Malcolm Needs

Yes, it is extremely scary! We usually recommend not transfusing if at all possible, but if it is deemed necessary, using IVIG and methylprenisolone cover. This seems to help.

I'm sorry shily, but to say that gel technology is safer than the LISS tube IAT is totally untrue. AMcCord is absolutely correct in saying that it may be more sensitive, but you lose specificity. If the LISS tube IAT is so dangerous, do you think that it would be the first line of attack at the International Blood Group Reference Laboratory and would have been used by such luminaries as Dr. Carolyn Giles, Dr. Elizabeth (Jan) Ikin, Dr. Kenneth Goldsmith, Dr. Robert Race, Dr. Ruth Sanger, Dr. Arthur Mourant, to name but a few, and do you think it would still be used by people such as Joyce Poole? :mad::mad::mad:

True, it shouldn't really matter, but when the inspector demonstrates that they do not have even rudimentary knowledge of what the laboratory does, but still insists on changes being made to fundamental processes, with no demonstrable improvement (and change should only be made if it can be measured), it most certainly does matter.

IN the UK, the BCSH Guidelines for compatibility procedures (2004) state: "It is essential that the request form and sample contain the following minimum patient identification (PIN) as described in BCSH Guidelines for the administration of blood and blood components and management of transfused patients (BCSH, 1999). (i) surname/family name (correctly spelt); (ii) first name(s) in full; (iii) date of birth (not age or year of birth); (iv) hospital number/accident and emergency number/NHS number/major incident number (in certain instances, such as a male partner of a pregnant lady, we will also accept an abbreviated address as an identifier, if none of the other criteria listed in iv are available - MN). The sample should be dated, labelled and signed by the person taking it. The request form should also include the patient's location and the location where blood units should be sent and the signature of the person making the request.... Provided that sample labels are printed and attached to the bottle next to the patient at the time of phlebotomy, hand-held bedside/chair-side scanners and printers utilizing bar-coded wristbands may increase security during phlebotomy. Labels produced in this way are not the same as addressograph labels, which are more likely to result in inadequate checking of PIN at the bedside (Sharp and Cummings, 2001). It is therefore recommended that any labels preprinted away from the bedside should not be accepted for either grouping or pretransfusion testing samples.... Samples received from trauma or unconcious accident and emergency patients are unlikely to contain the full PIN. There, however, must be at least one unique identifier, usually an accident and emergency or trauma number, and the sex of the patient identified on the sample label. The sample should be taken andlabelled and the form and sample should be signed by the prescribing medical officer as one continuous procedure. In the event of there not being at least one unique identifier on the sample in a life-threatening situation, group O blood only must be issued until a suitably labelled sample is available. If the patient is a female under 60 years old, group O D-negative blood should be given." When I was working in a hospital, we stuck rigidly to this guideline. Now I am working in a Reference Laboratory, many miles from some of our referring hospitals, and where it may be difficult to obtain replacement samples (particularly in an emergency), we may have to work on the samples under a concession form, if the mis-labelling is minor, signed either by one of our own Consultants or, in certain cases, me (as the Reference Service Manager). As all of our samples come through the hospital Blood Banks before referral to us, it is surprising how many we have to reject, or have to work on under concession! :rolleyes:

It isn't for the MHRA either. Almost all of them come from the pharmasuitcal industry. WIth the CPA, it is slightly better, in that they tend to be Biomedical/Clinical Scientists or Consultants, but, they don't necessarily have had to have worked in Blood Transfusion or even Haematology. :mad::mad::mad:

That's terribly cynical SMW, and I agree entirely with everything you say!!!!!!!!!

Oh John, I do apologise, but I'm going to have to disagree again! Anti-D was most certainly the first antibody studied for HDN, but it is by no means the only antibody to have been studied. Anti-c has also been studied extensively. Over here, for these two antibodies we do not perform titrations, but rather we perform quantification. All below assumes that the baby's red cells express the antigen (otherwise, of course, it would be nonsense). For anti-D, if the level is below 4IU/mL, there is little chance (not no chance, but little chance) of an affected baby. Between 4 and about 15IU/mL there is a moderate chance of an affected baby. Between 15 and 20IU/mL, there is a high chance of an affected baby. Over 20IU/mL, there is an almost certain chance of hydrops, unless there is intervention. For anti-c, up to 7.5IU/mL, there is little chance (once again, not no chance, but little chance) of an affected baby. Between 7.5IU/mL and 20IU/mL, there is a moderate chance of an affected baby. Over 20IU/mL, there is an almost certain chance of hydrops, unless there is intervention. We titrate all other antibodies, and are not really worried, unlesws the titre reaches well over 32, but in the case of anti-K and anti-k, we know that the antibody titre does not have to reach these stellar titres before severe HDNF can occur, because the Kell antigens are expressed extremely early on the red cell precursors in the bone marrow (much earlier than the Rh antigens). There are other antibodies that have been studied though (not least what used to be called anti-Tja, which caused recurrent spontanious abortions in the first trimester). Sorry John. :redface::redface:

It's because, if the unit is infected, the parents won't lose both twins or all three triplets.

I agree with you L106; performing a DAT on all cord samples is extremely excessive. You are quite right that, if anti-Fya is eluted (as long as the last wash control is negative) then there is no need to treat the baby's red cells and then group them. But I really agree with you wholeheartedly about the fact that I can't spell! :D

Hi Chun-kwok, I think there can be no better explanation than to quote directly from Geoff Daniels book, Human Blood Groups 2nd edition, 2002, Blackwell Science, "Abantu is another variation of Aend, found in about 4% of group A black South Africans (paper 245 cited), and in up to 8% of Bushmen and Hottentots, the ethnic group in which the Abantu gene may have originated (paper 301 cited). Anti-A agglutinate Abantu red cells more strongly than Aend cells." Paper 245 is, Brain P. Subgroups of A in the South African Bantu. Vox Sang 1966; 11: 686-698. Paper 301 is, Jenkins T. Blood group Abantu population and family studies. Vox Sang 1974; 26: 537-550.

Welcome Andy. Love the quote about the rings (but I don't think I'll pass it on to my wife - it could be very painful indeed!).

Hi Jeanne, I am not sure to which paper you allude, as there have been several that have come out of the UK on this subject (many by my own Consultant, Dr. Nay Win). The possible mechanism for IVIG (and steroids) is discussed in some detail in: Win N, New H, Lee E, de la Fuente J. Hyperhemolysis syndrome in sickle cell disease: case report (recurrent episode) and literature review. Transfusion 2008; 48: 1231-1238. I hope this is of help.

Then, on this point John, we must agree to disagree, but the thread has certainly brought about some lively discussion and identified the fact that there are (at least) two schools of thought on the subject, with each school adhering to their own ideas on the subject in an equally rigorous manner.

I agree with (almost) everything you say here Mabel. The only slight disagreement I might have with you is in the predictive nature of any anti-A that might be eluted. Whilst I would totally agree with you that titration of IgG anti-A (or anti-B come to that) is a waste of reagents, time and money, if the index neonate is affected in any way by the maternal IgG anti-A (albeit subclinically), the next and subsequent group A babies borne by the same mum will be affected at least as much as the first, if not more so, and at the same gestation period or earlier, so its demonstration does alert the neonatologist to watch for potential problems in future pregnancies. I also agree that the DAT due to ABO IgG antibodies can often be negative at birth, but equally as often, the DAT becomes positive after a couple of days. To "get ahead of the game", so to speak, it is sometimes worthwhile putting the cord sample in a fridge for a couple of hours and then examining it macroscopically for agglutination. IgG ABO antibodies can cause agglutination, and this agglutination is sure as hell not going to be caused by a "normal" maternal "cold" agglutinin, such as anti-I, anti-HI, etc. Just a thought.

Which one wil sort it out Rashmi? A single system or you retiring (remeber, you've just had yet another birthday???????????!!!!!!!!!!!!!!!!!!!!!!!!!!!!! SORRY; COULDN'T RESIST IT (BUT SHOULD HAVE DONE)!!!!!!!!!!!!!! :rolleyes::rolleyes:

Absolutely correct John, and I should have mentioned it.

As long as the unit is being given as a "top-up" transfusion, and the neonate was not given an IUT, and is not very small for age or very premature, then, yes, you can use blood up to its normal expiry, with no particular problems with, for example, potassium ion concentration in the suspending medium. It is also important that one complete unit is reserved for one neonate. There are two reasons for this. Firstly, and most commonly quoted, is the desire to minimize the exposure of the neonate to "foreign" antigens (although I've often wondered about this, as the neonates immune system is so immature that he/she is unlikely to be immunized, but may become "used" to the foreign antigens, and would not necessarily make antibodies to these antigens when challenged in later life). The second (more gruesome) reason is that, if the donation is infected by a bacterium, if it is transfused to one neonate, rather than several, only one neonate will die, rather than several. There are good arguments that all cellular blood components transfused to a neonate should be irradiated, on the grounds that, just by chance, there may be a shared HLA haplotype, and also by chance, some viable T cell lymphocytes present, that may result in transfusion associated graft versus host disease. This is particularly true with premature neonates, when their own immune system is compromised by age. One has to remember that not every single unit of cellular components will have been tested to ensure that the leucodepletion has "worked", and that one may slip through that has a near normal leucocyte count (and, of course, they will, almost by definition, be "fresh" blood components). All that having been said, the literature to support this theory is pretty scant! As for CMV negativity, unless you have tested the mum to ensure that she is CMV negative, and has not, therefore, passed on the CMV virus to her baby, and taking into account that, unless the CMV testing is performed by nucleic acid testing, there is approximately a 2% false negativity for serological testing for CMV, and looking at the data coming out of Scandinavia (admittedly by Pall, who make the filters) then leucodepletion is as good as, if not better than, CMV testing. PLEASE NOTE THAT, AS ALWAYS, THIS IS A PERSONAL POINT OF VIEW. :):)

I am in total agreement with you eric1980, and do not agree with all the points made by AMCWHC. It is not just a question of those patients with an antibody. ALL patients (except most of those who are group AB) have antibodies, and very dangerous ones, called anti-A, anti-B and anti-A,B. If you read my post in the thread on witnessing blood withdrawals AMCWHC, you will see a horror story that (nearly) took place at an (unnamed, but world famous) London Teaching Hospital. Now, I am not saying that transferring all of the patient records would have prevented this, but it would have minimized the chances. Yes, it is expensive (and a pain in the ****) but, as eric1980 says, it is probably less than the price of being sued. :eek:

In a way though, the anti-C3d is irrelevant. If there is an IgM element to the antibody, as well as an IgG (as can often happen with an antibody produced de novo during a pregnancy) you may still get agglutination prior to 37oC incubation.

No, not necessarily. We use cassettes that contain anti-IgG and anti-C3d (although cassettes containing anti-IgG only are available). But we often find that when an IgM antibody is present, particularly if it reacts better in the cold (well, cool) as most of them do, the sensitisation occurs before we put the cassettes in to incubate at 37oC, and you then get agglutination when you centrifuge. This is why did so much comparative work and change control. With experience, you can usually tell (although I'm sure we don't detect every time there is an IgM present).

True, but I did say "if at all possible".

galvania, that's just showing off!!!!!!!!!!!!!!!!!!!!!!!!!! What does it mean, for those of us who can only just speak English and have trouble with that if there are more than a couple of syllables?????????!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

Yes, thinking more about it, I also agree with galvania.

clmergen, I wouldn't mind betting it was a mixture of an IgG and IgM, and that you were detecting the IgM in the gel (same specificity, but a mixture of immunoglobulins).

Very true. I tend to forget that over this side of the puddle!