Malcolm Needs

My pleasure. :D:D:D:D

Who are "They"? Let me guess, "They" are people that have never worked in a Blood Transfusion Laboratory, are never likely to work in a Blood Transfusion Laboratory, but think that "They" know better than anyone who has worked in a Blood Transfusion Laboratory all their life. I could tell you of a similar situation myself, but if my own bosses read the post, I would be sacked. :mad::mad::mad::mad::mad:

Well, the point is, in this case, that it would be a good idea to "prove" the specificity before things get out of hand, but this is very easily done by using several samples of group A1 red cells, treated with a proteolytic enzyme. Assuming that I am correct (that the specificity is either anti-H or anti-HI), then all of these should be compatible. In such a case, therefore, all group A units of blood would be compatible, and providing blood would be simple (i.e. group A). That having been said, however, unless the patient were to undergo profound temperature loss ( and I can't see any reason why she should) group O blood would be perfectly okay for transfusion, because: 1. the transfused blood would soon reach body temperature (and so the anti-H or anti-HI would be irrelevant, and 2. do not forget that the "main" incompatibility was detected with enzyme-treated red cells and, of course, the red cells being transfused have not been enzyme-treated. This antibody would be clinically insignificant. :D

I had a telephone conversation with a friend of mine (who wants to remain anonymous - probably doesn't want to admit to anyone that he/she is really a friend of mine!!!!!!) about this. He/she knows a lot more about the subject than do I (which, come to think of it, is most of the world's population) and he/she said the following. It's all to easy to get bogged down with what to label the different stages of incident reporting and error management. The interpretations above are valid, but other other QA experts might talk about; Correction - putting right what went wrong Corrective action - making sure what went wrong does not happen again Preventive action - making sure you prevent other similar errors in other areas. Eg. Fridge failure resulting in components stored at the wrong temperature for 6 hours Correction - getting fridge fixed, discarding components, replacing lost components Corrective action - ensuring alarms work and that staff understand procedures for actioning the alarm and dealing with the problem Preventive action - ensuring all fridges, freezers and incubators have been serviced within the required timeframe, that all alarms work and that the procedures for dealing with alarms are robust when applied to all the equipment. As you can see depending on who you're asking, correction and corrective measures can be interchangeable terms, as can corrective action and preventive action. In the UK regulations, the generic term "corrective measures" is used to incorporate correction and CAPA. What's important is that you have a robust system for spotting errors and dealing with them. Usually a regulator will be less concerned with how you manage your incident reporting system as opposed to whether you comply. There are as many ways to crack a nut as there are to comply with the regulations, and where there might be "best practice" a regulator will not give a non-compliance if your system works. The BCR might well ask how long the CAPAs have been open, but this information on it's own is unlikely to trigger an inspection. The regulator may well ask for further detail, but as long as you have a justifiable reason for doing so, this should satisfy them. They would be far happier that an incident is still open after 3 months because several procedures needed to be rewritten, validated, document controlled and trained to all staff than to have the same incident closed after one week when the member of staff responsible re-read the old SOP. So, whether you split your documentation into sections and close down the incident in stages, or whether you close down the incident in one go, it is entirely the choice of the reporter. I hope this helps. Malcolm :D:D:D:D

The answer to your first question is, I don't know for certain, but I don't think so. The significance of mixed-field reactions is that, if these were present, it would prove that at least some of the transfused red cells were still present in the patient's circulation. It is highly unlikely that transfused blood would be of exactly the same types as the patient throughout from Rh to Kidd ( although it is not entirely impossible) and so one would expect to see some mixed-field reactions with some of the grouping reagents (although not Lewis, because transfused red cells take up the Lewis type of the recipient, as do Ch and Rg types come to that!). The fact that there was no evidence of mixed-field reactions strongly suggests that the transfused red cells are no longer in the circulation (although this does NOT necessarily mean that they have been destroyed by an antibody in the patient's plasma), but it does mean that the antigen typing will be that of the recipient. :):)

Hi rravkin@aol.com, No, the inconsistency of the antibody is not likely to be due to the apparent newness of the antibody; it is much more likely to be due to the specificity of the antibody and the nature of the antigen. Although fully recognised as a Blood Group System by the ISBT, both Ch and Rg are antigens that are adsorbed onto the surface of the red cell membrane from the plasma, rather than being an integral part of the red cell membrane. The Ch and Rg antigens are, in fact, C4B and C4A of the complement system, so that, if you are Ch- (as all good people should be!!!!!!!!!!!!!!), you lack C4A, and if you are Rg-, you lack C4B. The strength of the Ch and Rg antigens can vary greatly from one individual to another (hence the apparent difference in reaction strengths with different red cells and the same plasma), but, in addition, Ch- and Rg- are not all true Ch- or Rg-! This seems a weird thing to say, but there are 6 different Ch antigens and 2 different Rg antigens (together with a WH antigen that also belongs to the system). Therefore, the cell that only reacted weakly could be negative for one or more of the Ch antigens, but positive for the others, or negative for one of the two Rg antigens. The negative results with ficin-treated red cells does rule out the presence of an anti-e (although there are extremely rare examples of some Rh antibodies in the literature that only react by IAT, and not with enzyme-treated red cells - I published a poster myself [with others] a few years ago at a BBTS Meeting concerning an anti-E that reacted in just this way). I hope all that helps. Malcolm :):)

Hi klsmith, Actually, this is not that an unusual situation in a group A patient (reactions with all enzyme-treated red cells, DAT negative and auto negative) and the key to it is in the ABO group of the patient and the ABO group of your screening and panel cells. The patient, being group A, will have most of her H antigen (L-fucose) "hidden" by her A antigen (N-acetyl-D-galactosamine), whilst the screening and panel cells, being group O, will have all of their H antigen exposed. The patient can, therefore, make an anti-H or anti-HI that will appear to be an alloantibody (although it is actually an auto-antibody) that will react very much more strongly with group O red cells (particularly those that have been enzyme-treated) than group A red cells. Hope that helps. Malcolm :):)

I totally agree about the possibility of HLA antibodies, particularly as it is likely that this patient will have been transfused in the past, and will almost certainly be transfused with platelets in the future. One reason why the platelet count might not have gone up as expected (apart from consumption and HLA antibodies) is that the high-titre anti-A would also have sensitised the group A platelets (both those transfused and those native to the patient) and these could have been removed from the circulation). :confused::confused:

Very true David.

In that case then, as long as the present screen by IAT is negative, and there is no history of a clinically-significant antibody, BCSH Guidelines do not require an IAT cross-match to be performed, and I would be quite happy to cross-match by "immediate spin". However, I do know of some places that will take units off the shelf in such a situation (as if they are performing electronic issue, but without the computer) and this is an absolute NO, NO, as far as I am concerned (and as far as BCSH Guidelines are concerned). :eek::eek:

Tee hee!!!!!!!!!!!!!! :haha::giggle::haha:

Do you mean do an "immediate spin" cross-match instead, or do you mean just grab a unit off the shelf? :confused::confused:

You have to remember that I am talking purely from a UK point of view here. I don't know what goes on in the rest of the world. The answer is that SAG-M blood is never used for neonates, except in extremis. I know of one case where we had to supply SAG-M blood for an exchange transfusion on a bay whose mother had an anti-k, and the only fresh liquid blood available (it was too urgent for frozen blood to be reconstituted) that was K+k- was a SAG-M unit. Actually, the baby showed no sign wahtsoever of hepatotoxicity. In other words, SAG-M blood is reserved for children over a certain age (which escapes me at the moment I'm afraid) and adults. It would only be used for babies when the hospital is completely out of packed red cells, and they are too far away from their Blood Centre to get more too them, even using "blues and twos". It hardly ever happens, I might add. When we are using packed red cells, the expiry date is much shorter (like you, I think it is 7 days), it has to be CMV- and has to be HbS-. If it is being used for a top-up, rather than an exchange or an IUT, it does not have to be irradiated in the UK unless the baby has had an IUT before birth, is extremely premature, or, of course, the donor is a close relative (although some hospitals do prefer to have it irradiated at all times). :)

A SAG-M unit is unit of packed red cells that have been resuspended in the additive solution sucrose, adenine, glucose and mannitol. This is a "cell preservative" that "preserves" the red cells by allowing them to metabolise (if I remember correctly, and this is going back decades, via the Rappaport-Luberen shunt of the citric acid cycle - not too sure of the spelling). The problem is the the mannitol is supposed to be hepatotoxic to babies. It will be CMV-, HbS-, but it can be used up to 35 days (I think it's 35 days anyway), but it will not necessarily be irradiated.

Hey, and there was I thinking it might just be sample from one of TimOz's countrymen!!!!!!!!!!!!!!! :rolleyes::rolleyes:

Sounds good to me! I don't think there is anything else you could do at the moment, except, as you say, give R2R2, K- as a precaution. Ficin works just as well as papain for what I was saying. :D:D:D

The first thing I would do would be to test the patient's plasma/serum with papain-treated red cells. Apart from some very rare cases of extremely avid antibodies, the Ch and Rg antigens are desroyed by the action of papain, but at the same time, papain will enhance the reaction between anti-e and the e antigen. I would also type the patient for other antigens, M, N, S, s, Fy(a), Fy(, Jk(a) and Jk( for two reasons. Firstly to see if there are any mixed-field reactions, showing that some of the red cells from the transfused units are still present (it is extremely unlikely that the units given would be exactly the same phenotype as the patient). Secondly, to see what other antibodies the patient could make in the future. Certainly, it is doubtful that an anti-Ch or an anti-Rg would have caused all three units to have "disappeared" from the patient's circulation (sporadic reports of "transfusion reactions" caused by these antibodies suggest more of an HLA-type reaction, rather than a delayed haemolytic transfusion reaction), but I wonder if there may be another cause for the units to have "disappeared" so quickly (if, indeed they have), such as a chronic bleed, compensated by an active marrow. I wonder if you could tell us what the underlying pathology from which the patient is sufferring to require transfusions so often? This may give a clue. All of that having been said, if we have a patient who has anti-Ch or anti-Rg, we would tend to give them Rh and K matched blood in any case, just so that they are not stimulated to make further atypical alloantibodies. I have recently read a paper that stated 20% of patients who have produced one atypical alloantibody go on to make further antibodies when transfused, but almost all of these had a specificity within the Rh Blood Group System (C, c, D, E or e) or were anti-K. Only a very small minority produced antibodies directed against antigens in other blood group systems. I hope that helps in some small way. :):)

Thanks conwaysbb. I think that it is vitally important in such a case to differentiate between a delayed haemolytic transfusion reaction causing a less than expected increase in haemoglobin and other possible causes, such as your patient's disease state. A positive DAT alone after a transfusion, even if the DAT were negative prior to the transfusion, is not diagnostic of a delayed haemolytic transfusion reaction. Nor is a positive DAT and a less than expected rise in haemoglobin. The former could just be what George Garratty terms a delayed serological reaction (where tests such as the DAT become positive, but there are no clinical sequelae for the patient). The latter may be a combination of this and a less than expected rise in haemoglobin due to the patient's disease state. If it were the latter, then you would still need to keep the patient in for a longer period, and perform all the extra tests, but it might well prove that the transfusion was coincidental, rather than causitive. :confused::confused:

Oh, I agree, that is what you should do, but I would still put in a strongly worded and well-argued complaint that the kit is NOT testing the proficiency of the entire test. :mad::mad::mad:

I totally agree. Thanks Cliff. :D:D:D:D

Well yes, obviously for tests like an FMH and a KB, but I (and I think Peter Issitt) was talking about a serological test. :)

I would totally agree with what you say in the last part of this post. One only has to think of the number of anamnestic responses to a weak anti-Jka in the literature. What kind of reaction was it? Was it a full-blown acute transfusion reaction with rigors, dark/black urine, etc, a lower rise in Hb than would be expected, or what? I ask out of interest, rather than trying to catch you out (in case it reads like that). :confused::confused:

There was a survey done in the UK a couple of years or so ago, which raised some horror stories about observations during transfusion. One that stuck in my mind in particular was of a neonate being transfused in a side room, with no observations being done (and, of course, the poor little thing couldn't shout if he or she was feeling unwell). I know babies don't have their own antibodies usually (although some are born with their own ABO antibodies), but that does not mean that they have not got unrecognised maternal antibodies in their circulation, or that they cannot become over-loaded, etc, etc. :eek::eek:

In at least one of his three editions of his book Appkied Blood Group Serology, Peter Issitt wrote that microscopes should be banned from a Blood Transfusion Laboratory. I agree with him 100%. :):)

My immediate thought is, why are they sending out samples like this? The DAT involves washing, and always has done, unless it is being performed in column agglutination technology, in which case it usually involves centrifugation, followed by resuspension in the chosen medium, to the chosen concentration of red cells. If they want to ask you to perform a realistic test, and that, I would have thought, is the whole point of the test, then send out a whole blood sample, with the (presumably) IgG antibody sensitising the red cells and in the plasma; otherwise, what are they testing other than the AHG? :confused::(:confused: