Malcolm Needs

Well, no not really, because you can't perform an IS in a card. Even if you only incubate for a couple of minutes, you still need to centrifuge for about 10 minutes, whereas with tubes, you would incubate for a couple of minutes, and then centrifuge (low) for about a minute (or less). This is why I can never understand Hospital Blood Banks who sy they cannot perform IS because they haven't got tubes, centrifuges, SOPs, etc, and yet are major trauma receiving hospitals; it doesn't add up to me - sounds like an excuse! :confused:

Well, what I am saying is that if there is any suspicion whatsoever that there is microbiological involvement, the blood supplier should be informed immediately. As to who should perform the culture, I think it would be best to get a decision from the blood supplier's Microbiological Consultant at the time, rather than me trying to say here, and probably making a complete horlicks and getting the answer wrong! (NOT that unusual, as you know!). :eek::eek:

Nice idea, but exceedingly difficult to do. There are so many other causes of these kinds of reactions (e.g. hyperhaemolysis in patients other than sicklers) that it is usually impossible to identify such cases other than be trial and error (and the trail and error could be a really big error for the patient). :confused::confused:

Sorry scodina, I am in the same position as Rashmi over this one; I haven't got a clue either. Having been at a meeting on Friday, however, I can answer Rashmi's question a little more fully. In most cases, a reaction caused by microbiological contamination strongly resembles a full blown acute immediate transfusion reaction. Therefore, in such a case, if you cannot detect any serological reason for the reaction, suspect microbiological contamination immediately, and let your blood supplier know immediately, so that any other blood components made from the same donation can be put into quarantine immediately. An awful lot of "immediatelys" here, but speed is of the essence. :)

If you are performing an "immediate spin" cross-match, then, presumably, you would be performing this in a tube, rather than by column agglutination technology (CAT). This would detect ABO IgM antibodies, in almost all cases, as long as there is a slight incubation period of a couple of minutes or so (which is why I always put "immediate spin" in quotation marks [whenever I remember so to do - it's an age thing]). If you look back at various NEQAS (for those not in the UK, this is the National External QUality Assurance Scheme) reports, they do suggest that a short incubation time is essential to detecting such antibodies. In addition, addition of EDTA to the process helps, but, of course, these days almost everyone uses EDTA samples anyway. CAT will detect IgM antibodies actually, as these will sensitise the red cells during the incubation period, thus causing agglutination, and the agglutinated red cells will stay at the top of the column (in most cases). Whether this is true of other "new-fangled" techniques is another thing entirely! I agree with you entirely that we have to be ready to adapt the antigenic make-up of our screening cells, with our changing ethnic mix of patients, but in the UK (for the moment anyway) we are lucky that most of the ethnic minorities lack a high-frequency antigen more often than they stimulate an antibody against what is a low-frequency antigen in our native population (whatever our native population may be; Saxon? Viking?, Jute? Norman?). I also agree that haemovigilance schemes, such as SHOT and/or SABRE are probably our best allies in this. :):)

I have heard of this scary situation twice before in 37 years of my professional life; both involving Rh antibodies (although neither was proved by PEG because it wasn't around at the time, but only by the fact that the patient, in each case, tolerated antigen negative blood). One was described in a US patient either by Malcolm Beck or George Garratty in a meeting in the UK (both were lecturing, and I can't remember which of them described the case), and one by Bill Chaffe in the UK. Both involved anti-E. It really is incredibly worrying when one hears of these cases. :eek::eek:

Ah, this one is an easy one. It's just a bit of UK jargon! NISS is normal ionic strength saline. LISS is low ionic strength solution. By the way, I entirely agree with the feelings that you posted after this. I think that you were very brave, but absolutely right. :D:D:D:D

This is an excellent idea on the face of it, but I think that it would be hugely expensive. :confused:

No, not really. Rh antibodies that do not react with enzyme-treated red cells are really exceptionally rare (of the same order of rarity as an Rh antibody that stimulates the complement system - and I have only ever seen one of those, when I was working at the International Blood Group Reference Laboratory as a very Junior Technician). I think that it is quite reasonable to assume that all but the rarest Rh antibody/antigen reactions are enhanced by enzyme treatment of red cells. It's me talking about zebras again!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! :D:D:D:D

I am extremely pleased that you agree with my posts, especially the bit about all the best people being Ch-!!!!!!!!!!!!!!!!!!!!!!!!!!!! :D:D:D:D

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: