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I sometimes think that management monitor the temperature in many of the laboratories where I have worked by seeing how many of the staff faint. If it is more than 50%, it is regarded as too hot. Anything less than 50% and it is okay!!!!!!!!!

Reminds me of a donor we had once when I was a reference lab sup. He had donated 12 times as O NEG. The next time he donated, they picked up weak typing with Anti-A,B and with further testing, turns out he was a very weak subgroup of A! Unbelievable. I agree with A subgroup. I see a lot of people want to automatically classify the subgroup....but without further testing, that is actually erroneous. Best to just leave it at subgroup. Brenda Hutson, MT(ASCP)SBB

There was a period of time it was so hot in our lab due to construction issues that a door to the main hallway had to be open or our chemistry analyzers wouldn't work. It was still tropical with the door open. We threatened to work naked, in view of everyone that passed by. We did get a couple of big fans after that until the problem could be resolved. As for monitoring temps, we do pretty much what Scott does.

Another good source is towards the back of the Blood Group Antigen FactsBook.

Please discuss the importance of donation with this donor, and register the donor with the American Rare Donor Program. I remember having a pregnant patient with anti-Rh17. I believe there were only a couple of units available nationally. If I remember correctly, we had to resort to autologous donation, iron, and EPO.

Just for info - CellStab is not a LISS solution and Diluent 2 is - but you can't store red cells in dil 2 because they will haemolyse after a while

Definitely an A subgroup. But clearly with an anti-A1 so best to transfuse group O. Tube is actually MORE sensitive than gel for ABO

The rationale for irradiation is that congenital cardiac anomalies are associated with immune deficiency syndromes. Some of these are not easy to diagnose in the first months or even first few years of life. Our own policy is for infants and younger children (<5 years of age) to transfuse only irradiated, ABO identical red cells and the first red cell is washed. We only wash red cells <21 days of age because of data that washed red cells are associated with less inflammation and clinical complications if of shorter storage (<21 days), but greater inflammation and poorer clinical outcomes if >28 days of storage. Pediatr Crit Care Med. 2015 Mar;16(3):227-35 Despite the long standing policy of using "fresher" red cells for these patients, the safest red cells are probably about 10-21 days of storage according to our data and meta-analyses of the randomized trials. Fresher red cells are associated with a higher incidence of post-operative infections, the major cause of morbidity and mortality in this population. I would never transfused red cells <7-10 days old to any patient at this point in time. We have some mechanistic data that is as yet unpublished that the mechanism is dysregulation of oxidation/reduction in freshly collected red cells. Blood. 2016 Jan 28;127(4):400-10 Washed red cells reduce the risk of post-operative inflammation in the only published randomized trial and there is also a trend towards reduced mortality in the washed arm of the study. This may be controversial but it's the only data we have to go on, certainly the only randomized trial. Pediatr Crit Care Med. 2012 May;13(3):290-9.

The reverse grouping red cells in the UK often react with an anti-c. I would be happy (on the evidence you give) to transfuse c-, E-, K- cross-match compatible blood. As you KNOW that the patient is group A, I would ignore the bit about giving group O blood, which is totally over the top.

I can see no reason why you should not transfused D Positive red cells.

That would be like back when everything was manual and we had multiple racks of reagents out being used by more than one tech. Every rack had to be QC'd.

I have found most of the standard blood bank reports useless for transfusion review. I don't specifically remember data mashed up and becoming unreadable, but it is difficult to do a proper review with the multi-line reports that they give you. I had my NPR writer develop a transfusion review report for me which pulls all of the data I need in a semi-colon delimited format. I download this report, export it into Excel, and then each transfusion is on its own line with headings that I can sort any way I need. This has been a lifesaver!

It is 2 different systems. they both need to be QC'd. Had this problem at a recent client's facility. Talked to the regulatory folks (JCAHO in this case). Both systems need to be QC'd for the testing performed using them.

The D--/D-- or D../D.. phenotypes (the two are almost synonymous, but the D--/D-- type is negative for the Evans antigen, whereas the D../D.. type is positive for the Evans antigen) are both EXTREMELY RARE. Unfortunately, these individuals have a nasty habit of producing anti-Rh17 (essentially, an antibody directed against the C, c, E and e antigens), and can only safely be transfused with units that are themselves D--/D--, D--/D.. or D../D.., and if these are not available, units of Rhnull blood. An exciting find, but I wish you luck!

FDA and AABB had gone back and forth over the years on storage vs transport. In the past few "Ask the FDA" sessions I've been at during the AABB Annual meetings both FDA and AABB have said coolers are transport. People even brought up newer cooler technology reminding them that coolers can be out of the blood bank for an extended time. We validate our coolers to hold temp at 1 - 6. We do not take temps every 4 hours.

Yes. Our OR nurses document every four hours. If the cooler temp reaches 6 degrees C, they call and request a new cooler with fresh blocks. We have quite a few cases that easily exceed four hours. We also put temp indicator stickers on each unit to make sure they weren’t left out of the cooler. We validated at RT, Trauma Bay (warm extreme), and CV surgery suite (cold extreme). We did those for both maximum (6 units) and minimum (1 unit). Message me if you need more specifics!

It is important to remember that there is a sort of continuum between the various A types (including A1 and A2) in terms of the number of A antigen sites expressed per red cell, and that there is no such thing as an absolute A1, absolute A2, absolute A3 and so on and so forth. In addition, of course, the lectin Dolichos biflorus is NOT an anti-A1, but is a lectin that "recognises" the A antigen, the Tn antigen and Cad antigen, as well as the A1 antigen. It will not recognise the A antigen if it is diluted correctly, but every now and again, there will be an "overlap" between a "strong A2", and a stronger than normal Dol. b. reagent. In addition, there are people who are Aint, or A intermediate, who are somewhere between an A1 and an A2. SUch people usually hail from the south of the African continent, but not always. As we are looking at ABO, I am not for one minute surprised that the reaction strength increases with cold incubation. The next thing to remember is that, with gel, it is all but impossible to add the reagents to the reaction chamber so that they remain exactly at 37oC, which means that IgM antibodies, such as anti-A1, which it looks like this pregnant lady has in her circulation, will sensitise A1 red cells prior to true incubation at 37oC, but will not elute quickly enough to give negative reactions after 37oC incubation, particularly after centrifugation. Anti-A1 is NOT clinically significant, unless it reacts STRICTLY at 37oC, and this can really only be shown by a pre-warming tube technique, in which case A2 blood (or other A subtypes, such as A3, Ax and Am) can safely be transfused, keeping your precious group O units for group O recipients. Anti-A1 has NEVER been implicated in clinically significant HDFN. None of this is pregnancy related.

Yes, frequency, incidence and prevalence are all interchangeable with either "high" or "low" before any of them. For some reason (I know not why), low prevalence has suddenly become the "word of the day", but there is no particular reason for this (as far as I know). Those low prevalence antigens within the 700 series, and, come to that, the high prevalence antigens within the 901 series, are, as you say, placed there as they do not belong to any known blood group system. However, do not run away with the idea that all low prevalence antigens are in the 700 series, and all high prevalence antigens are in the 901 series. The antigen KREP, of the Diego Blood Group System has only ever been reported in one Polish individual and one Slovakian individual, and yet it is not in the 700 Series of antigens. Conversely, and as far as I know, DOLG of the Dombrock Blood Group System has only been found to be negative in one Sri Lankan woman, and yet is not in the 901 Series of antigens. This is because, in each case, the chromosome and the particular loci have been identified, and they are mapped to known areas of the genes which encode each of these antigens.

When I was working in RCI at NHSBT-Tooting Centre, we used to store our liquid reagent cells in Cellstab, but wash them an resuspend them in Dil2 for use. We found the reactions we got were much, much sharper (I don't mean that the reactions were more sensitive to detecting weak antibodies, although we believed that they were, but that it was far easier to "see" the reactions as clear reactions, rather than "fuzzy" reactions), and, in addition, it meant that we didn't detect reactions caused by antibodies directed against the preservatives in the Cellstab. We were able to show this with multiple photographs. Despite all the evidence, we were told that we couled not continue to do this, as we were not standardised with the other NHSBT RCI Laboratories (standardisation is everything these days, even if it means dumbing down, rather than bringing everyone up to an excellent standard, and because it was more expensive. The only problem was that we were able to show that it was actually LESS expensive, because it meant less testing, and no testing for antibodies against preservatives. This did not fit with management theory, however, and so we had to stop. Since then we got "fuzzy" reactions, leading to many cases of repeat testing, and many cases of antibodies against preservatives and, hence, more expensive testing in terms of reagents, staff time and fairly simple investigations into moderate or even complex investigations, but hey, what did we know! At least we are now standardised (and expensive)!

Very true.

Yes, but c.261delG characterizes deleterious O alleles and is not present in alleles A. If this mutation is homozygous, I would suspect a cross-reactivity.

Well, one reason why anti-c is detected more often in the reverse group than is anti-e is simple that anti-c is a much more common antibody specificity than is anti-e. There are two possible reasons for this. Firstly, apart from the rarer c Negative Rh types, the most common c Negative Rh type is R1R1 (all the best people are R1R1!!!!!), and the R1R1 is not that rare, but, except in certain circumstances, it would be unusual to deliberately give an R1R1 individual R1R1 blood, unless they have already produced an anti-c. This means that such individuals are often given blood that is c Positive (R1r, R2r, R1R2 and rr) and so their immune system is challenged. Secondly, apart from the rarer e Negative Rh types, the most common e Negative Rh type is R2R2, and the R2R2 is comparatively rare, and, except in certain circumstances, it would be unusual to deliberately give an R2R2 individual R2R2 blood, unless they have already produced an anti-e, or anti-C. This means that such individuals are often given blood that is e Positive (R1r, R2r, R1R1, R1R2 and rr) and so their immune system is challenged. That having been said, anti-c is, as I said above, much more common than is anti-e, and so this also suggests that the c antigen is much more immunogenic than is the e antigen, and all of this serves to show why anti-c is detected with the reverse grouping cells, more often than is anti-e. This is the kind of thing about which Geoff was writing. As for your other question about E Positive units being given to patients with anti-E, you may be talking about patients with an auto-antibody that mimics anti-E, rather than someone with a genuine alloanti-E, but I would need a few more details to be certain.

It COULD be that the patient is a secretor, and is secreting sufficient A substance, which is then adsorbed onto the group O red cells, for some very strong anti-A reagents to detect this adsorbed A substance (remember that the patient will still secrete A substance throughout his life, as the secretion is not affected by the bone marrow transplant). This is a bit of a long shot, but I have seen it happen on very rare occasions.

I think because Rh antisera is usually not IgG and will agglutinate with cells in buffer cards so it is really not QCing the IgG activity in your IgG card.

Most states in the US do not require a license. I suspect after that it is up to the individual facility on what the requirements are. We require our techs to be ASCP certified, you might want to look into that.

We have order sets available to providers, but will go into action with a phone call for MTP and emergency release. The order does need to be placed for that to happen. The patient comes first. CAP specifically says that blood products the patient needs should not be delayed so as to endanger that patient by sticking to paperwork rules. The orders do need to be placed as soon as it is feasible, but sometimes some of those orders are placed by lab. Our procedures spell that out. TRM.40770 Life-Threatening Situations Phase II Adequate policies and procedures have been established for the investigation and handling of life-threatening situations (such as the use of uncrossmatched blood or abbreviation of testing) that include the written authorization of a qualified physician. NOTE: Written policies and procedures must be available to expedite testing for transfusion in a life-threatening situation. If an institution's procedure allows abbreviated testing in massive transfusion situations, records should indicate that the procedure was followed. Records must include the authorization by a qualified physician. (If approved by the institution and recorded in the laboratory's procedures, the physician responsible for the transfusion service laboratory may accept this responsibility.) If an incompatibility is discovered on completion of an incomplete crossmatch, the responsible physician must be notified in a timely manner and this notification recorded. 29 of 85 Transfusion Medicine Checklist 08.21.2017 Red blood cells released before testing has been completed must be conspicuously labeled as uncrossmatched on the tag or label. Records of completion of compatibility testing for units released uncrossmatched must be maintained. Evidence of Compliance: ✓ Records of emergency release authorization by a qualified physician REFERENCES 1) Food and Drug Administration. Current good manufacturing practice for blood and blood components. Laboratory controls. Compatibility testing. Washington, DC: US Government Printing Office, 1999(Apr 1):[21CFR606.151] 2) ibid. Records and reports. Records. Washington, DC: US Government Printing Office, 1999(Apr 1):[21CFR606.160]

My EXACT point on another thread. I think it is about time we all, and I mean ALL, told these people where to go, unless they can justify their rules.

I remember seeing a blurb about QCing each methodoly in use but can't find it in CAP. It might have been somewhere else. But CAP does say that QC is required for only 1 vial reagent/lot in use TRM.31400 Antisera/Reagent Red Cell QC Phase II There are records of acceptable reactivity and specificity of typing sera and reagent cells on each day of use, including a check against known positive and negative cells or antisera, or manufacturer's instructions for daily quality control are followed. NOTE: Unless manufacturer's instructions state otherwise, the following apply: ■ Each cell used for antibody detection must be checked each day of use for reactivity of at least one antigen using antisera of 1+ or greater avidity. ■ Typing reagents such as anti-D, anti-K, anti-Fy(a), etc. must be checked each day of use. ■ Anti-IgG reactivity of antiglobulin reagents may be checked during antibody screening and crossmatching. ■ Typing sera and reagent cells must be checked for reactivity and specificity on each day of use, including a check against known positive and negative cells or antisera. This checklist requirement can be satisfied by testing one vial of each reagent lot each day of testing.

Unfortunately, what you say is far from "universal". Certainly, it is unusual to see an antibody directed against a low prevalence antigen causing either HDFN or an HTR, but it is by no means unknown. For example, anti-Bea has caused very severe HDFN, and anti-Wra caused a fatal HTR only a couple of years back in the UK. In terms of the 901 series (and, come to that, anti-U of the MNS Blood Group System) it is possible that it is to do with the IgG subclass, but it is more likely to do with them being (occasionally) IgG2 and/or IgG4, but, as far as I know, this remains a theory, rather than having been proven.

They are from different clones and titer. We repeated the blood group using BioRad Newborn Card and it showed 2+ with anti-A,B but negative with anti-A.

Ortho On Demand has a three part series on Titrations that you might like. Ortho Clinical Diagnostics is pleased to present a Spotlight Series focusing on Standardization and Validation of Titrations in Perinatal Clinical Situations. https://presentations.akamaized.net/Shows/OrthoONDEMAND/Microsite/LoginPage.html

There are MANY more mutation than this leading to O alleles.

I prefer to call it an A subgroup. Maybe some human anti-A can do help, since it is polyclonal, not monoclone as our reagent anti-A.

I've seen anti-c reacting with the reverse grouping cells many times. I've only seen anti-e reacting like that a very few times.

We use fresh (less than seven days old) irradiated RBCs. We wash the units only if they are not fresh.

I just answered this question. My Score PASS  

"Tube testing is notoriously variable, while gel testing is believed to reduce some of those nuances. " Yes, but it is also - according to years of CAP survey results - routinely 1-2 endpoints higher on every titration run. So, make sure you are telling your physicians that your facility is doing titers with gel and that the actionable titers for their patients might be at higher endpoints than those historically with tube testing. "It does need to be reliable/robust and give the same end point each time, even with the acknowledged variations in serological tests (reagents, test cells, techs, etc.)" I wonder if the inspector would have been OK with procedures with this kind of control if it was used when there was no retained sample (no control avail) and not used when the new specimen was run in parallel with it's retained pair (internal control avail)?? I guess we will have to see, because that is what we are going to try doing.

Well, it may seem subjective to YOU... The particular problem we had was with a few panel cells on a new panel coming up only slightly hazy--not even a weak 1+. (These are R1R1 cells that should be clearly positive with our usual QC anti-sera which contains anti-D and ant-e. So that is what is under investigation.) Ortho said that we should be seeing a definite 1+ at the least. We are used to seeing 2+ or 3+ with these gel panel cells. Scott

Did "they" expand on what they think of as "a decent reaction"? This sounds very subjective to me.

I just answered this question. My Score PASS  

I just answered this question. My Score PASS  

I am not sure what the various regulatory inspectors would say, or exactly what standards they would cite. I do think that any facility that is going to do transfusions would want a armbanding procedure that established an unbroken chain of identification from the initial T&S draw, through processing and testing, to the transfusion. As can be seen by the various responses here, this can be accomplished in a number of ways. Scott

Here's my 2-cents, 2-pennies, or 2-any other small denomination coins: First, I am NOT a regulatory expert, but I am familiar with assay development and validation. All assays should be controlled in some fashion, to give the practitioners some confidence that the results are valid AND that batch-to-batch variation is limited. In a titration, especially a serological titration, this is a little more difficult than having one or two pass/fail samples that are typically included in many laboratory tests. If a control is needed for a titration, it doesn't need to be the same specificity as the test antibody (as Malcolm highlights). Ideally, yes, but not necessarily. It does need to be reliable/robust and give the same end point each time, even with the acknowledged variations in serological tests (reagents, test cells, techs, etc.). Tube testing is notoriously variable, while gel testing is believed to reduce some of those nuances. As Malcolm suggests, it might be necessary to have a control for an IgM titration (ABO) and/or a different one for an IgG titration. At the very least, the end-points may be different. An IgM control might be as simple your routine anti-A reagent; a simple IgG control might be an IAT-reactive anti-D or other specificity. A clever option might be a control that contains both - an IgM component and an IgG component. If a test system is adequately controlled each time (and passes), in my opinion, there is no reason to routinely perform parallel testing of successive patient samples. Retention samples might be useful for investigatory reasons if/when a patient's antibody titration changes radically from one sample to the next, or if there's some other medical indication. I getting a sense of deja vu, I think I've written this before.

We do perform in parallel if we have a previous specimen from the same pregnancy.

Our fetal bleed screen kit (Immucor Rapid Screen) is only approved for postpartum testing with known infant type. Antenatal bleeds and losses > 20 weeks require a KB in our facility. Which screening kit do you use?

Lily at CAP said it was only for the FS kits and daily QC is fine for everything else. When I called back in October with my list of questions, I got the feeling she thought we over interpreting many of the items

Thanks, Cliff, for the Velcro idea! It took a few hours to get all the old labels off without alarming the poor fridge but I relabeled our shelves this week.

Attached is my SOP and form for documentation. It's pretty basic but it covers the bases that I think it needs to cover - what should I check, what do I expect to see, what do I do if there is a problem and how do I document all of that. It's general because it applies to all the labels I might receive/use. I also have a similar one for reviewing new batches of forms that come in from the printers. As you can see, it has been around for awhile. In my 'spare' time I should probably combine the label and form policies into one. Inspection of Labels.doc

We would do an extended Gel XM as long as the current screen is positive. It's required by the LIS. The computer system disqualifies them for electronic XM in this instance. If the screen becomes negative in the future, they would qualify for electronic XM as the antibody is classified as not clinically significant

Hi Dave, Now things make sense, thats why I don't and you do perform the AHG for D neg. Ok! Great, thanks for that.