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All, I am about to blow your mind.... Our plasma freezer is down and so is our backup. The freezer will not get colder than -18 C. I was preparing to move all the products into boxes with dry ice until I had a conversation with my 87 year old dad, a retired blood banker from University of Chicago. He said to me, do not take the plasma out of the freezer and put it in boxes, PUT THE DRY ICE IN THE FREEZER, IT IS THE BEST STORAGE BOX YOU HAVE!!!! MIND=BLOWN!!!! I did that. Our freezer is currently reading -25.1C and getting colder. Furthermore, the probes in the freezer continually monitor the temp in the freezer so you don't have to record temps every 4 hours, the chart is doing that for you!!! Isn't that cool? That perfectly illustrates the difference between wisdom and knowledge there. I wish we could hire my dad. I just had to share this here. PS. Freezer is now at -26.4C.

You did everything that was required in this situation. The patient was a trauma and needed emergency transfusion. The risk of death outweighed the risk of a hemolytic transfusion reaction in that scenario, according to the treating physician. I once had a trauma surgeon tell me "I can treat a transfusion reaction but I can't treat death!" That put things in perspective for me. That is why thy sign the consent. Next step would be to report this to your risk management department so that follow-up can be made, including monitoring the patient for the s/s of DTR.

Our Red Cross just informed us that it will discontinue providing CPDA-1 rbc. We primarily used it to provide volume reduced red cells to pediatric patients under 3 years of age. We will volume reduce AS-1 or AS-3 by centrifugation or washing (Terumo 2991) instead. Probably unnecessary for most patients, but this is a long standing practice here, and it doesn't seem worthwhile trying to adjust pediatric practice in this regard. Most patients do not need the additional volume provided by the anticoagulant-preservative in AS-1, etc., and avoiding unnecessary volume is a reasonable goal in many patients. There is no inherent virtue to CPDA-1 vs. AS-1 and similar solutions, and rbc preservation is slightly better in AS-1/AS-3 by in vitro metrics. There is absolutely no factual basis for using CPD-A1 in preference to AS-1, etc. in pediatrics. Purely expert opinion and probably unduly conservative. I've attached a nice presentation by Dr. Saifee at the University of Washington, who createdAdditive solution AS-1 in Children Univ. Washington presentation Dec 2021.pptx it to educate her colleagues about using AS-1 instead of CPDA-1. Additive solution AS-1 in Children Univ. Washington presentation Dec 2021.pptx Pediatric RBC White Paper - November 2021.pdf

It is usual for the C+, D- red cells (e.g. r'r) to react with an anti-G more strongly than a C-, D+ red cell (e.g. R2R2), BUT, this is by no means "diagnostic". As Jsbneg says above, it would be far safer to perform the proper tests, to ensure you have ascertained the correct specificity/specificities. The attached PowerPoint may or may not help (ignore if it is not helpful). The G Antigen and Anti G.pptx

There are no data suggesting a particular limit. Survival is very unusual after 30-50 units of red cells, but everyone has exceptional cases like those mentioned above. We have discussed futility of care many times, and our practitioners are quite amenable and forthcoming. We have stopped resuscitation in a young man having a liver transplant go badly, when there was no surgical path to hemostasis after about 250 units, but this is unusual too. Bottom line, a case by case decision as to whether care is futile and/or the patient's needs endanger the well being of other patients needing transfusion. Those are the key issues in each case to my way of thinking.

I have issued 148 units of products to a guy who was cycle vs car massive haemorrhage - he survived. I have issues 120ish units on an obstetric massive haemorrhage (as well as 20 6-packs on the twins) - all 3 survived. I've issued similar on AAA (with eventual bypass) - survival. I think the key is to use TEG to see whether the clotting is screwed - if they are clotting then keep going... In the grand scheme of things blood is cheap

For those of who works in transfusion service laboratory and would like to learn more reference cases, I can post some mock-up cases here. If you would like me to do it, please hit the "heart" button on this post. If enough folks want to practice case studies on reference lab cases, I can post mock-up cases here weekly or so..

So, this PROVES that CAP do not know the A from their elbow. ALL Blood Transfusion Reference Laboratory Staff, not to mention MOST Blood Transfusion Hospital Laboratory Staff KNOW that not all antibodies can, by any means, be detected by ALL serological techniques (saline, albumin, enzyme, LISS, IAT, inhibition tests, recombinant blood group proteins, etc), let alone by ALL technologies (glass, tube, plastic tube, liquid phase microtitre plates, solid phase microtitre plates, column technologies, etc), BUT THOSE WHO RUN CAP KNOW BETTER THAN EVERYONE. They should be thoroughly ashamed of themselves, and go back to kindergarten.

I've never heard of that. While I can understand the rationale, I'm afraid that if there was enough of a fetal bleed to impact antigen testing mom there are bigger problems than just getting the antigen type right. Just my thoughts.

We don't recheck antigen typings here in our hospital in Canada. The typings that have been performed at Canadian Blood Services, are embedded in the barcode on the bag, with all negatives printed on the End User Label. Every unit is antigen typed for K so if it isn't printed on the bag the unit is K Pos. Antigen typings we do are all linked to the unit through barcode. The reason of, "We were typing a lot of units and may have mixed them up", is not acceptable in a blood bank setting. Go work in a different department if you can't organize yourself. Anyway, there is also a full gel or whatever you use crossmatch at the end of that phenotyping, as long as the antibody is reacting, an anomaly could be discovered there. You have to have a little faith that people before you are doing their job properly, or you can cause yourself a lot of undue stress.

I realize this is "fighting city hall" but is there a more useless requirement than having everyone review and sign off on procedures that haven't changed one iota? In our laboratory, this is many hundreds of procedures (including the one on how to write a a procedure :). Bureaucratic make work of no value whatever. An unfortunate example of the administrative/legal mindset versus the scientific/clinical mindset in our society. Probably an early small sign of the coming end of our civilization when non-productive work receives such priority. Seriously.

I've had further thoughts upon this case (having told you not to worry about it - I live a sad life - NOT!). It struck me that the patient has an Rh type of D+ C+ c+ E+ and e+, suggesting that the probability is that the patient has a genotype of DCe/DcE (R1R2), but this may not be the case. She could have one of the rarer Rh genotypes, such as DCE/Dce (RzRo), DCE/dce (Rzr), Dce/dCE (Rory), etc, and this may be potentially important. Some years ago, Joyce Poole explained to me that most grouping reagents labelled as anti-C are, in fact, a mixture of anti-c and anti-Ce, and this, she told me, included most monoclonal anti-C reagents (which surprised me, to be honest). This is because the vast majority of the red cells transfused that stimulate an anti-C would have the haplotype of either DCe or dCe, or both, and will, therefore, also stimulate an anti-Ce. As a result, these "hybrid" anti-C/anti-Ce reagents will react more strongly with red cells expressing the Ce compound Rh antigen (Rh7) and the C antigen (Rh2), than with red cells that only express the C (Rh2) antigen. This would not, incidentally, explain the stronger than normal reaction with the e antigen. However, if the patient does express one of the rarer Rh types mentioned above, say she is RzRo, she can actually produce an allo-anti-Ce, and most antibody panels only contain C+ red cells that are only Ce+ as well. In other words, her antibody in the plasma MAY be identified as an anti-C, whereas it is actually a monospecific anti-Ce, which would neatly explain why she has an apparent anti-C. Of course, she may also have an auto-anti-C, or a mimicking auto-anti-C (and, possibly, an allo-anti-Bg of some sort). Sadly, for a nerd like me, I doubt if we will ever know! I think it was John C Staley who once accused me of looking for zebras, when I hear horses hooves (I may be wrong, but I think it was John). Anyway, this proves that he was absolutely correct about me!!!!!!!!!!!!!!!!!!!!!!!!

Not a sensible approach in my opinion. No real chance of mistyping due to fetal bleed. At very least, you'd see a mixed field if there were a fetal bleed with a different type. So get rid of this requirement in my view.

Well, the first thing to say is that red cells CANNOT be either homozygous or heterozygous (or, come to that, hemizygous). These terms apply ONLY to genes, and red cells do not contain a nucleus. The antigens can only be described as, at best, "homozygous", "heterozygous" or "hemizygous" expression, or, alternatively, "double" or "single dose" expression. Then, it HAS to be accepted that, unless the maternal antibody is an autoantibody, it must be an alloantibody (or, possibly, an isoantibody), which means that to mimic the state of the foetal red cells, the red cells used to titrate the antibody MUST have a "single dose" expression. However, that in itself presupposes that the foetal red cell antigens are all expressed at the same time, which we know is untrue (just look at the A, B and H antigens as an obvious example, but also the Kell antigens that are expressed much earlier than are the Rh antigens) or are ONLY expressed on foetal red cells, as opposed to other tissues (such as on the placental cells, which have, in some cases, been proved to adsorb the maternal antibodies). Then, there is the fact that not all antibodies can be detected by all techniques. This is why Reference Laboratories SHOULD have more than one technology available (and their workers should be provably competent in these techniques. However, even then, not all techniques can predict the severity or otherwise of HDFN. For example, antibodies within the Indian Blood Group System always show that they can cause severe HDFN by certain techniques, such as MMA, but they don't! There is also the fact that the immunoglobulins may be IgM, IgA, IgG1, IgG2, IgG3 and IgG4 (to mention just a few), and I have yet to come across, or read about, an IgG4 immunoglobulin causing HDFN. So, my answer is that there is a HUGE amount of knowledge known about the various antibody specificities, their titres, the expression of their cognate antigen, etc, etc, that there CANNOT be a single answer to your excellent question, but that the best thing that can be done is to read around the subject - and read around the subject from every source available - not just from a single country. OKAY THEN, RIP ME APART!!!!!!!!!!!

Agree! Save the life first. Our medical director would likely order at least one DAT the next day, possibly for additional days, to monitor. Anti-E is generally relative benign (though I have seen one patient who had an acute hemolytic reaction), We might also monitor plasma Hgb or haptoglobin, depending on the antibody involved.

The same phenomenon is seen if you use a spun sample for DATs. The cells at the top can be negative and the ones from the bottom positive if recently transfused.

"The bottom line was, if the treating physician wanted to use up the entire inventory trying to save a life, we could not deny them the blood, even though it places other patients at risk. " I would call this some combination of cowardice and insanity, speaking purely personally. Taking responsibility for difficult decisions is why physicians get paid well, and avoiding decision making is irresponsible.

I am waiting for some conscientious, firm inspector to insist we add the blood bank director's hat size and astrological sign to each procedure. About as relevant to health care as most of the stuff the accreditation and regulatory agencies obsess about.

I could not agree more. I believe that, if unchecked, some of the accrediting agencies will eventually regulate themselves into irrelevance.

Another bureaucratic authoritarian idiocy? Sorry, couldn't restrain myself, but there is a cadre of "quality gurus" who are constantly thinking up irrelevant, pointless make work stuff for the rest of us. This is how civilizations come to an end. Why in the world would an SOP have to have the address, name, GPS co-ordinates, topographic elevation and postal code of the facility? How does that address any patient care issue in the universe?

@Neil Blumberg, I wish we had you at all of our facilities to educate our medical staff. Sadly, convincing Hematologists and Oncologists (at least here in America) that it is better to postpone platelet transfusions than give ABO incompatible platelets is, more often than not, rejected, especially in light of the fact that many patients are having to wait because of lack of platelet inventory to begin with. What we really need is a push for better transfusion therapy education in medical school. Along with this, continuing education for practitioners needs to become a priority. It is, however, quite difficult to get time with these practitioners. Even when we convince our laboratory medical directors to advocate for these issues, in my experience, clinicians rarely change. All that said to say, in the "trenches," the practice will likely continue to prioritize inventory over safety.

I should add the good news is that when one starts prioritizing ABO identical platelets over inventory management, one reduces the platelet transfusions needed by perhaps 50%. So our platelet shortages will disappear in large part if we stick with ABO identical as much as possible. See attached randomized trial from eons ago :). ABO identical reduces transfusion reactions as well, HLA and rbc alloimmunization. Not to mention decreasing bleeding and mortality. ABO randomized trial UR european j haematology 1993 copy.pdf ABO plt tx revisited cumulative effects.pdf Platelet transfusion worsens ICH Stroke 2020 copy.pdf

Another point. Since group O whole blood has proven as safe or even safer than typical component therapy (A platelets, A or AB plasma) in massive transfusion of trauma patients, perhaps group O low titer platelets would be safer than group A or B platelets for an AB patient :)? No one knows, but worth considering. The big problem is probably giving non-O platelets to O patients. There is evidence this increases bleeding and mortality. Just like red cells, only O platelets for O recipients is a good practice. The AB patient may be less of a problem, since giving some small amount of antibody may be less dangerous. A risk of hemolytic reaction of about 1 in 700 or so. The risk of mortality in transfusing an O patient with A platelets is probably 1 in 5 (see attached). ABO incompatible platelets intracranial bleeding 2021.pdf ABO plasma incompatible platelets and hemolytic reactions.pdf

"Since AB+ people are considered the "universal recipient" , we give them any type platelets, usually starting with the one with the closest out date. " I grant you that this is widely shared idea in our field for decades. It is also seriously wrong. It prioritizes inventory management over patient wellbeing. Our approach to ABO and platelets is distinctly different from ABO and red cells with no rational basis. Antibody and complement destroy red cells and platelets equally well. The only difference is that instead of free hemoglobin being released, it's mediators such as VEGF, IL-6 and other platelet pro-inflammatory, immunomodulatory and pro-thrombotic granule contents are released. ABO mismatched platelet transfusions at least double the refractoriness rate in repetitively transfused patients (see attached for references), and actually increase bleeding and mortality. The answer to the question is ABO identical is by far most effective and safest. If you have to give ABO mismatched, there is probably no good answer other than washed/volume depleted O's, A's or B's, where most of the incompatible plasma is removed. If that's not possible, postponing platelet transfusion until ABO identical is available when feasible, giving half doses of ABO identical if two patients need the one available unit, etc. are also reasonable. Sadly, ABO mismatched platelets are probably worse than no platelets at all. They provide little or no hemostatic benefit and increased risks of bleeding, organ injury and death for the patient. If I were the attending physician, I would generally give no platelets if ABO identical or washed O's weren't available in a stable, non-bleeding patient with a count of over 5,000. The good news is we can improve outcomes by just doing what we do for red cells. Do not transfuse ABO incompatible antigen or antibody. It's bad for red cells, platelets and endothelial cells, all of which have complement and Fc receptors that bind immune complexes, and all of which bear ABO antigens on their surfaces. Carr ABO mismatched refractoriness copy.pdf ABO story expanded.docx ABO endothelial cell paper.docx NEJMc2034764 copy.pdf NEJMc2034764_appendix copy.pdf

I used this case study as part of my Higher Specialist Diploma in Blood Transfusion. The IBMS have asked if I would like to give my PowerPoint presentation ('What the f?') at the 2023 Congress. Thank you to all the contributors - I will certainly big up PathLabTalk if I do get to do it. Rich

I agree with both Bet'naSBB and jayinsat in that it is probably an antibody directed against a low prevalence antigen. The problem with identifying the specificity of such an antibody is that there are so many! To make certain that it is not a "fool's errand", it might be worthwhile trying to get a sample of blood from the putative father, if he is available and/or known. As the baby is, like the mother, group O, there is a 50% chance that the father will also be group O, in which case it is simple to see if his red cells can be sensitised by a maternal antibody. If he is not group O, everything is not lost as, as jayinsat suggests, an eluate from the baby's red cells should be clear of all anti-A and/or anti-B. If the putative father's red cells are compatible by all methods, either there is another explanation for the positive DAT, or he is not the father (or both). The other thing that springs to mind is that, even if there is an antibody directed against a low prevalence antigen, as you have not identified a specificity using your standard panel, and should the baby develop a clinically significant case of HDN (it is too late for HDF) and require a transfusion, acquiring crossmatch compatible blood, suitable for the baby, should be a simple task.

It is all over the place, to be honest. It is Caucasian, rather than caucasian, It is group O, D Positive, and group A, D Positive, rather than either group O Positive or group A Positive (see the early editions of Peter Issitt's book). It is Oh (with a subscript "h"), and not "Bombay". The FUT1 gene, or, rather, the lack of a functional gene through various different genetic mutations, leads to the "Oh" phenotype, but this should NOT be called the "Bombay phenotype". Although this phenotype was first described by Bhende YM, Deshpande CK, Bhatia HM, Sanger R, Race RR, Morgan WTJ, Watkins WM. A “new” blood-group character related to the ABO system. Lancet 1952; i: 903-904. DOI: 10.1016/S0140-6736(52)92356-8, Another example of the Oh phenotype can be seen in the rare recessive condition, Leukocyte Adhesion Deficiency Type II where, to all intents and purposes, the patient will have a normal H gene, and yet the red cells are of the Oh phenotype, and anti-H can be found in the plasma. the phenotype has been identified in many different parts of the world (and is not just confined to mutations in India or even Asia (Hidalgo A, Ma S, Peired AJ, Weiss LA, Cunningham-Rundles C, Frenette PS. Insights into leukocyte adhesion deficiency type 2 from a novel mutation in the GDP-fucose transporter gene. Blood 2003; 101: 1705-1712. DOI: 10.1182/blood-2002-09-2840). The other thing is, of course, that "Bombay" no longer exists - it is now Mumbai! I APOLOGISE FOR BEING A COMPLETE PEDANT!

Does acquiring more good blood banking staff count?

It's never safe to assume that everyone, or for that matter, anyone knows what you are talking about when providing one short sentence. Especially us old, retired guys. Both Malcolm and I thought you were looking for some philosophical discussion. Hope you find the key you are looking for.

Just to be clear, these regulations are almost totally arbitrary and can be overridden by a physician's judgement. There are no data to support this 30 minutes nonsense nor the 1-10 degree storage requirement. Just so we all understand there is almost no scientific or clinical basis for our regulatory rigidity and we are usually discarding perfectly safe units of blood. Rant off :).

The first, and most important, thing to remember is that ABO antigens are "carbohydrate-based" and are not, therefore, direct gene products (not that any antigens are, as every one of them undergo post-translational changes). The direct gene products are, of course, the A, B and H transferase enzymes. At birth, it is incredibly rare for the enzymes to be "working" at its optimum/maximum, so that it is rare for the ABO antigens to be expressed maximally (or anything like) at birth. I am certain that you know all this already, so that I am probably "teaching my Grandmother to suck eggs", as the old (and in this case, almost certainly, insulting) adage goes. As a result of the above, however, unless you can perform A, B and H typing by molecular techniques (NOT to be recommended - see Geoff Daniels book, Human Blood Groups), you either have to decide to ignore all serological cord ABO types, and call all of them O, or, you have to use serological methods that will enhance the antibody/antigen reactions. Herein, there are inherent problems. Firstly, whatever enhancement you use, you MUST use a suitable negative control. It is fine (in my opinion) to vary the incubation temperature from RT to 4oC, but, to so do, it is very necessary to use another cord blood from a known group O cord sample (i.e. where both parents are KNOWN to be group O themselves, and so an A or B subtype in terms of the control is not a problem). Similarly, the same can be said for enzyme-treating the baby's red cells, as long as the control cells are also treated in EXACTLY the same way with the proteolytic enzymes. Finally (at least for now!!!!!!!), it should be remembered that we routinely use monoclonal ABO antibodies these days. These are extremely avid, which is fantastic, but are also VERY specific, which can be a drawback. By this I mean that the old polyclonal human-derived ABO antibodies we used to use (when I was middle-aged, and Karl Landsteiner was a young boy) had the single (and probably only) advantage that they were not quite so specific, and would, therefore, detect ALL (or most) ABO antigens, including those that the monoclonal antibodies would not necessarily detect. For an explanation of this, there was a recent paper in Vox Sanguinis (Cripps K, Mullanfiroze K, Hill A, Moss R, Kricke S. Prevalence of adsorbed A antigen onto donor-derived group O red cells in children following stem cell transplantation: A single-centre evaluation. Vox Sang 2023; 118: 153-159. DOI: 10.1111/vox.13386) talking about the A antigen being adsorbed onto the surface of group O red cells in vivo. One of the references they use is the first peer reviewed paper that I ever wrote, concerning A and/or B substance being adsorbed onto the surface of donor-derived red cells in vivo. What I failed to say in this paper was that this phenomenon was far easier to detect with polyclonal ABO reagents than monoclonal ABO reagents (36 years, and I still regret this omission!). Anyway, IF I HAVEN'T SENT YOU TO SLEEP YET, my point is that, as long as you use suitable controls, particularly NEGATIVE controls, there is no reason why you should not use any modification to any technique (GIVEN THAT IT IS IN YOUR SOP, with all the qualifications given above), and, even then, if you feel it safer, GIVE GROUP O BLOOD.

Also, fetal bleed screen testing on a spun sample. Those giant fetal cells will be on top. Mix well before testing!

The most likely answer has been given above: newly formed autologous red cells have a lower gravity than transfused cells and will concentrate at the top of the re cell pellet whereas transfused cells will seat at the bottom. I hereby attach a paper describing that phenomenon. I hope Grifols will thank you for giving them the answer :-) 20230301142735376.pdf20230301142735376.pdf

Was the patient recently transfused? We had a situation several years ago where the patient sample results were one type on the Vision and another type in tube. I learned that the instrument samples red cells from the bottom of the patient specimen which, after centrifugation, is where the majority of the more dense transfused cells are vs. the top of the red cell layer where the less dense autologous red cells are. This cause for a forward typing discrepancy was confirmed after communications with Ortho. The theory was confirmed with manual gel testing where red cells were sampled from the top, middle and bottom of the red cell layer of the patient's specimen. The top layer of red cells were Group O, the middle and bottom were primarily Group A. This patient was discovered to be Group O after receiving several Group A RBC transfusions. The reverse typing showed reactivity only with Group B red cells at that time.

I'd go up the food chain ladder and consult with this inspector's supervisor. Clearly if the lab receives five samples, giving them all to one technologist does not in any way mirror clinical practice, and thus violates the regulations. Thus my initial take on this is that is another extremely bad idea from an inspector who has no idea what they are doing. Sort of the old joke about some physicians: "Occasionally wrong, but never in doubt."

I did allo-adsorptions on eluates for quite a while and never once detected anything in the adsorbed eluate. My own experience suggests that it is a waste of time and resources, but others may disagree.

i had an AABB inspection years ago. At the summation the inspector said: "I know I'd have to dig to find something in Dave's lab." That should have been a warning. My only deficiency (which was cited by the Area Chair, who determined the deficiencies based on the Inspection report form) was that I did not have my facility ID on my antibody panel sheets. I immediately called my area chair and told him I wanted to inspect his lab (UT@Knoxville), which of course is not allowed. I became an AABB inspector/assessor after that fact.

@Neil Blumberg Exactly. We've all had the odd cases that survive when it doesn't seem they should, and I agree that it's certainly case by case and dependent on hemostasis and coagulation like @Auntie-D said above. We use TEG for coagulation eval as well. I think my trauma surgeons are looking for a prompt to make them aware of how many products they've used, so they can evaluate the futility of continuing versus stopping. Anesthesia is the group transfusing these products, and they can easily lose track as well, so we're looking for an estimate of when the blood bank staff might give them a nudge to let them know they've hit a threshold, and to evaluate the entire picture of the patient with that knowledge, rather than being tunnel visioned into fixing the damage only. I have heard 30-50 units of red cells is the sweet spot as well. We consider more than 30 units of red cells to be a super massive transfusion, so that would jive.

A lecturer I listened to discussed MTP and stated that using Rh positive packed cells keeps the patient alive. He said that if anti-D is built, it can be dealt with when the woman gets pregnant. If she dies because she didn't get transfused with Rh positive packed cells, she certainly won't even have the opportunity to become pregnant. So, there's that.

If the baby is not anemic and has no evidence for hemolysis, I'd just leave it at that. There are variant plasma antigens that can elicit antibodies and these can be hard to identify using red cell serologic techniques. If the eluate is negative against panel red cells, this is high probability. Perhaps mom is sensitized to a paternal immunoglobulin variant and these immune complexes are adhering to red cells. There are no standardized tests for such anti-plasma protein antigens, to my knowledge. Not very satisfying, but the clinical findings are the most important issues here, not the serologic issues.

Do you think it too passive aggressive to ask if you are required to QC ALL the low and high incident antigens on the panel especially those that you have no antisera for (or the cells to QC that antisera)? You could also ask them if and how you should QC the antigen variants on each panel!

I only wish I could know another language anywhere near as well as Yanxia knows English! She has always impressed me with her blood bank knowledge as well.

If we have to hunt for a sample to use for this that will give consistently comparable results, we aren't testing the method, we are testing our ability to find a suitable sample. I heard that CAP will sell you one that will consistently give the same results. If we aren't going to change anything (can't recalibrate gel!) based on the answers we get (like chemistry would), then why are we doing this? I talked TJC out of it last inspection (I probably got a little heated over the stupidity of it because I had to come in the day after a concussion to meet with them, but maybe they took pity on me and didn't cite me because of my unfiltered brain). No one has been able to explain to me any meaningful takeaway from doing this comparison. If I am ever forced to do it, we will just keep copies of sample results that we run by two methods to solve a problem and make a note that they are acceptable because we expect these differences between methods. If anyone can give me a valid use for this, I would be very appreciative.

Our window opens in October. I will not budge! If our inspector gives a deficiency for this item I will take my fight to CAP. If I do not win, then I will make the change. I am hoping by then they get their collective heads out of their posterior waste removal orifices and accept the rational and logical process.

Thank you all very much for your responses. I'm glad to hear that this is not a common practice and I do agree that the risk of mistyping would be extremely rare. This was my first time as well seeing this kind of practice. Definitely worth an SOP change.

I've been Blood Banking for 35 years......... (albeit in the same hospital) but I've never heard of that - nor do I know of any AABB or CAP regs that would imply that...... (and we've just been inspected by both!)

I was joking about the specificity being between "anti-O" and "anti-Q", in that anti-P, the specificity almost always involved in a case of PCH is a "cold-reacting" IgG anti-P that "fixes" complement (and P is between "O" and "Q" in the Western alphabet). A pretty poor attempt at a joke, I fully admit! While I am not saying definitely that it is a case of PCH, the fact that the patient has a suspected AIHA, that the auto-antibody appears to be "cold-reacting", that it is IgG and that it also involves activated complement, strongly suggests that this may be the line to go down as an investigation. We didn't perform a DL test routinely by any manner of means (despite being a London based Red Cell Immunohaematology Laboratory). It was always discussed between our own Consultant (or, at night, weekends or Bank Holidays) by the on-call Consultant, but all of the staff knew how to perform the test, even if they were a lone worker. We always used to dread being asked to perform such a test as a lone worker, as it took so long to do!

"Pettifogging".....an 'olde worde" that is so relevant today. Thank you for reminding me. I shall try to work it into as many conversations as possible.

Reading between the lines, I believe you're saying that C+D- (r'r) panel cells are nonreactive, thereby excluding the presence of anti-C, If that's the case, and since said cells should carry the G antigen, it is very unlikely you're dealing with anti-G. Anti-LW may mimic an anti-D pattern by demonstrating reactivity only with D+ cells. It's also very remotely possible that one of the donors carries a rare form of D-antigen that is not readily detected by typical commercial reagents. However, those are very rare and their ability to stimulate an immune response is not well understood.

Short answer would be any ABO type if a one time thing, along with a prayer card for no hemolysis or post-transfusion purpura. You could make a case for type A as the anti-B is likely to be lower titer, lower biologic activity than the anti-A in group O platelets (unless low titer) or group B platelets. But this is largely theoretical hand waving.