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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.

When I was working in the Reference Laboratory at the NHSBT and, come to that, when I was working for a short time in a Hospital Blood Bank, we would ALWAYS test for the C, c, E and e antigens, together with the K antigen, both for patients and donors, and we would also test for the antithetical antigen, as well as the cognate antigen (in other words, as in your example, the Jk(a) and the Jk(b) antigen. We ALWAYS did this, except when the grouping reagent was exceedingly rare (e.g. anti-Dib) or the antibody AND the antigen were extremely rare (e.g. anti-Kpc). The reason we did this, particularly in the NHSBT Reference Laboratory, was because we wanted to identify very rare phenotypes, such as Kp(a+b-), or even rarer (in most cases), null phenotypes, but there was also a paper that showed that people who were transfusion dependent, such as sicklers and thal patients tend, once they have made an initial atypical antibody (particularly anti-C, anti-c, anti-E, anti-e or anti-K) to make all sorts of specificities (I'll try to look up the paper and get back to you on here). Other papers comparing their findings actually agreed with them. I say ALWAYS, but then, of course, the Bean Counters, who know nothing about Blood Group Serology, or about Patient Requirements, and care even less, came along, and we were banned from doing this as, apparently, IT COST TOO MUCH MONEY, except in special circumstances, such as patients from the Black populations, where we were privileged to be able to test for both Fya AND Fyb, in case they were Fy(a-b-) - and, of course, most of those who were found to be Fy(a-b-) had the FYB gene, so would very rarely produce an anti-Fy3, as they were homozygous for the GATA1 gene mutation. Unfortunately, what these "suits" seem to forget, despite counting beans for a living, is that, if the patient goes on to produce other, clinically significant, atypical alloantibodies, they will occupy a hospital bed for longer while suitable blood is identified, including, sometimes, cryopreserved units, ALL OF WHICH IS FAR MORE EXPENSIVE THAN THE INITIAL TYPING WAS IN THE FIRST PLACE - but what do we professionals know! RANT OVER!!!!!!!!!!!!!!!!

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..

There is reason NOT to use the freshest possible units. They may be more toxic than intermediate stored units. This is something that made sense but was almost certainly wrong. See below for the reasoning and published data. We use <21 days as fresh for this reason and avoid <7 days storage for everyone based upon the randomized trial data. BMJ 2019;366:l4968 doi: 10.1136/bmj.l4968 (Published 5 August 2019) Page 1 of 1 Letters Trivella and colleagues present some caveats around the subject of duration of red cell storage and clinical outcomes.1 Studies have been widely interpreted as showing that transfusion is not associated with adverse clinical outcomes. I think this is a serious misinterpretation of the data. In addition to the concerns raised by the authors, another valid hypothesis, which has received little attention, is that very short storage red cells might be more dangerous than medium storage periods (say 7-21 days) and equally dangerous as longer storage red cells (say 28-42 days). An inverted U shaped curve. The evidence for this comes from a meta-analysis finding that “ultra short” storage of red cells was associated with a post-transfusion increase in nosocomial infection.2 Shorter storage red cells have a greater imbalance of oxidation-reduction potential than longer storage red cells in preliminary studies in vitro.3 Red cell storage duration is also a poor predictor of post-transfusion free haemoglobin and heme, putative mediators of toxicity from transfusions.4 5 We need better metrics for predicting red cell transfusion efficacy and toxicity. The simple expedient of fresher red cells is clearly not that metric and might be leading us to transfuse more toxic red cells (very fresh) in the most fragile patients, such as premature newborns. A new approach is clearly called for by the current data. At our centre we define fresh as <21 days of storage, and we generally never transfuse a red cell that has been stored for much less than 7-10 days, for the above reasons as well as logistics of supply. Competing interests: None declared. 1 Trivella M, Stanworth SJ, Brunskill S, Dutton P, Altman DG. Can we be certain that storage duration of transfused red blood cells does not affect patient outcomes?BMJ 2019;365:l2320. 10.1136/bmj.l2320 31186250 2 Alexander PE, Barty R, Fei Y, etal . Transfusion of fresher vs older red blood cells in hospitalized patients: a systematic review and meta-analysis. Blood 2016;127:400-10. 10.1182/blood-2015-09-670950 26626995 3 Schmidt A, Gore E, Cholette JM, etal . Oxidation reduction potential (ORP) is predictive of complications following cardiac surgery in pediatric patients[abstract]. Transfusion 2016;56(Supplement S4):20A-1A. 4 Cholette JM, Pietropaoli AP, Henrichs KF, etal . Elevated free hemoglobin and decreased haptoglobin levels are associated with adverse clinical outcomes, unfavorable physiologic measures, and altered inflammatory markers in pediatric cardiac surgery patients. Transfusion 2018;58:1631-9. 10.1111/trf.14601 29603246 5 Pietropaoli AP, Henrichs KF, Cholette JM, etal . Total plasma heme concentration increases after red blood cell transfusion and predicts mortality in critically ill medical patients. Transfusion 2019;59:2007-15. 10.1111/trf.15218 30811035 Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/ permissions LETTERS

If the unit if leukoreduced, as all red cell transfusions should be, there is no need for CMV negative in my view.

In this paper from 1985, "The Lui elution technique A simple and efficient method for eluting ABO antibodies c. s. FENG, K. c. KIRKLEY, c. A. EICHER, AND D. s. DE JONGH, TRANSFUSION 1985; 25:433-434.", the authors thank A. Lui. MT(ASCP)SBB, who introduced this technique to them. Therefore, I believe Lui is the name of the MT who invented this elution method.

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.

The three months was chosen following a paper written by Laine EP, Leger RM, Arndt PA, Calhoun L, Garratty G, Petz LD. (In vitro studies of the impact of transfusion on the detection of alloantibodies after autoadsorption. Transfusion 2000; 40 1384-1387. DOI: 10.1046/j.1537-2995.2000.40111384.x.) that showed that red cells that had been transfused (or entered the circulation via a feto-maternal haemorrhage could adsorb out weak alloantibodies for up to three months in a patient with AIHA. This in vivo adsorption would, of course, also apply to individuals who did not have AIHA, but could lead to a secondary stimulation, leading to a stronger antibody (higher titre and higher concentration per mL of plasma), if the alloantibody was "missed" in the antibody screen and/or cross-match, particularly as it is unlikely that the full phenotype of the transfused (or foetal) red cells would be known.

I've been a BB'er for 35 years (at the same hospital) my very first manager (who was a good, seasoned BB'er) used to tell us........., "if you have to hunt for it - it's not there". As you become more adept at reading tube reactions - your eyes will not fail you! Trust your gut. As for your technique - it all sounds good! Practice with a few techniques to find the one that works best for you I "tilt and giggle", button up, The tilt helps with seeing Mixed Field - which we tend to see a lot here - It also helps with seeing "how" cells are falling off the button - are they chipping off or are they "swirling" off.....or is there a little of both? (For some reason I always think of the "tail" of an old RPR test .....which probably dates me, LOL!)

It sounds to me like you are doing everything that you should do, without either over-shaking the tube, or over-reading the contents. I am extremely glad that you are not using a microscope, as, if you did, you would almost certainly see the odd couple of red cells "kissing each other", even if they have been incubated in isotonic saline. The other thing is (and I speak with some 43 years of working in blood group serology) if the reactions in the tube are THAT weak, the chances of any atypical alloantibody that you might miss being clinically significant are absolutely minute. If you are still worried, however, get a more experienced worker to read your tests as well, until you feel confident. That is how I learned when I started. I wish you the best of luck in your future career.

I'm all for the concept of quality and the strive to provide the safest blood products to patients, but I won't deny that sometimes many of our current practices in blood banking in terms of achieving that "quality" seems excessive, unnecessary, and sometimes it feels like a mere quality charade for inspectors and regulators. Considering the hight cost that blood banks have to incur to meet all quality regulations, it may be worth studying the financial impact of the many quality measures that regulate the practice of blood banking and to what extent these measures are actually contributing to achieving the quality needed to provide the best blood products to patients.

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?

In emergencies, we always accept verbal orders for transfusion. These should be followed up by a request documented in our electronic medical record, but that's after the fact. If you have a paper system, then the followup order is documented that way. There is a regulatory/accreditation requirement, which I consider bureaucratic, obstructive and useless, that these emergency requests require a signed release from the ordering practitioner, if the transfusion is not fully tested for the recipient.

I would most strongly advise you to send a sample, possibly even multiple samples throughout the pregnancy, to a Reference Laboratory. As the patient is pregnant, there is the possibility that the Jk(a) antigen you are detecting is actually being expressed on the red cells of the foetus, and you are detecting it as a result of a foeto-maternal haemorrhage. However, the Jk(a) antigen is not necessarily straight forward, as there are weakened forms of the antigen (and the Jk(b) antigen come to that) where there are amino acid substitutions remote from the site usually associated with the Jk(a) and Jk(b) antigens (280 of the mature protein). In addition though, you have, obviously, to consider the health of the unborn baby who, even if the antibody does turn out to be a maternal auto-anti-Jka, may cause haemolytic disease of the foetus and newborn, albeit this will usually be be very mild. I attach a PowerPoint which may, or may not help you in your decision to send a sample to your local Reference Laboratory (also tell them the ethnicity of the patient). Interesting case - please keep us informed. In Depth Lecture on The Kidd Blood Group System.pptx

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 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!

In New York State, we also are inspected by the state. FDA, NY State, AABB, CAP. You can make a sound argument that this is wasteful and duplicative. Obviously we don't have any choice about FDA and NY State. CAP and AABB, as accreditation organizations, will accept the results of each other's inspections, which is a plus, but you are still dealing with two sets of requirements. My advice to smaller facilities is to pick one if you can do so, and not duplicate your efforts and expense. Both organizations are essentially trade organizations, not scholarly/research societies. They both provide important educational opportunities, but you don't need both to keep your staff current, in my view. With the shortage of medical technologists, reducing non-productive non-clinical effort is a priority to prevent staff burnout and keep everyone focused on the main mission, patient care.