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    Malcolm Needs

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    Mabel Adams

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Showing content with the highest reputation since 03/19/2023 in all areas

  1. 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.
    12 points
  2. 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.
    11 points
  3. Neil Blumberg

    CPDA-1 Blood

    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
    9 points
  4. 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.
    8 points
  5. 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.
    8 points
  6. 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!)
    7 points
  7. 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.
    7 points
  8. 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.
    7 points
  9. 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!!!!!!!!!!!!!!!!!!!!!!!!
    7 points
  10. 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.
    7 points
  11. 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!!!!!!!!!!!
    7 points
  12. AMcCord

    Incompatible Blood

    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.
    7 points
  13. 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.
    6 points
  14. 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
    6 points
  15. My motto was "when in doubt, shake it out". Seemed to work for me.
    6 points
  16. 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.
    6 points
  17. 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 :).
    6 points
  18. 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.
    6 points
  19. A few references you might find of interest: Management of Blood Donors and Blood Donations From Individuals Found to Have a Positive Direct Antiglobulin Test. Transfusion Medicine Reviews 2012. Volume 26, Issue 2, Pages 142-152, Garratty G. The significance of IgG on red cell surface. Transfus Med Rev. 1987;1:47–57. Petz LD, Garratty G. Immune Haemolytic Anaemias. 2nd ed. Philadelphia, PA: Churchill Livingstone; 2004.
    5 points
  20. 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.
    5 points
  21. Blood bank methods aren't expected to correlate perfectly. We use their differences to avoid rouleaux, clinically insignificant, and weak warm auto reactivity so we can better detect any significant alloantibodies. No method will detect 100% of significant antibodies. I am going to tweak the above to say we can "better detect' antibodies so it works better with the next sentence and doesn't imply that we can detect "any" significant antibodies.
    5 points
  22. 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.
    5 points
  23. 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.
    5 points
  24. I'm annoyed! Yes, there are differences in results between automation, GEL and tube testing. Automation is the most sensitive and tube testing is the least sensitive (but the BB gold standard method), with GEL in-between. I wrote that bit of information in my procedure so an inspector would know I am aware of the possible differences. We are doing this exercise to make sure the methods compare, if the specimen is positive in automation, it should also be positive in GEL and tube testing and should appear to be the same antibody on the antigrams. If I am doing an antibody screen and an AB ID, I am using the same METHOD whether I am testing using 3 screening cells or a panel of 10 or more cells. Yes, we have the rare antibody screen that gives wonky results in automation and and is stronger in GEL. That tells me we need to do the ID in GEL so we can actually get an answer we trust. Different antibodies work differently in different methods but the screen and AB ID should be the same within the same method. Our screening cell method in tube is the exact same method as our panel tube testing. If I am doing the comparability testing, I am using a strong antibody that has a 3-4+ result so I can be assured I will get similar results across all 3 methods. I'm not going to use a weak or wonky antibody that would give shady results an inspector could question when they view my forms at an inspection. This is Method Comparability, not Test Result Comparability. Does CAP have to have a quota of standard changes they have to meet? I'm on a soap box and I am sorry to rant but this seems unnecessary and extra work for the same AB screen results across the different methods.
    5 points
  25. Malcolm Needs

    Patient hx

    Extended cross-match, UNLESS, the history of which other hospitals the patient has been treated is known. Of course, in the UK we have a national database of patient's antibodies, which makes life an awful lot easier, even if the data is just a "snap shop".
    5 points
  26. 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.
    5 points
  27. 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!)
    5 points
  28. In the UK, such a unit would be offered to the National Frozen Blood Bank, and would only be frozen AFTER a thorough aseptic wash, followed by addition of a chemical to prevent the formation of sharp ice crystals, and then more washing upon thawing. There would be no allo-anti-Kpb left!
    5 points
  29. Just be aware that dry ice turns into a gas. I presume your freezer is not fully airtight, but it could open rather violently depending on how tight it is sealed, and how long since the last time it was opened.
    5 points
  30. I don't think the AABB comments are evidence based. Washing with 37 degree saline is extremely unlikely to cause false negatives with clinically significant antibodies, and I'm unaware of any evidence that this is so. Any such antibody would be very low affinity to be washed away by saline at any temperature, and unlikely to have in vivo/clinical significance. As argued persuasively above by Malcolm Needs, anything that doesn't react at 30 degrees or above in typical serologic testing isn't going to cause clinical problems. Patients are neither at 30 degrees nor centrifuged :). Our serologic techniques are overly sensitive, in general, for clinically insignificant agglutinins. No need for cold panels ever, with rare exception, and more for intellectual curiosity than clinical decision making. Perhaps a mini-cold screen someetimes just to confirm you are indeed detecting a weak cold agglutinin in 37 degree testing, which disappears with prewarm technique. Like Malcolm, I've never seen a patient with an hemolytic reaction due to an antibody that disappears with prewarming, in close to 50 years of clinical practice. I know there are in vitro examples of clinically significant antibodies that weaken or disappear with prewarm, but I've never seen any clinical consequences.
    4 points
  31. Thanks for your input. I was hoping you might respond. The Daniels book says that "No case of HDFN caused by anti-Lua or -Lub and requiring any treatment other than phototherapy is reported, although raised bilirubin or a positive DAT may be detected." Does this description equal "clinical significant HDFN" by your definition or is there newer information on more severe HDFN from these since Daniels published the 3rd edition? My thought is that, if there is no evidence of any case needing any early intervention, then there is no point in running titers to determine when to begin early intervention.
    4 points
  32. I wouldn't bother, to be honest. Apart from the fact that the Lutheran antigens vary in strength of expression, making it difficult to ensure that the recorded titres would "match up" one to another, but the expression of the Lutheran antigens on foetal and cord erythrocytes is known to be weak. On top of that, of course, there is the problem of finding a regular source of adult erythrocytes with heterozygous expression. In addition, anti-Lua and anti-Lub can be either IgG or IgM but are more commonly IgM. It might be worth your while treating the maternal plasma/serum with a reducing agent such as 0.01M dithiothreitol, 2-mercaptoethanol or ZZAP to see how much, if any, IgG is present. Even if the antibodies are IgG, they are thought to be adsorbed on to foetal Lutheran glycoprotein on the placental tissue. Lastly, as you so rightly say, clinically significant HDFN caused by anti-Lub is incredibly rare, and so, all in all, you could be giving yourself an awful lot of work for very little return. If you do decide to test the maternal plasma/serum with reducing agent, and you find that there is an element of IgG present, it might be worthwhile just performing a titre once, in order to see that you have not got one of these incredibly rare examples that might cause clinically significant HDFN, and, as lone as the titre isn't massive. I would rest easy. If you want, I can cite references to back up what I have written above, but I haven't done so straightaway, as actually finding some of these papers to read is equally hard work!!!!!!!!!! I hope that helps.
    4 points
  33. Something one of my mentors said early in my career: "Don't worry about junk. If it's a real antibody and you transfuse against it, it'll be nice and strong by the next time you see the patient."
    4 points
  34. I'd also add that none of the cell washers are FDA approved for washing platelets. We've been washing platelets on the 2991 for about 40 years :). I believe there may be a paper on using the ACP-215 to wash platelets but as yet we do not have any hands on experience. We have developed a manual method of platelet washing using a Sorvall centrifuge. If your volume isn't too high, you might consider a manual wash method. It takes a bit longer, but actually has higher recoveries (>90% vs. about 80-85% with the 2991). Folks will tell you that washed platelets don't work clinically and the count increment is Washed Tx Leukemia.pdfWashed Tx Leukemia.pdflower. The increment is indeed lower, but if you employ platelets that aren't ABO incompatible with the recipient and remove the supernatant, the clinical results are actually better than the clueless advice to give ABO major incompatible platelets routinely (e.g., group A to group O recipients). The PLADO study had a bleeding rate using this abominable practice of about 70%. Our bleeding rate avoiding infusion of ABO incompatible antigen or antibody is 5%, with or without washing. A fourteen fold difference. So by all means give washed platelets to patients with severe or recurrent reactions, or avoid infusion of ABO incompatible plasma, and, if you believe our randomized trial data, to improve the survival of younger patients with acute myeloid leukemia. References attached if anyone is interestedWashing AML Greener_et_al-2017-American_Journal_of_Hematology.pdf. Washing Review IJCTM-101401-the-clinical-benefit-of-washing-red-blood-cells-before-transfusion.pdf Washing AML Greener Am J Hemat AML Washing Supplementary Figures and Tables.pdf Jill's washing paper.pdf Plt Washing Vo.pdf
    4 points
  35. Well, the thing is John, when I first left school, I started to work as a VERY, VERY junior member of staff at the International Blood Group Reference Laboratory when it was in London. At that time Dr Kenneth Goldsmith was the Director, but others working there were Dr Carolyn Giles, Dr Elizabeth (Jan) Ikin, and a VERY young Joyce Poole. Across the carpark was the MRC Blood Group Unit, run by Drs Rob Race and Ruth Sanger, where Dr Patricia Tippett worked, along with Geoff Daniels, for a while Christine Lomas (before she went to the USA and became Christine Lomas-Francis) and, for a short time, Dr Marcela Contreras (before she became a Dame and a Professor). Just up the corridor was another set of laboratories run by Profs Walter Morgan and Winifred Watkins (and the janitor was one Sid Smith - after whom the SID Blood Group System was named). As you can imagine, with all those "NAMES" working in such a small area of London, it was like a magnet for all of the other world's greats to come and visit (I even met Dr Arthur Mourant and Dr Philip Levine on visits). With all these people, ALL of whom were amazingly helpful to even me, as someone who had just left school, what else could I do but fall deeply in love with the profession, and count my blessings from day one until I retired 43 years later. I have been one lucky man.
    4 points
  36. Was the physician happy for his/her patient to expire if there was literally no group O, D Negative blood available, or, indeed, to condemn some other patient to death if, for example, they were exsanguinating and also had an anti-D??????? RIDICULOUS!!!!!!! NOT you, the physician.
    4 points
  37. If you will be getting any of those units back then a FDA inspector may want to see their storage records. Some will, some won't, depends on the inspector. Better to be prepared for the one that wants to see them. In this case a little paranoia may be a good thing.
    4 points
  38. I'm afraid I still can't agree with this methodology, for a couple of reasons. Firstly, antibody/antigen reactions are, largely, governed by the Law of Mass Action. As a result, and given a steady state of conditions (e.g. temperature), however long the incubation time may be, once a state of equilibrium is reached, there will be no net gain of antibody coating antigens, however long the incubation time may be extended. Certainly, LISS will increase the rate of association of antibody and antigen enormously, but this will apply equally to the auto-antibody as any allo-antibody that may be present, however, of course, some antibodies will only react visibly with red cells that have homozygous expression of a particular antigen, and, if such an antibody is present, it will be very difficult to detect in the presence of an auto-antibody, but can still cause a haemolytic transfusion reaction, albeit, usually a delayed reaction, but it can still cause damage to the renal system in particular. For these reason, I would always perform an adsorption, to get rid of the auto-antibody, even if I had no intention of performing specificity tests on the auto-antibody (although, it goes without saying, I would go all out to try to ascertain the specificity of any allo-antibody detected). I am trying to write a book at the moment, called "Human Red Cell Serology and Blood Groups for Beginners", and Chapter 2 deals with Serological Techniques. I attach the draft copy, which also gives relevant references, the odd diagram and abbreviations I use throughout the various chapters. Chapter 2 Serological Techniques in Routine Blood Transfusion and Red Cell Immunohaematology Laboratories.docx Chapter 2 Serological Techniques in Routine Blood Transfusion and Red Cell Immunohaematology Laboratories Figures.docx Abbreviations.docx
    4 points
  39. 4 points
  40. Does anyone remember the humorous/terrifying thread on here more than a decade ago of all of the insane things we had heard of? "I can't hang this plasma on my patient, it's liquid and the doctor ordered FROZEN plasma". Or, "I don't care if the plasma isn't thawed yet, I need to hang it stat! Send it up now!" "I ordered that blood culture stat and it's been 2 hours. Why don't I have a result yet?!"
    4 points
  41. While it is infrequently referenced, universal leukoreduction is one strategy for minimizing pulmonary and cardiovascular adverse responses to transfusion (see attached). When we instituted it in 2000 our rate of TRALI decreased by 80+ % and TACO decreased by 50%. Probably mechanism is that white cells, DNA, histones and neutrophil extracellular traps (NETs) cause acute lung injury and inflammation when infused (good animal model data exist). Thus the failure to implement universal leukoreduction in the USA during the last 23-25 years was a terrible and tragic mistake, and this fatal error persists to this day. ULR TRALI TACO PMC version.pdf
    4 points
  42. I had the ENORMOUS honour of lecturing on a course with Sue in Cressier in Switzerland in 2015, and I can assure everyone that she is a consummate lecturer, who has the ability to get across the most difficult subjects, and make them fully understandable to even the most junior of staff.
    4 points
  43. Stop blaming the Canadian Smoke. We in Canada, do result as No Antibodies detected. If the patient had an antibody in the past, that is maybe below detectable limits, but was previously identified, those are also in report as historical and as such the patient would have a full crossmatch in gel as well as phenotypically matched for previously discovered antibodies.
    4 points
  44. The trouble was that, in those days the anti-D immunoglobulin was known as "anti-D for Mum's Bums" in the UK, as the shot was given in the gluteal muscle. But, there was an awful lot of fat in that muscle, so the anti-D had a habit of "staying there", rather than being adsorbed into the blood stream. This meant that, even when the dose of anti-D immunoglobulin was calculated from the Kleihauer-Bekte test, the actual dose reaching the circulation was far lower than the calculated dose, and women used to produce allo-anti-D as a result. Nowadays (at least in the UK) the shot is given in the lateral deltoid muscle, where there is a good deal less fat, and so the shot is adsorbed into the circulation much easier, and so there are fewer cases of maternal allo-anti-D. I realise that this is a very vague explanation, and that there are many other causes of anti-D immunoglobulin being less than effective (such as giving it to the father, or even to the ambulance staff (SHOULD be unbelievable, but is actually true), but it does show just how complicated such a simple thing as this can be.
    4 points
  45. Most blood bankers I know have a pain tolerance only slightly less than their resistance to change!!
    4 points
  46. This may or may not help. Clinical Aspects of Transfusion Reactions.pptx
    4 points
  47. Okay, so as long as the said antibody is tested each and every time, to ensure that the antibody specificity has not "broadened", but also that the thermal amplitude has not changed, so that, "this time" it may be a clinically significant "cold-reacting antibody", rather than a clinically insignificant "cold reacting antibody". Sadly, it is not even THAT simple (if only), but it depends upon the specificity of the antibody and, to a certain extent, the ethnicity of the patient. "Cold-reacting" anti-M, for example, is known to be much more clinically significant in people from the Far East (particularly Japan) than in any other ethnic group, as far as I know. However, if you take the "antibody" out of the computer system, so that it no longer flags, there is the very real possibility that a formally clinically insignificant "cold-reacting antibody", that has developed into a clinically significant "cold-reacting antibody" may be ignored - not "not detected" (far from it) but ignored, because "it was okay last time"! All that having been said, I have NEVER understood why time and money is spent on determining the specificity of a genuine cold-reacting antibody, rather than just determining the thermal amplitude, to determine the clinical significance, and bothering to provide antigen negative blood, when there is zero chance of a haemolytic transfusion reaction!
    4 points
  48. Hi mpmiola, I apologize for my late reply. Grifols just confirmed the phenomenon that was described in the discussion above as the cause of the ABO discrepancy. They stated that the probe in Erytra analyzer goes down to 2mm from the bottom of the tube to pick up red cells. in this case, the transfused cells (group O) are more heavier (more dense) than the patient's own cells (group A) and therefore they occupied the bottom of the tube after centrifugation. Since the probe only takes cells from the bottom of the tube, it only picked up the transfused cells (group O). Hope this makes it clear to everyone.
    4 points
  49. Yes, we've seen this a few times with patients whose plasma has reacted to red cells kept in DiaMed Preservacell, but not in DiaMed Diluent 2. Apparently, it is an antibody directed against one of the antibiotics in the former, that coats the red cells. DiaMed told me this, or, rather, Imelda Bromilow of DiaMed told me this, and I have huge respect for Imedla, and so I am quite content that this is the true reason. :D:D:D:D
    4 points
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