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    Malcolm Needs

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Showing content with the highest reputation since 05/26/2018 in all areas

  1. Malcolm Needs

    Gold Medal.

    I am enormously honoured to announce that I am going to be awarded the Gold Medal of the British Blood Transfusion Society at their Annual Scientific Meeting in Brighton this year. It is awarded to an individual for their exceptional and long standing services to the Society and to the practice of blood transfusion in the UK. Sorry if this sounds egocentric, but I am very excited.
    37 points
  2. 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..
    19 points
  3. I'm going to be blunt. This is ridiculous!! You have the potential of causing far more problems by removing the cubes from their protective container.
    17 points
  4. 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
  5. 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
  6. Very proud to have received this through the post earlier this week, to go with being elected to Fellowship of the British Blood Transfusion Society earlier this year.
    11 points
  7. This is not a popular concept but at some point we have to accept there are things we can not control. Once the blood leaves the blood bank we are at the mercy of other humans and as long as the human factor is involved there will be human error be it unintentional or intentional. Attempting to complicate a process will only provide inventive humans the opportunity of coming up with creative work arounds to circumvent your best of intentions. At some point you just have to step back, do your job and hope for the best. I had a corporate transfusion QA director who could not accept that human error could not be completely eliminated with out eliminating human involvement in the process. Her directives became horribly complex solutions with multiple, redundant checks and balances only resulting in increasing problems. Bottom line, pick your battles and fight those you have a reasonable chance of winning. Make suggestions, offer insight, provide training opportunities but at the end of the day realize that you have to accept some things are simply beyond your control and even your influence. On that happy note I'll step off my soap box and stop my philosophical ramblings.
    11 points
  8. If you put a drop of blood on something like a filter paper, and then add a drop of 1M NaOH, if it is adult blood, after a couple of minutes it will turn a sort of yellow/brown colour, as the Hb is denatured by the alkaline, whereas, if it is blood derived from the baby (including cord blood), the red cells will stay red, as HbF is not denatured by the alkaline for much longer. It is rather like doing a Kleihauer, but by "bucket chemistry", as it is known!
    11 points
  9. 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!!!!!!!!!!!!!!!!
    10 points
  10. We had a melanoma patient on Nivolumab = Opdivo who apparently has hemolytic anemia but his IgG was only microscopically positive and his complement was negative. Hgb 5.5. Retic % slightly elevated, absolute retic normal, immature fraction retic very high. Bili and LDH normal. Hpt <14 and responded to steroids. They blamed this drug so I hunted up this article. This was new to me so I wanted to share it. Clinical Trial Am J Hematol 2019 May;94(5):563-574. doi: 10.1002/ajh.25448. Epub 2019 Mar 13. Clinical and laboratory features of autoimmune hemolytic anemia associated with immune checkpoint inhibitors Rebecca Karp Leaf 1, Christopher Ferreri 2, Deepa Rangachari 3, James Mier 3, Wesley Witteles 4, George Ansstas 5, Theodora Anagnostou 6, Leyre Zubiri 1, Zofia Piotrowska 1, Thein H Oo 7, David Iberri 8, Mark Yarchoan 9, April K S Salama 10, Douglas B Johnson 11, Andrew D Leavitt 12, Osama E Rahma 13, Kerry L Reynolds 1, David E Leaf 14 PMID: 30790338 DOI: 10.1002/ajh.25448 Free article Abstract Immune checkpoint inhibitors (ICPis) are a novel class of immunotherapeutic agents that have revolutionized the treatment of cancer; however, these drugs can also cause a unique spectrum of autoimmune toxicity. Autoimmune hemolytic anemia (AIHA) is a rare, but often severe, complication of ICPis. We identified 14 patients from nine institutions across the United States who developed ICPi-AIHA. The median interval from ICPi initiation to development of AIHA was 55 days (interquartile range [IQR], 22-110 days). Results from the direct antiglobulin test (DAT) were available for 13 of 14 patients: 8 patients (62%) had a positive DAT and 5 (38%) had a negative DAT. The median pretreatment and nadir hemoglobin concentrations were 11.8 g/dL (IQR, 10.2-12.9 g/dL) and 6.3 g/dL (IQR, 6.1-8.0 g/dL), respectively. Four patients (29%) had a preexisting lymphoproliferative disorder, and two (14%) had a positive DAT prior to initiation of ICPi therapy. All patients were treated with glucocorticoids, with three requiring additional immunosuppressive therapy. Complete and partial recoveries of hemoglobin were achieved in 12 (86%) and 2 (14%) patients, respectively. Seven patients (50%) were re-challenged with ICPis, and one (14%) developed recurrent AIHA. Clinical and laboratory features of ICPi-AIHA were similar in DAT positive and negative patients. ICPi-AIHA shares many clinical features with primary AIHA; however, a unique aspect of ICPi-AIHA is a high incidence of DAT negativity. Glucocorticoids are an effective first-line treatment in the majority of patients with ICPi-AIHA, and most patients who are re-challenged with an ICPi do not appear to develop recurrence of AIHA.
    10 points
  11. I think you should invite members of that committee to remove a bag from its cube, try to label it sufficiently (substance, lot #, expiration, etc.), attach that label in such a way that it will stay attached when the bag 'collapses' as it's emptied, hoist the bag up to the level of a cell washer without the aid of the box (especially this part), and suggest ways to keep the collapsed bag at an angle that will ensure all the contents are used. I'm willing to bet they'll come around.
    10 points
  12. No, there is a lot more to it than that. Anti-A and anti-B are isoantibodies, rather than alloantibodies. In other words, they are "naturally occurring" and do not have to be stimulated by either red cell transfusion or pregnancy. They are usually stimulated by particles in the air (including human cells that have been shed into the air) that either express chemical compounds that mimic the A and/or B antigens or, in the case of shed human cells, actually do express these antigens (remember, the A, B and H antigens are histoantigens). On the other hand, genuine alloantibodies (for example, let's say an anti-Jka) that are stimulated by transfusions and/or pregnancy, have, by definition, shown the individual to be a "responder". It is by no means unusual for an individual who has produced a genuine alloantibody (such as the anti-Jka mentioned above) to produce an alloantibody of another specificity (or alloantibodies of other specificities). Such other alloantibodies may not be easily detectable by routine serological techniques for various reasons. Three of these are that the antibodies may not become serologically detectable at the same time (one may be detectable as early as the other, as not all antibodies "read the books"), that an antibody may be evanescent (or "disappears" from the circulation quite quickly - such as many Kidd antibodies - but these can remain clinically significant if re-stimulated), and thirdly, that the cognate antigen is not expressed on either the screening red cells or the red cells used in the antibody identification panel (for example, in the UK, to give two examples, the Jsa antigen and the Wra antigen, and both of these antibodies can be exceedingly clinically significant). For this reason, it is very important that a serological cross-match is preformed (and found to be compatible), even if the blood provided is antigen negative for a known cognate antibody. You may well ask, "Well, what about an anti-Wra (for example) that is present as a monospecific antibody? Is that not clinically significant?", and the answer is "Yes"! Indeed, there was a fatal case of an acute transfusion reaction caused by anti-Wra within the last decade in the UK, and the court decided that it was death by misadventure, because anti-Wra is known to be quite a common antibody, whereas the cognate antigen is sufficiently rare for the Law to recognise that it does not need to be expressed on screening cells (otherwise the Reference Laboratories would be overwhelmed with samples that have anti-Wra in their plasma/serum - and this is only one such specificity). This may be one of the few times that our judiciary have used their brains (did I say that??????????!!!!!!!!!!!!!!!!!) and the decision may have been influenced by an editorial in Transfusion, written by the late, great Professor George Garratty (Garratty G. How concerned should we be about missing antibodies to low incidence antigens? Transfusion 2003; 43(7): 844-847. DOI: 10.1046/j.1537-2995.2003.00492.x.). SORRY THIS IS A BIT (VERY) LENGTHY!
    10 points
  13. This issue - the switch to plastic - seems to bubble up every few years (pardon the minor pun). When I was a puppy in my early years, last century, labs were already tossing around the idea to avoid potentially dangerous, sharp glass tubes. When broken, the plastic used for test tubes is also sharp, possibly worse that glass, as Malcolm suggests. As others have mentioned, static is always an issue with the plastic version, rather than occasional with glass. Other than that, and in my experience, plastic test tubes tubes work almost as well as glass for serological testing. However, many "tube reagents" are not formulated for, or qualified in plastic. The Directions for Use/ Package Inserts may be restrictive. Two points - personal opinion of a cranky old man: 1. One event does not indicate a trend - changing the whole system to address a single cut-finger incident is unreasonable. 2. The various safety apparatuses (however they be mis- or confusingly named) exist to limit institutional legal liability, i.e., prevention of legal action ("please don't sue us"). The workers' actual safety is often secondary.
    10 points
  14. Ah, inform them that by their logic; phlebotomist's should not use needles due to the many unintended sticks in hospitals each year
    10 points
  15. It simply means that the P1 antigen is particularly strongly expressed on these red cell samples. Therefore, if you come across a weak anti-P1, it may apparently react with these particular red cell samples, whilst apparently not with, for example, the third red cell sample shown in your antigram. Although not identical to dosage, per se, it is fairly synonymous with dosage at a phenotypical level. The strength of the expression of the P1 antigen is an inherited trait.
    10 points
  16. I just saw this seminar being offered by Bio-Rad with our own, infamous, Malcolm Needs as the presenter. I registered and thought I'd pass the word to all of us here. Here is the link:https://info.bio-rad.com/ww-IHD-transfusion-w-registration-lp2.html?elq_mid=48765&elq_cid=10201434&elqCampaignId=30837&utm_campaign=30837&utm_source=eloquaEmail&utm_medium=email&utm_content=Email 13ER EM-R-CM-385201-FY21-TCHS-AWEN_BR-JRNL-TRF News 19 Nov&elqTrackId=6ecbbea5f2bb46849981687404578a8e&elq=7c5f74470efa434dbd4351e512f7ae7a&elqaid=48765&elqat=1&elqCampaignId=30837
    10 points
  17. Does your Pathologist not understand that Lewis antigens are not intrinsic to the red cell membrane (in fact, in all probability, if they were discovered now, they would almost certainly NOT be recognised as red cell antigens by the ISBT). As such, even the small amount of plasma contained in packed red cell units is sufficient to adsorb out most of the patient's Lewis antibodies in vivo, during the actual transfusion. Those transfused red cells that survive in the circulation (i.e. about 100%) will very quickly assume the Lewis type of the recipient. He or she might like to read Sneath JS, Sneath PHA. Transformation of the Lewis groups of human red cells. Nature 1955; 176: 172, as this may serve to stop the worrying.
    10 points
  18. I always considered antibody identification both art and science with a little magic thrown in for good measure.
    10 points
  19. 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
  20. 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
    9 points
  21. 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.
    9 points
  22. 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
    9 points
  23. 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
    9 points
  24. If the unit if leukoreduced, as all red cell transfusions should be, there is no need for CMV negative in my view.
    9 points
  25. 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.
    9 points
  26. In terms of the function of the various ABO blood types, there have been a huge number of peer-reviewed papers written on the subject (and the number has exploded with the advent of COVID19). I would seriously defy anyone to keep up with all of these, but I would recommend reading pages 42-43 of Reid ME, Lomas-Francis C, Olsson ML. The Blood Group Antigen FactsBook. 3rd edition, 2012. Academic Press. ISBN: 978-0-12-415849-8. In terms of how they evolved, it is so far back now that it is anyone's guess, but slides 28 to 32 of the attached lecture may give you some idea. In Depth Lecture on The ABO and H Blood Group Systems.pptx
    9 points
  27. I have never understood this obsession with looking at reactions down a microscope in blood bank, except looking at things like a Kleihauer or when teaching, to show mixed-field reactions. The great Peter Issitt, not a bad roll model to have, wrote, many years ago now, a passage that I attach from page 69 of his "Applied Blood Group Serology" book, 3rd edition, 1985, Montgomery Scientific Press. That having been said, all reactions seen MUST be recorded, it is just that macroscopic reading is almost all that is ever required.
    9 points
  28. Ok, here we go. First is from a personnel stand point. When promoted from with in you are no longer "one of the guys". This means that some of the staff will try to leverage your close friendship which in turn will cause problems with others. Both you and the rest of the staff need to recognize that things have changed on a personal level, at least in the work place. This does not have to be dramatic and should not be, but it is real. Some can do this and some find it very difficult. Now, when coming from outside your are exactly that, an outsider. Now the level of this can vary immensely depending on the situation. One time when I changed facilities it was just across town and I new many of the staff at the new facility so a lot of the unknowns were minimized. On the other hand, I also moved to another facility out of state and pretty much walked into an unknown from a staffing standpoint except for what little I could glean from the interview. As I noted in my previous post, be very judicious when using the phrase, "this is how we did it." I've had new employees who would say this at every opportunity and then go into detail about how we were either doing it wrong and that their way was just much better. This became very trying to everyone else on the staff and we finally just tuned them out. Because of that we probably did miss out on some good ideas. One last point, in either case be aware of any others staff who may have either applied for the position or simply been over looked. Depending on their personality they can either be a great help or a significant hinderance. Do everything you can to get them involved and engaged. They can be your greatest asset but it may take a little extra work on your part. For me, the personnel issues were always the most difficult. I'm assuming that you are new to the lead position and not knowing your previous experience here a couple of generalizations. Unless something is an obvious hazard to either patients, staff or the ability to pass an impending inspection/assessment don't be in a big hurry to make changes. As they say in the military, you need to understand the lay of the land. Become familiar with the blood bank/transfusion service medical director and let them have the chance to become familiar with and confident in you. They can and should be your greatest allies. Ultimately most of what you want to change will have to be approved by them. You need to understand the current processes before trying to change them. At one of the facilities I moved to I noticed that many of the staff were not following their procedures "to the letter". The way I dealt with this was at the monthly staff meeting we would go through a procedure as a group, line by line and I would ask the questions, "Is this how you are really doing it? If not, why not and how are you actually doing it?" This is when I would make suggestions for changes and generally a lively discussion would ensue. It took quite awhile to go through the procedure manual but by picking, what I considered the most important one first it was time well spent. This is getting a little long so I'll end with how I described my position as Transfusion Service Supervisor at a 350 bed level ll trauma center. My job was to provide the staff with the tools (equipment, knowledge, material and support) for them to do their jobs at the highest level possible. All this while keeping the dragons (administration) away from the door. Good luck and if I can think and anything else that others may miss I share a few more golden nuggets of wisdom with you. Above all else have faith in your self. Wow I think that's the longest post I've ever made.
    9 points
  29. I would pull the unit from inventory and contact the supplier. They should have the resources to investigate the problem with the donor.
    9 points
  30. PLEASE do not worry. Your midwife is COMPLETELY wrong, and really should not comment about something she patently does NOT understand, and about which she has a pitiful amount of knowledge. She should never have answered your questions with her lack of knowledge, but should have left it to your Obstetrician. I note that you are a fellow "Brit"! Within the British population, the percentage of people who have the R1R1 type (which is a type within the Rh Blood Group System) is 16%. Also within the British population, the K- type (which is part of the Kell Blood Group System) is 91%. What that means is that 91% of 16% of the British population is R1R1, K-, or, give or take, a few decimal points, 15% of the British population (about an eighth of the British population). On Friday, 19th October 2018, the British population was measured as 66,690,116! Let's call that 16.5 million in round numbers. This means that, give or take, 9, 975, 000 in Britain are R1R1, K-. Now, admittedly, your midwife will only be looking after women, but, even then, that means 4, 987, 500 women will have the same Rh type and K type as you! How your midwife has only come across your "rare" type four other times in her career, is beyond belief (and I genuinely mean BEYOND belief), unless, as I say, her knowledge of blood groups and blood group serology is incredibly poor, and I repeat, she should NEVER have worried you like this. Just in case you think that I do not know what I am talking about, I have worked in the field of blood transfusion/blood group serology for 43 years, have been an internationally invited lecturer and am the Chief Examiner in Transfusion Science for the Institute of Biomedical Science in the UK, and am a co-author of the British Society of Haematology's Guidelines for Blood Grouping and Antibody Testing in Pregnancy. I don't write that to "blow my own trumpet", as it were, but to try to reassure you that I actually do know what I am talking about. I should warn you that "consulting Dr Google" is equally as useless as listening to your midwife. You should really relax. YES, it is possible for you to produce red cell antibodies during your first pregnancy, but it is INCREDIBLY RARE. It is even more rare for such an antibody to cause any problems in a first pregnancy. I notice that the report from the Blood Bank was that they detected WEAK reactions with 26 of 30 panel cells, but they could not identify a specificity. They have requested three further samples of blood to send to the Reference Laboratory. Again, to give you some comfort, I hope, I ran a Reference Laboratory in London for 16 years before I retired in 2016, and we saw, quite literally hundreds of cases like yours. For a red cell antibody to cause any problems within you pregnancy, it would have to have a titre of 32 or above (this means that it would still be detectable when it has been diluted THIRTY TWO times). I can assure you that the mere fact that the Blood Bank reports weak reactions means that there is ZERO chance that the titre will be 32 or above. If a Hospital Blood Bank, however big or famous the hospital may be, cannot identify an antibody, it is almost universal practice that samples will be sent to a Reference Laboratory for further testing - AGAIN, DO NOT WORRY ABOUT THIS. There are many, many red cell antibodies that are clinically insignificant, both in terms of transfusion reactions and haemolytic disease of the foetus and newborn (which is what your midwife has left you worried about). I KNOW it is difficult, but PLEASE do not worry. PLEASE take no notice whatsoever of your midwife on this matter (I am sure she is an excellent midwife, but she is patently no expert in the field of blood groups), but DO talk to your Obstetrician, who, I hope, will have talked to your hospital's Haematology Consultant, who, in turn, will have spoken to the Consultant in Charge of the Reference Laboratory, and I am sure that they will echo my opinion that there is NOTHING to worry about. Oh, and lastly, I am R1R1, K- myself!!!!!!!!!!!!!
    9 points
  31. SMILLER

    Just for fun

    LOL! We would send it to our reference lab! We have other things to do here... Scott
    9 points
  32. I will quote (one of my favourite quotes) from Issitt Peter D and Anstee David J. Applied Blood Group Serology. 4th edition, 1998, Montgomery Scientific Publications, pages 63-64 (only because I cannot get to my copies of earlier editions at the moment - as while looking for them, a large number of my text books almost knocked me sideways, as they fell off the top of my wardrobe, and my wife nearly "brained" me too for making our bedroom look a mess!). "Reading Methods for In Vitro Tests. Now that most routine tests are carried through to an antiglobulin reading the question of how to read them does not often arise. They are usually read macroscopically in order that the cells and serum are left in the tube for progression of the test. A few cells may, of course, be removed and examined microscopically at any stage if this type of reading is required. However, one of us (PDI) has believed for years that routine use of the microscope in the blood bank creates far more problems than it solves. Almost any cell suspension, including those in which washed cells have never been exposed to antibody, if examined carefully enough under the microscope will be found to contain a few small clumps of red cells. Thus, while reading aids such as mirrors or hand lenses are acceptable, routine use of the microscope is not condoned. This reasoning also applies to the reading of antiglobulin tests. Again if agglutination cannot be seen with the naked eye, a hand lens, a convex mirror, or the type of microscope in which the contents of the tube are viewed while still inside the tube by placing the tube itself on the microscope slide, IT IS NOT THERE. Were it not for special tests, such as those in which mixed-field reactions may have occurred or when a small percentage of fetal cells might be present in a maternal sample, the microscope should be banned from the blood bank. Enzyme tests for agglutination or following conversion to antiglobulin reading, should NEVER be read microscopically." Several things should be noted about this quote. Firstly, there is NO distinction here between the indirect and direct antiglobulin test. Peter Issitt (see PDI, although I happen to know that Dave Anstee agrees with him) talks about reading antiglobulin tests. Secondly, this quote was originally written well before 1998. Since that time, there have been huge steps made in improving the sensitivity of tests within blood transfusion and blood group serology (often at the expense of specificity, and certainly at the expense of making diagnosis from the results of these tests straightforward - see the introduction of the term "delayed serological transfusion reaction", when there is laboratory evidence of a transfusion reaction, but no clinical evidence of a "delayed haemolytic transfusion reaction" (Petz LD and Garratty G. Immune Hemolytic Anemias, 2nd edition, Churchill-Livingstone, 2004). Thirdly, both Peter Issitt (1986) and Dave Anstee (1997) have been awarded the AABB Emily Cooley Memorial Award and Lectureship (amongst numerous other international awards - Dave was the President of the British Blood Transfusion Society, the Kenneth Goldsmith Award in 1985 and the James Blundell Award in 2003; these two are far from idiots! Lastly though, looking down a microscope is no panacea to detecting a transfusion reaction. I would draw your attention to Sachs UJH, Röder L, Santoso S, Bein G. Does a negative direct antiglobulin test exclude warm autoimmune haemolytic anaemia? A prospective study of 504 cases. British Journal of Haematology 2006; 132: 651-661. This paper talks about the production of de novo antibodies and anamnestic antibody production post-transfusion, as well as WAIHA. It comprehensively debunks the fallacy that a mixed-field reaction can, in all cases, be detected by the use of a microscope. So, perhaps the question should be, if the DAT is negative to the naked eye, should we perform an elution in each case? I REALLY, REALLY hope that nobody (seriously) answers YES to that suggestion (believe me, it was made with my tongue very firmly in my cheek)! Sorry about the rant!
    9 points
  33. galvania

    Rh Pos or Rh Neg?

    I would just like to add one 'grain of salt' to this debate. You cannot detect all D variants - whether D weaks or partial Ds by serological methods alone. Neither D weaks or Partial Ds behave in a way that allow one to say that all D weaks or partial Ds react with such and such a strength. You will always miss some. You will miss some D+ donors because their D antigen is so weak that it is not detected by even the most sensitive of routine serological tests - or because despite using at least two different monoclonals the donor has an extremely unusual variant that is detected by neither. You will miss some 'D-neg' patients because they have sufficiently large numbers of D-antigen sites that they give a normal reaction with the anti-D reagents used. Follow the manufacturer's instructions for the reagent and method used and you will detect as many as you can hope to detect. And before you shoot the manufacturers because their reagent/instrument gave a 4+ reaction with a partial D known to have 10'000 D-antigen sites per red cell, and discovered because the lady made an anti-D and she is pregnant - please take a minute to think about the theory behind the serology. Maybe in years to come there will be a foolproof routine method for catching every single one……...
    9 points
  34. Sorry guys but you've got it wrong about the witches. she was a witch if she DID NOT drown - in which case she was burned at the stake. whether she had anti-D or not!
    9 points
  35. 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
  36. 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
  37. 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.
    8 points
  38. Malcolm Needs

    why 3 months?

    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.
    8 points
  39. I did check our IFU and they did specifically state to use glass tubes. No more arguments.
    8 points
  40. The mechanisms of what have been termed TRALI (actually a subset of acute lung injury/acute respiratory distress syndrome) and TACO (actually something very common, congestive heart failure) have been widely misunderstood due to unjustified assumptions/dogma. There are many biologic mediators other than antibodies that can cause lung injury after venous infusion which directly subjects the lung vascular endothelium to these mediators (antibodies, activated cells, lipids, mediators such as sCD40L, DNA/histones). Likewise there are many mediators that can cause or exacerbate cardiac failure after venous infusion (inflammatory mediators, excess volume). Cardiac failure is not just volume overload, but can be caused by fever, inflammatory cytokines and vascular/myocardial muscle dysfunction. The notion that these are distinct entities is also at variance with clinical experience. Many patients have signs of both cardiac failure and pulmonary failure simultaneously. So the definitions and pathophysiology used in reviews and texts are lacking in validity and just plain oversimplified and wrong, in my view. There are compelling data to support these iconoclastic contentions for TRALI, and some for TACO. Most germane (see attachment), when we introduced universal leukoreduction, we saw a sustained 83% drop in reports of TRALI and 50% in TACO over the following years. This suggests that white cells/DNA/histones play a role in causing lung and heart inflammation and dysfunction. This clinical observation was confirmed in animal studies from Denisa Wagner's lab at Harvard demonstrating that neutrophil extracellular traps (NETS) infused intravenously can cause acute lung injury (see attachment). To me these observations are convincing evidence that leukoreduction alters cardiorespiratory injury and failure post-transfusion and represents one of the strongest arguments for universal leukoreduction. Needless to say, this challenge to dogma has been ignored by the transfusion medicine community which continues, at least in the USA, to infuse deadly white cells and their degradation products (free DNA/histones) to patients, one of the great tragedies of the last 20 years in the USA blood bank field. We got this entirely wrong and tens of thousands of patients have probably died unnecessarily due to complications of non-leukoreduced transfusions. ULR TRALI TACO PMC version.pdf NETS and TRALI Wagner 2012.pdf
    8 points
  41. jojo808

    Transfusion Errors

    I think we need to add an OMG emoji to our selections!
    8 points
  42. I was immensely honoured to receive this through the post today (with a lapel badge).
    8 points
  43. Hi Rich, I am not a clinician but as far as I know IVIG can be given to obstetrical patient in diff. conditions (autoimmune disorders, recurrent pregnancy loss, ...). I thought about IVIG when I saw the DAT becoming positive plus additional reactions coming up over the time. Anti-A and Anti-B are indeed the most prevalent antibodies in plasma derived products but other specificities of low titre can be present sometimes such as anti-D, anti-K and a bunch of antibodies of undetermined specificity reacting with several to not say all RBCs. Just a thought that can be doublechecked with the clinician..? Hereunder is a very great (not recent though) paper to be read and re-read again: Problems Associated With Passively Transfused Blood Group Alloantibodies George Garratty, PhD, FRCPath American Journal of Clinical Pathology, Volume 109, Issue 6, 1 June 1998, Pages 769–777, https://doi.org/10.1093/ajcp/109.6.769
    8 points
  44. And to give credit where credit is due, whatever I have achieved has been with the invaluable contributions of my collaborators, including physicians, scientists, medical technologists and nurses. In particular, my most important collaborator has been my wife, Dr. Joanna Heal MBBS, MRCP, whose brilliance and dedication to patient care made all the difference. That's her in the picture :).
    8 points
  45. Thanks ELondon. Could I just say again, even if the Reference Laboratory does detect an antibody (or more than one, come to that), it is not a particularly abnormal thing in pregnancy, but it does not mean for one minute that the pregnancy will be affected; Mother Nature has seen to that. There is another Blood Group System named Lewis. The antigens within this system are soluble in the plasma part of your blood, and are adsorbed onto the red cells from the plasma (they are not intrinsic to the red cell membrane). During pregnancy, the concentration of plasma lipoproteins (fatty proteins in the plasma) can increase enormously (about four-fold). These plasma lipoproteins "mop up" the soluble Lewis antigens, and a pregnant woman, who would normally be, for example, Le(a-b+), can become Le(a-b-), and may even, temporarily, produce antibodies against the Lewis antigens (an individual hardly ever produces antibodies against an antigen that they express - but strange things happen in pregnancy!). In addition, ALL babies are born as Le(a-b-), so any Lewis antigens Mum produces will NOT affect the baby! There are many, many other antibody specificities that will not affect the pregnancy at all. Now, I should say two things. Firstly, I cannot say, from a distance, what is the antibody in your plasma (that can only be done by the laboratories at the Hospital and the Reference Laboratory, but it does not sound at all serious). Secondly, i am what is called a Biomedical Scientist, not a doctor, and so I am, by Law, not allowed to diagnose (as far as I know, neither is the midwife), and this is why I am so glad that you are going to see an Obstetrician, who, I hope, will be able to reassure you even more. Mean while, sleep easier, and enjoy your pregnancy!
    8 points
  46. My advise for safe patient care is confirmation of the patient blood type by a laboratory professional.
    8 points
  47. Incubating patient plasma with patient red blood cells and then applying the antiglobulin test is no longer a Direct Antiglobulin Test but an Autocontrol test which is an Indirect Antiglobulin Test. Some may think an Autocontrol test gives the same results as a Direct Antiglobulin Test, but that is not always true.
    8 points
  48. I'd say that you have to consider the capabilities of your staff. I do ask my techs to use the microscope for DATs. They are all generalists and their time in blood bank is limited. Some of them shake too hard, in spite of my best efforts to fix that problem. They use a mirror, but some don't use a mirror well. So, in order to not miss weak positive reactions they use the scope with a tube roller. We also have a definition for microscopic agglutination (right out of the Technical Manual) that says it is a clump of 4-5 cells (though I do tell them that they should be cautious with this - if tests look suspicious, check them out, don't blindly ignore what you see). When I train, I stress the difference between a clump of cells that are friendly/kissing and a clump of cells that 'love each other' (agglutination). They do very well - false positives are rare. I don't see a lot of unnecessary work being done.
    8 points
  49. I would do a bit more work on it. There are two things I would do. Firstly, I would incubate a 4oC (but would include a group O cell in the reverse in case there is a "cold" auto- or allo-antibody there). Secondly, I would papain or ficin treat the reverse red cells (including a group O cell again as a negative control). As long as the group A and group O red cells remain negative, and the B cells react more strongly, but not as strongly as normal, I would be happy to call it a group A.
    8 points
  50. KKidd

    Retirement

    I will be retiring on August 9 and wanted to tell everyone that the forum has been a great source of information (and amusement at times). I have spent time reading Malcolm's posts trying to imagine what he sounds like (just love a British accent). Thanks for keeping the forum a place where we can all learn from each other
    8 points
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