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Showing content with the highest reputation since 09/29/2021 in all areas

  1. 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
  2. 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
  3. 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
  4. 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
  5. 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
  6. 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
  7. 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
  8. 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
  9. If the unit if leukoreduced, as all red cell transfusions should be, there is no need for CMV negative in my view.
    8 points
  10. 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
  11. 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.
    8 points
  12. We had an over zealous infection control team (made up of 100% nurses) come to our lab last year making the same demand. We told them, in essence, we will not comply because the risk of injury from handling those containers were greater than the risk they were trying to alleviate. Furthermore, the risk of accidently confusing saline with formalin, whose containers look exactly alike, was to high when removing from the cardboard containers. In addition to that, we told them the man hours required to keep up with that would require additional FTE's, which would not be approved. They conceded and we continued on, business as usual. TJC does not really inspect labs that are CAP, AABB, or CLIA certified. Those organizations understand the logistics of the cubes and do not have a problem with it. Most infection control officers are nurses and think from the nursing perspective only.
    8 points
  13. I did check our IFU and they did specifically state to use glass tubes. No more arguments.
    8 points
  14. 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
  15. 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
    7 points
  16. Here is an interesting paper showing that antibodies to red cell/platelet... may be transmitted via breast milk indeed, causing prolonged HDFN. Milk contains mostly IgA but IgM and IgG may be present of course and IgGs can cross the different barriers up to blood circulation (not on the same model - not actively - as the placenta though). The surprizing part here is the mother and baby are group A, A antigen is ubiquitous so the anti-A titer in breast milk should high enough to interfer with reverse group despite the adsorption of anti-A on various tissues. https://pubmed.ncbi.nlm.nih.gov/30720868/
    7 points
  17. To paraphrase Malcolm: A proven responder may have "other stuff", too. A serological crossmatch is probably the best, and sometimes, the only way to detect it.
    7 points
  18. With all due respect, if you do not trust the results given to you by your IRL, why did you send samples to them in the first place? The other thing is that the term "least incompatible" has been "rubbished" by LaTwrie Petz almost 20 years ago now (and you can't get much better than him!) - see Petz LD. "Least incompatible" units for transfusion in autoimmune hemolytic anemia: should we eliminate this meaningless term? A commentary for clinicians and transfusion medicine professionals. Transfusion 2003; 43(11): 1503-1507. DOI: 10/1046/j.1537-2995.2003.00583.x. I apologise if this reads as I am being personally rude to you; that is DEFINITELY NOT my intention.
    7 points
  19. Danielle, I love the lights. When i'm feeling stressed, I come here and break em. If you haven't noticed, move over them with your mouse and they break with the most refreshing sound of glass breakage. I hope you all don't think less of me now...
    7 points
  20. NicolePCanada

    John Judd.

    My favourite John Judd quote from a University of Michigan Symposium I heard him at. "Phenotypically matched RBC units for a corpse is not a medical breakthrough." If the patient needs blood get them blood, worry about the rest later. RIP John Judd
    7 points
  21. What about RH pos plasma products or platelets? Though they don't tend to cause an anti-D, they can "spike" one that dropped below detectable levels, I believe. And that far back, if any platelet concentrates were given, they would have had more RBC exposure than they do now with platelet pheresis units. Just a thought.
    7 points
  22. We do not routinely transfuse neonates (have not done one here in 30 or so years). We would give the freshest O= we have; irradiated if we have one. We are 3 hrs from our blood supplier. Chances are the infant will be transfused before we could receive appropriate products.
    6 points
  23. We only type for the actual antigen corresponding to the patient's antibody for anything other than Rh. For those Rh antibodies, we will type for the C, c and E as appropriate genetic-inheritance wise, as you described above. We don't typically type for e unless the patient has an e antibody (to prove it's creation) or is E positive (checking for heterozygosity), since 98% of people are e positive (we assume e pos unless given reason to check that). We would do a full pheno with whatever sera we have in house (pretty much all common antigens) for those patients where it might be useful (sicklers, WAA, etc.).
    6 points
  24. yan xia, there are two mutations present. The first, RHD 4.0/RHD DAR3.1. This will lead to the expression of a Partial/Weak D. The second mutation is a hybrid of the RHD and RHCE gene, with exons four to seven of the RHD gene being replaced, or substituted, by exons four to seven of the RHCE gene. I hope this helps a little.
    6 points
  25. Some caution may be appropriate. Most "colds" are indeed clinically insignificant and mere laboratory annoyances. Most of these are autoantibodies that can be avoided by pre-warming methods. However, some can be clinically important - there are examples of anti-Vel that behave exact as LaurieD describes, but are IgM, cold-reactive alloantibodies that can cause serious in vivo hemolysis. I think one case reported by Jill Storry was actually fatal. Another nasty beastie in this category is anti-P+P1+Pk (anti-Tja, in the old vernacular). I would suggest that a Reference Laboratory take a look at the sample (the Blood Bank of Hawaii is close ), just to give some assurance that the troublemaker is "just a cold auto". Pre-warming without an antibody ID may be dangerous. Just my two cents.
    6 points
  26. When I first read this post yesterday I was tempted to answer but thought I would wait to see what Malcom had to say. Glad I waited. My thoughts were much the same but Malcolm presented it in a much more succinct and detailed manner. As expected I have nothing to add other than my agreement .
    6 points
  27. I also should get up earlier to contribute! thank you all for the suggestions! In response to some of the ideas - her pregnancy loss end of last year and surrounding OB care was entirely through my institution, and I know we didnt give her any RhIg of any sort. Could find no evidence of ITP (handful of CBCs over months have been dead normal), no evidence of any underlying autoimmune disorder. No evidence of getting IVIG or any other antibody-based treatment. The only possible autoimmune trigger I recognized was the strep throat, but that's a long shot and anyhow she was promptly treated. And we don't use gel. Overnight we came up with some of the same ideas as y'all - warm auto with anti-D specificity, an anti-LW, or a D antigen variant. Just hearing from the manager we ran her against some O negative cord cells this morning; does not look like an anti-LW. We are opting to use what is left of the sample to send to reference for the D chip. I'll definitely update once we have more info!
    6 points
  28. All of the above are excellent suggestions. I will have to get up earlier to contribute.
    6 points
  29. Does the patient have ITP? Is it possible that she is receiving WinRHO (same as RHIG) for ITP? Does she have a low platelet count. I haven't seen this situation in several years but there was a time when patients with ITP who were rh pos would be treated with WinRHO (as long as they had their spleen). It would present as this very scenario you are describing. Another possibility is anti-Lw?
    6 points
  30. To emphasize Exlimey's point: "One event does not indicate a trend - changing the whole system to address a single cut-finger incident is unreasonable". Also of concern is the use of plastic, who knows in the near future if this will be available in test tube form in abundance? We need to look at how and why this accident occurred? Everything in our lives cannot be padded so we don't fall, trip, get our feelings hurt (sorry had to add that), or get a cut. I know it's very serious to get a cut from a blood-contaminated item but I personally would look at what is reasonable and prudent. I know we have 'seasoned' techs on this site, probably 20-30 years in the field that would think it strange for that incident to happen, I would think getting a cut from grabbing "clean" tubes from the dispensary would be more likely because you are grabbing a bunch of tubes but normally you grab tubes with samples in them (contaminated tubes) from either the centrifuge or tube rack and can clearly see what you are grabbing.
    6 points
  31. Don't use plastic tubes, stay with borosilicate glass. Static from the plastic will affect drop size adversely. As Malcolm said using CAT is better overall.
    6 points
  32. As Joanne mentioned above, no system is fool proof and there are lots of creative, inventive fools to prove it. Keep your system as simple as possible which should minimize the need for creative people to find ways around it. Now to your question, does it actually help prevent problems? Probably a few but certainly not all! I've seen people become lax in their diligence when they assume they are protected by the system. They seem to assume that if they make a mistake someone down the line with catch it. This is something to be avoided if possible. The only way that I know of to prevent this type of mind set from developing is through education and convincing everyone involved in the process that their step is critical and by keeping it simple they will be more likely to perform their step as instructed.
    6 points
  33. All the talk about statistics is great but in the real world you never know: I once screened over 30 units for K. All were positive. As I was the night guy, the day folks were laughing until they got the same results. All we could figure is the blood center was screening for K and shunted all the +s to a shelf which we received in bulk. I've also screened for Fya in past. Once i screened 4 units and found 2. The next time I had to screen 16 and the last 2 were negative. As I said, the stats look good but reality is sometimes a bit different.
    6 points
  34. Here the Medical Director or designee is the one responsible for contacting the patient's physician. If the patient's physician refuses to contact the patient, our Medical Director or designee will end up having to do it.
    5 points
  35. Malcolm Needs

    Why 3 days?

    The timing for fresh samples is somewhat different in the UK than in, for example, the USA. The timings, and the reasons for these timings, are set out in paragraph 3.7 of the BCSH Guideline "Guidelines for pre-transfusion compatibility procedures in blood transfusion laboratories" (written by Claire Milkins, Jenny Berryman, Carol Cantwell, Chris Elliott, Richard Haggas, Joan Jones, Megan Rowley, Mark Williams and Nay Win, for, and on behalf of the BCSH, and published in Transfusion Medicine 2013; 23: 3-35. doi: 10.1111/j.1365-3148.2012.01199.x), with the Key Recommendation of this paragraph being, "Serological studies should be performed using blood collected no more than 3 days in advance of the actual transfusion when the patient has been transfused or pregnant within the preceding 3 months." As I understand it, this timing was based on the work originally carried out by Professor Patrick Mollison many years ago, who found that a new specificity of an alloantibody, or a nascent antibody that has become undetectable by normal serological techniques, can appear (or reappear) in the plasma of an individual within three days, after stimulation. The problem is that not all patients know whether or not, or when, they have been transfused, or may deny it for religious reasons (I once cross-matched for a patient who had been a life-long Jehovah's Witness, who had an anti-Fya in his plasma that had a titre well in excess of 128). I hope that helps.
    5 points
  36. We don't actually see many T&S orders from the ED. Those are usually patients who may be surgical candidates (like broken hips, bowel obstruction, etc.) and unless they are anemic, usually not transfused. There are more orders for 1 unit and transfuse, almost 100% look appropriate when reviewed. Instead we saw a pattern of ED providers ordering blood types in order to have a Blood Bank specimen available. We've persuaded them to use a BB Hold order instead of charging a patient for a blood type that was rarely needed - a specimen is collected but nothing done until they order a Prepare/T&S. We do use some discretion with the BB Hold orders. If the H&H is low or the patient is a really active GI bleed or it's a trauma case that looks bad, we put the specimen on the Echo just to get a head start. Nothing is reported until we get an order but it can definitely help the TAT. I've never actually looked at stats on ED orders, but I've wanted to (in my abundant spare time ). Another project I've wanted to tackle is to look at our emergency releases (especially on medical, rather than trauma, patients) and MTP orders to see what % of our patients we are actually transfusing or MTPs that only use a unit or two (or none), to see if we have any interesting provider ordering patterns. Also, how many times we ship blood with transfer patients vs how many times they are actually transfused in route or the unit(s) wasted. I would like to compare that information with the score ED assigns to the trauma patients to see if we are correlating well.
    5 points
  37. All potentially clinically significant antibodies like this can be managed pretty well by non-invasive fetal monitoring for anemia by ultrasound (doppler velocity), so the management should be the same for all such antibodies. Clinical variation is great, as you all know, so the drill is to monitor the fetus. No anemia, no worries. Anemia leads to intervention. Serology is largely irrelevant (e.g., titers) but habit is to measure them by most clinicians.
    5 points
  38. I do know of one case in the UK that involved an IUT given by Professor Kypros Nicolaides (a world renowned foetologist) at Kings College Hospital involving anti-Kpa in pregnancy, but I never saw it written up, and there was certainly no clinical sequalae, and so it could be that the anti-Kpa (the titre was not all that high) may well have been coincidental to some other pathological condition (KCH was one of "our" hospitals in terms of Red Cell Immunohaematology). In all my years in blood transfusion/blood group serology, I never saw an unequivocal case of anti-Kpa that caused clinically significant HDFN, and it was a fairly common antibody at our laboratory. That probably doesn't help that much, but that is my experience on the subject.
    5 points
  39. We got the same song and dance from our infection department some years ago. Our manager told them the instruments would not work correctly if the saline/reagents were not in the manufacturer's container, the interior plastic bag would droop and possibly break without the cardboard support to contain it. The solution/compromise was to make a notebook of "acceptable" cardboard containers, e.g. saline/reagent cubes. If an inspector questioned, we would show them the book with pictures of what had to be in cardboard to maintain lot numbers or integrity of the reagent. I agree, the rule is to reduce incoming exterior dirt and insect infestation for patient areas but the lab is not a patient care area. Some committees make a mountain out of a molehill and go too far.
    5 points
  40. I QC reagents before I put them into use; usually not upon receipt.
    5 points
  41. Here is a follow up. The baby had tested with anti-A on 27, April and transfused with O washed cells the same day, but on 10, May she had no anti-A and received A type packed red cells with no transfusion reaction. She has stoped feeding on her mother's milk for 14 days. I tried to persuade her mother to do some tests. The results came out and she has no anemia, with normal reticulocyte count and percentage. Her bilirubin and LDH are normal too. But she has not tested her haptoglobin. She has not received any blood transfusion and IVIG. She just diagnosed with slight anemia during pregnancy and after birth. She had taken iron supplements during pregnancy,. This is her eventh pregnancies and the third baby, she had several miscarriages. She told me her case seems like a mystery both to her and the doctors she know. She just want to know if she is ok and the baby will be healthy in the future.
    5 points
  42. I would report the crossmatch as compatible and recommend use of a blood warmer for transfusion. No further workup necessary.
    5 points
  43. I had an OB patient with an antibody to anti-Goa that we picked up on prenatal screening. One cell was positive on the screen and nothing showed up on 2 panels, Because it was an OB case, I sent it to the ref lab and they identified the culprit.
    5 points
  44. I highly recommend you use this opportunity to discontinue using a separate BB ID band. Using the patient’s regular ID band works great. If you’re using scanned PPID from the wristband for specimen collection & labeling, adding another ID band into the process no longer adds any safety benefits. You’ve already created your closed loop system using the regular hospital ID band and scanning it for both specimen collection and blood administration in BPAM.
    5 points
  45. Arno

    Ortho MTS Gel cards

    This thread is pretty old but as it comes up again.... this "air gap" is required to avoid having the Anti-Human Globulin (AHG) present in the gel matrix getting partly "neutralized" by the excess of human immunoglobulin from the plasma. Keep in mind that plasma is full of various human Immunogloblins which will be recognized by the rabbit AHG. This "partial" neutralization may weaken the reaction indeed. Same as in tube but there is no washing step requires as the air gap is there to prevent this neutralization. Once cells are sensitized after the 37°C incubation step, the card is spun and the AHG will catch the Ig bound to the RBCs leading to positive reaction.
    5 points
  46. Excellent. It's not often that the IFU comes to our rescue.
    5 points
  47. Not that I am aware of. There are publications reporting an increase of DAT positive samples amongst Covid-19 patients. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7414594/ According to the authors, the eluate (IgG) reacts only with cells from Covid patients and this state is likely to be transient (related to hyperinflammation in these patients).
    5 points
  48. In our institution the most inappropriate use of group O cells is for trauma patients where we haven't received a sample so that we can switch patients to their own ABO type. We exhort our trauma team to send the first sample they send to us. ABO mismatched red cells is a suboptimal use of group O red cells, and in the long run, probably harms patients. We switch patients as soon as we can when they are A, B or AB to their own red cell type. I know there are some old dogmas that you should keep patients on group O once you've started. No data whatever to support that, practice some data suggesting it's harmful and it's obviously terrible for the supply of group O red cells.
    5 points
  49. I did a swiss cheese diagram after the fatality in the US a few years ago to hit home what COULD happen. Attaching, feel free to tweak for your use. It speaks to just one of the reasons why we require the sample confirmatory sample, and probably the most important one, WBIT. Swiss cheese TX incompatible transfusions patient death1.pptx
    5 points
  50. We used to have sign in our BB: The Buck Stops Here. Of course someone altered the posters to "The Buick stops here". My boss was pissed off about that. The concept being that if you have a system of multiple checks and balances you better make sure the first one works. I have seen this concept evidenced too many times in my career. People get complacent.
    5 points
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