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  1. 8 points
    Malcolm Needs

    Phenotying

    I agree entirely with exlimey, except to say that even today's monoclonal antibodies need a potentiator. Many of them include a small amount of bovine albumin in the reagent bottle. I don't, however, agree with you Jermin. The reason being is that there is no such thing as a silly or daft question. The only silly or daft question is the one you (anyone) don't ask, because, if that question is not asked. the person who doesn't know the answer will never know the answer. Sadly, there are numerous examples of silly or daft answers!
  2. 7 points
    Absolutely the advice given to you was correct. For a start off, as you say yourself, 80% of A2B individuals do NOT make an anti-A1, but of those 20% who DO make an anti-A1, how many will make that anti-A1 as a result of immunisation as a result of transfusion or pregnancy? The answer to that, if you read any book concerning blood group serology (and that is NOT a criticism of you - we all started somewhere, including the very best, such as Herr Dr Willy Flegel, and others - and I have HUGE respect for Willy), you will see that a clinically significant anti-A1 is amazingly rare. For an anti-A1 to be clinically significant, it has to react strictly at 37oC, and that is a VERY rare "animal", and no example of anti-A1 has EVER been implicated in a case of HDFN, so, PLEASE, do not worry about giving A1B (or even A1) blood to an A2B individual, even if they have an anti-A1 in their circulation, UNLESS they have an anti-A1 that is actually active at strictly 37oC.
  3. 7 points
    The INR is a largely useless predictor of bleeding risk except for those on coumadin/warfarin, and not so good a predictor in those patients. It is known that the range of 2-3 is a reasonably safe and effective one for anti-coagulation to prevent recurrent thrombosis (usually DVT or PE). Beyond that, INR numbers like 6 or 12 tell us next to nothing except that factor VII is quite low, which may or may not be clinically important. The INR of liquid plasma or FFP is around 1.6-1.8, and is not affected by the citrate anticoagulant, since exogenous excess calcium is added in the performance of the INR. INRs of 1.5 to about 2.0 are not associated with substantial increases in bleeding, either spontaneous or procedure related, and do not need to be corrected at all, in my view, and this opinion is supported by an extensive observational literature. FFP will not correct such an INR in any case, and thus represents risk without benefit. Medical specialty society recommendations for INRs of 1.5 prior to procedures are without any evidence support whatever, and represent old, no longer valid expert opinion. If an INR needs correction for any reason, factor concentrates are more effective and less likely to harm the patient than FFP. FFP should never be used to reverse warfarin/coumadin in my opinion, because of these efficacy and safety issues. Unfortunately factor concentrates are also much more expensive than plasma/FFP. However, this considers only the cost of the product, not the cost of any clinical complications such as thrombosis, volume overload, ICU admission, etc., not to mention death, all of which are more likely with plasma/FFP. Meta-analyses of randomized trials of FFP vs. factor concentrate, demonstrate that FFP is associated with a two fold mortality increase. 'Nuf said. One ICU admission for a few days can balance the increased costs of factor concentrates for the overall health system. Factor concentrates, preferably II, VII, IX, X concentrates that also contain some protein S and C; in the USA=Kcentra; in Europe=Beriplex are preferred over three factor concentrates, but both are superior to FFP.
  4. 6 points
    exlimey

    Rule out Anti-K

    I agree with Malcolm. In theory, there may be examples of anti-K that only react with K+k- cells, but in practice it's a very rare event. One of my former colleagues/mentors once said that one shouldn't worry about missing a weak antibody. If the patient were unfortunate to be transfused antigen-positive blood, the former weak antibody would be super-strong next time around !!! Problem solved.
  5. 5 points
    Jermin

    Phenotying

    Thanks exlimey for a really good explanation, with background information. Always nice to put an answer in an easy to grasp wording. Cheers Malcom, gives me more confidence to seek out answers to questions (which I have plenty of)
  6. 5 points
    Malcolm Needs

    Rule out Anti-K

    In my opinion (and that of the BCSH Guidelines) you do not need a K+k- red cell to rule out anti-K. If you look at the antigen profile of the red cells you use every day as screening cells, they will not have a K+k- cell, and yet you are ruling out the presence of anti-K (and any other antibodies directed against the major blood group antigens) with each sample that gives negative reactions with these red cells. In addition, if you look at the screening cell profile that the BCSH Guidelines recommend, they say that the K antigen MUST be represented, but NOT that these cells must be K+k-.
  7. 4 points
    John C. Staley

    5 Day Plasma

    I had hoped that the validation mania had subsided. It's good to see that there is still some common sense out there. I never did understand why so many of us felt the need to continually reinvent the square wheel when all the work on the round one had already been completed.
  8. 4 points
    Malcolm Needs

    Phenotying

    The reaction with anti-D may well be enhanced - but not for the right reasons! Thorpe et al1, 2 reported that monoclonal anti-D molecules possess a V4-34 moiety, that is also present in anti-I and anti-i. As a result, if papain-treated D- red cells are tested with such antisera, or untreated D- red cells are tested with such antisera that have not been brought to room temperature, they may agglutinate, and you will get a false positive - which is the very last thing you want. 1. Thorpe SJ, Boult CE, Stevenson FK, Scott ML, Sutherland J, Spellerberg MB, Natvig JB, Thompson KM. Cold agglutinin activity is common among human monoclonal IgM Rh system antibodies using the V4-34 heavy chain variable gene segment. Transfusion 1997; 37: 1111-1116. 2. Thorpe SJ, Ball C, Fox B, Thompson KM, Thorpe R, Bristow A. Anti-D and anti-i activities are inseparable in V4-34-encoded monoclonal anti-D: the same framework 1 residues are required for both activities. Transfusion 2008; 48: 930-940.
  9. 4 points
    exlimey

    Phenotying

    The Rh typing reagents are designed to react that way. These days, the reagents are monoclonal, IgM in nature and give direct agglutination in a very short amount of time (similar to anti-A and other ABO reagents). Centrifugation is also usually part of the process. Antibodies to Rh antigens in patients (or donors) are typically IgG and require incubation and an antiglobulin phase. Most manual tube testing systems these days also use a potentiator to enhance reactivity and/or reduce incubation times. In the "bad-old-days", Rh typing reagents were human-source, IgG in nature and usually required incubation and an antiglobulin phase.
  10. 4 points
    exlimey

    Rule out Anti-K

    I like that ! None of this wishy-washy, barely reactive stuff.
  11. 4 points
    BldBnker

    Rule out Anti-K

    That is what my former supervisor used to say (he was a tech for over 50 years)! Get the titer up where you can work with it! God rest him!
  12. 3 points
    How do you know that the positive DAT is due to ABO incompatibility, unless an elution is performed. Surely, you are making an assumption (a very likely assumption, but an assumption nevertheless)?
  13. 3 points
    I think that this is very possible. We have seen some thawed plasma look like egg drop soup after several hours in the refrigerator. If you place it back in the water bath for about 5 minutes, cryoprecipitate will go back in solution and should be fine to transfuse. If it still looks the same after warming, then you shouldn't use it.
  14. 3 points
    SMILLER

    Antigen Tested Units

    There are two types of "antigen negative" units we can get from our supplier here in Michigan. One is "historically negative" -- those have to be retested when they arrive. The other type is "confirmed" -- those units have been confirmed negative for a particular antigen at the supplier and do not need to be retested here. Scott
  15. 3 points
    Personally, I think people are getting a bit "hung up" about this - not least the people who "write the rules", and I think that a lot of these problems are caused by the sloppy use of nomenclature (see my first ever post on BloodBankTalk back in March 2009 - before it became PathLabTalk). When you are using antibody screening red cells, you are using, I presume, R1R1, R2R2 and possibly rr red cells, but are you actually? These are "most likely genotypes", that are derived from phenotypes, but I very much doubt if the donors, from which these red cells have been derived, have been genotyped. Even if they have been genotyped, it is extremely unlikely that full gene sequencing has taken place on the RHD and RHCE genes to determine, whether either the RHD gene is present in a homozygous state, a hemizygous state, or a heterozygous state, where one RHD gene is of the wild type and the other is mutated, and would produce a variant D antigen. or the RHCE gene is homozygous for the production of, in order, the C and e antigens, the c and E antigens and the c and e antigens, or whether they may be hemizygous with a silent gene (either with a normal RHD gene to encode a D-- or D.. haplotype, or with a silent RHD gene to encode an Rhnull haplotype), or whether they may be heterozygous with, for example, a normal C and e antigen and a CeS antigen in, for want of a better way of putting it (although this, strictly speaking, only applies to genes, rather than antigens) in trans. The same principle applies to all of the other antigens and their genetic backgrounds. So what am I saying? I am saying that, day after day, we are excluding the presence of an anti-D, an anti-C and an anti-E (and, possibly, an anti-f) with screening cells that we actually do not know what antigens they are actually expressing, and yet we do not worry about this. It is only when we detect a reaction with the screening red cells that we bother to perform an antibody investigation to determine the specificity of the antibody causing the reaction. What, I ask, does this say about our logic? I would contend it says nothing flattering! So, if you are detecting an anti-D, and you (that is the collective "you", JustaKIDD, not a personal "you" - I am certainly NOT attacking you as an individual) are worried about the presence of an anti-C or an anti-E, because you only have one example of r'r or r"r red cells to exclude the specificities, I, unlike the people who "write the rules" would say "so what", but, if you are worried, why not just assume the antibody/antibodies is/are present, and cross-match rr units (if, indeed, the red cells in the bag actually ARE rr ). Lastly, in all the years since anti-C and anti-E have been described (1941 and 1943 respectively), how many patients, with anti-D in their plasma, have had a fatal transfusion reaction due to the presence of an undetected anti-C and/or anti-E? Not many (if any) I would suggest, and yet we, as a whole, get ""hung up" about such things, for no apparent reasons.
  16. 3 points
    R1R2

    Rule out Anti-K

    I have seen dosage a couple of times and a >K reacting at room temp only. I agree with Malcolm and his reasoning why K+k- cell is not required to rule out >K.
  17. 3 points
    Malcolm Needs

    Presence of H antigen

    All of my books say O>A2>B>A2B>A1>A1B. The only impact this may have on your routine work is either if you come across a patient who has auto-anti-H or auto-anti-HI in their plasma (in which case, cross-match ABO compatible units and ignore the results of the panel - because the panel will be group O and so give very strong results with such auto-antibodies), or if you are taking an examination, and the examiner is particularly sadistic or trying to show just how much they know, rather than trying to find out what the candidate knows. Do, however, watch out for a genuine Oh individual, with an allo-anti-H (which you could come across at any time - if you are unlucky), but such an anti-H is usually, but not always, pretty damn strong!
  18. 3 points
  19. 3 points
    Amazing how conservative they can be with transfusions when motivated.
  20. 2 points
    galvania

    Lewis A

    Malcolm, are you really trying to kill Mr. Lewis??????????
  21. 2 points
    SMILLER

    Lewis A

    From you to our pathologist's ear, Malcolm! Scott
  22. 2 points
    Malcolm Needs

    B(A) Phenotype?

    It is important to remember that the A, B and H antigens are not direct gene products, but are their as the result of the action of specific transferase enzymes. In the case of a group AB individual, the N-acetyl-D-galactosaminyl transferase (the A transferase) "competes" against the D-galatose transferase (the B transferase), and it is not unusual to come across a case where "one transferase has beaten the other". This results in an apparent weakened A or B antigen, and this could be the answer in this case. It could also be, of course, that there is a "genuine" weak expression of the A antigen, due to the patient inheriting an A2 gene (or other weak A gene). This could be checked by adsorption and elution tests with an anti-A. The reaction with the A1 reverse grouping cells could be due to an anti-A1 in the plasma, but this would not account for the reaction with the A2 reverse grouping cells. This latter reaction could be due to a "cold" auto-antibody, such as auto-anti-H, auto-anti-HI or auto-anti-I, or to a "cold" reacting allo-antibody, such as anti-M or anti-P1, where the corresponding antigen is not being expressed on the B reverse grouping cells. This, of course, would all have to be proven with appropriately typed reagent red cells. Depending upon the anti-A reagent you are using, but I assume that you are using a monoclonal reagent, I would be happy myself to call this an AB, and not waste my group O stocks unnecessarily. Lastly, as far as plasma is concerned, I would try to give group AB, but also wouldn't hesitate to give either A (preferably) or group B, unless the patient is of small stature, in which case I would definitely go for AB.
  23. 2 points
    Yes, you are completely right Yanxia. Briefly, the patient's plasma and reagent red cells are incubated at 37oC, as for a normal tube IAT, to allow the antibody in the plasma to sensitise the antigens on the red cells. The tests are then washed free of unbound antibody (as for the normal tube IAT), but then, instead of adding AHG at this stage, fresh ABO compatible serum (it has to be serum, rather than plasma, to ensure there is complement there to initiate the classical complement pathway), which is known not to contain any atypical antibodies (we used to use AB serum from a source that had been extensively tested and found to be free of any such antibodies) and mixed with the red cells. The tests are then incubated again at 37oC, to allow for the complement cascade to be initiated, and then washed again, as for a normal tube IAT. Lastly, monospecific anti-C3d is added, and the tests GENTLY centrifuged, and examined for agglutination. A negative control, using the inert AB serum, rather than the patient's plasma, must be set up and tested in parallel. Of course, such a technique can only be performed by tube, capillary, tile or liquid-phase microtitre plate techniques, as column agglutination and solid-phase microtitre plate techniques cannot be used.
  24. 2 points
    Malcolm Needs

    Lewis A

    Sorry Scott. In my personal opinion, and it is only my personal opinion, it's not 20th century........it is at best 18th century!!!!!!!!
  25. 2 points
    Malcolm Needs

    D weak transfusion

    No! Sorry Amra23. You do probably have a baby with a Weak D Type 1, but you do not necessarily have a baby with a Weak D Type 1. Depending on what your monoclonal anti-D reagent(s) are designed to detect, you could, for example, have a baby with a Partial D VI, and the very last thing you want to do is give a female patient with such a partial D type, D Positive blood. Certainly, for the time being, I would cross-match D Negative blood until the D type has been proven (either using a whole lot of different anti-D reagents designed to detect various weak or partial D types, or at a molecular level). It may well be a Weak D Type 1, and so it could be argued that it is a waste of D Negative blood to give this to her, but, personally, I would be devastated if I gave a baby girl D Positive blood, before I had a definitive D type on her, only for her to make an allo-anti-D, which could have a terrible effect on her ability to produce children herself later in life.
  26. 2 points
    AMcCord

    Antigen Tested Units

    How do you handle those that you don't have antisera for - like Vel for example?
  27. 2 points
    Malcolm Needs

    Lewis A

    Probably! We haven't screened for the Lea antigen for anyone with an anti-Lea for years in the UK, and we haven't come across a transfusion reaction - although there are reports in the literature.
  28. 2 points
    AMcCord

    Choosing an anti-D reagent

    Inevitable discrepancies, I'm afraid, dependent on which clones are used in the reagent.
  29. 2 points
    ZoeS

    Just saying Hi

    It's great having Malcolm in the lab to fire questions at! He really is a walking, talking Transfusion textbook and a true gentleman.
  30. 2 points
    Cliff

    Just saying Hi

    Welcome, anyone who has Malcolm as en employee is very fortunate.
  31. 2 points
    Firstly, and if possible, we would use an IgM monoclonal agglutinating antibody. Secondly, we can elute off the auto-antibody using mild treatment with DTT or ZZAP, leaving the red cells relatively intact (relatively, because some antigens are denatured by this, while some others are considerably weakened). Thirdly, and more commonly now in the UK, we can perform genotyping (but it has to be remembered that genotyping is only a prediction of what antigens may actually be expressed on the red cell surface).
  32. 2 points
    Christy Spence

    Antigen Tested Units

    This is our policy as well.
  33. 2 points
    TreeMoss

    RhIg administration

    This is also what we do. We treat this as a blood bank "critical value" and do a "write down, read back" to nursing.
  34. 2 points
    Carrie Easley

    Antigen Tested Units

    Our policy as well.
  35. 2 points
    BldBnker

    RhIg administration

    We do not notify our medical director. We alert the nurse taking care of the patient that more than 1 vial of Rh Immune Globulin is needed due to a positive FMH. The KB results are on the chart also. The nurses inform the patient's physicians.
  36. 2 points
    This is the way Meditech documents the splitting of products. Now with ISBT, the product code does not change when you split, so this is how the computer differentiates one split from another made from the same product. The split number (A, B, Ba, whatever) needs to print on the tag so you can tag the product properly and the blood bank and bedside staff know which split is being issued and transfused. I've had Meditech 27 years, we're a pediatric hospital so we make tons of aliquots, and no inspector (CAP, AABB, FDA, JC) has ever had a problem with this. Your CAP inspector should not cite you for something they don't understand. The previous post is correct - adding an A or B to the DIN when splitting has nothing to do with a closed or open system. I would challenge that citation.
  37. 2 points
    I have used Safe-T-Vue 10 and 6 versions. We had an extremely hard time getting the 6 version from turning red to say it was out of temp. We moved to the Hemo-Trac 6 indicators and we love them. They can be stored at Room Temp and work really well. We get them from Fisher.
  38. 2 points
    Jane12

    5 Day Plasma

    Awesome details. Thanks for all the information. I worked at couple of facilities that switched to 5 day plasma and I do not remember them doing any factor studies. They did a lots of validation with the ISBT labels. I do not remember the exact details. My supervisor said that since it has been approved by FDA, we do not need to repeat the factor studies but, has to make sure that the thawed labels match the product code for the frozen product. Is that right ?
  39. 2 points
    Eman

    5 Day Plasma

    Both the Technical Manual and Circular of Information include a table from a paper published a while back (2009) showing how the various factor and proteins C and S and anti-thrombin persist (or not) over 5 days. It's really not pretty but here is a copy/paste from the circular of information, which is also available from AABB (direct link, go to page 14 for easier reading of the table) I do QA and software support now, so read your question as about validating the computer/labeling process. Our facility skips the 24 hour FFP step, so when we thaw a plasma it is immediately re-labeled as 5 day Thawed Plasma [looks like our study results might not have passed at Kate's place, only about 70% of FVII remained after 5 days at 1-6 in FFP, but the FP24 would pass (it started lower but retained 86% of activity).] Table 3a. Coagulation Factor Activity in FFP and PF24 (whole blood) at the Time of Thaw and after 120 Hours of 1 to 6 C Storage (adapted from Table 1. Scott EA, et al. Transfusion 2009;49:1584-91) Thaw, mean ± SD (range) by product 120 hr, mean (range) by product %Change after 120 hr at 1 to 6 C Analyte FFP (n=20) PF24 (n=14)* FFP (n=20) PF24 (n=14)* FFP PF24 FII (IU/dL) 97 ± 10 (83-125) 97 ± 8 (80-113) 95 ± 10 (82-126) 96 ± 11 (74-120) 3‡ 1 FV (U/dL) 85 ± 13 (63-104) 86 ± 16 (54-124) 67 ± 19 (17-92) 59 ± 22 (15-109) 21‡ 31‡ FVII (IU/dL) 105 ± 25 (50-163) 89 ± 22 (54-145) 70 ± 18 (34-102) 77 ± 27 (50-159) 33‡ 14‡ FVIII (IU/dL)§ 81 ± 19 (47-117) 66 ± 17 (30-100)† 43 ± 10 (27-60) 48 ± 12 (26-73) 47‡ 28‡ F IX (IU/dL) 82 ± 13 (62-108) 88 ± 13 (70-105) 80 ± 12 (64-107) 84 ± 12 (65-99) 2 4‡ FX (IU/dL) 94 ± 10 (71-112) 94 ± 11 (72-112) 87 ± 11 (65-111) 91 ± 12 (67-114) 7‡ 3‡ vWF:Ag (IU/dL)§ 98 ± 27 (57-156) 132 ± 41 (78-211) 97 ± 30 (48-150) 127 ± 40 (79-224) 1 4 vWF:RCo (IU/dL)§ 101 ± 26 (61-152) 123 ± 47 (58-238) 93 ± 30 (48-149) 102 ± 38 (50-191) 8‡ 17‡ Fibrinogen (mg/dL) 280 ± 52 (223-455) 309 ± 70 (211-500) 278 ± 50 (223-455) 303 ± 50 (205-490) 1 2‡ Anti-thrombin (IU/dL) 97 ± 9 (85-118) 97 ± 11 (77-110) 100 ± 10 (85-131) 101 ± 14 (73-116) 3 4‡ Protein C (IU/dL) 107 ± 20 (74-148) 88 ± 16 (65-120)† 107 ± 19 (77-148) 89 ± 17 (65-115)† 0 2 Protein S (IU/dL) 97 ± 18 (61-123) 92 ± 18 (54-121) 90 ± 22 (52-134) 78 ± 19 (46-114)† 7‡ 15‡ *N = 25 for FII, FV, FVIII, Fibrinogen, vWF:RCo, and Protein S. †p < 0.05 compared with mean activity in FFP of the same age. ‡p < 0.05 when comparing mean activity at thaw to mean activity after 120 hours of 1 to 6 C storage. §Only results from group O products were used for statistical comparisons of factor VIII, vWF:Ag, and vWF:RCo activities.
  40. 2 points
    Malcolm Needs

    Rule out Anti-K

    I have an idea I may know who that was!
  41. 2 points
    And I would like to stress one thing. There is NO serological method that will allow you to detect ALL partial and weak Ds. Variant Ds come in all shapes and sizes. There are some weak Ds that have so few D antigens that the most sensitive 'normal' serological techniques will not pick them up - they will be typed as D- (including donors). On the other hand, some partial Ds have a sufficiently high number of D antigen sites that you will detect them as a normal D+ (even patients). And there are some Partial Ds that react with all commercially available Anti-D clones. So you will pull these up too as D+ (even for patients). The message behind this is - You WILL misgroup some D variant patients as D+ and you WILL misgroup some D variant donors as D-. And you have been misgrouping them for ever. Until (and if) genotyping becomes as easy, fast and cheap to do for every routine group, then you have to learn to live with it!
  42. 2 points
    Oh dear, whatever happened to common sense? If you are testing an antibody screen, for example, why do you need a negative control? The majority of your samples will give a negative result. So you know that the negatives are working. But you DO need a positive control to make sure that the reagents are working. similarly, if you have an anti-k reagent, where are you going to get a k-neg cell to use as a control each time (in a normal lab)? For ABO, if you have an A, a B and an O you have covered everything, even the reverse group, as with the A and the B one of the reverse group cells will be negative each time.....
  43. 2 points
    The INR was never intended to predict bleeding risk, it was intended to normalize PT results from lab to lab in order to provide physicians a more standard indication of their patient's anticoagulation status. There was a good presentation at AABB by Dr. Mary Townsend about this topic in the Blood Bank Mythbusters session.
  44. 2 points
    Congrats!!! If by "weak antigen positive; unable to isolate" you mean positive antibody screen unable to determine specificity - I would not worry about this. There are many reasons for a result like this., too many to go into detail. IF you are in the US, the methods used in antibody screening and detection are very good but false positives do occur. A repeat at 16 weeks is a good idea. Don't worry and keep us posted.
  45. 2 points
    cthherbal

    Blood Bank Software

    Soft Bank is by far the best BB LIS I've worked with.
  46. 1 point
    I just answered this question. My Score PASS  
  47. 1 point
    I just answered this question. My Score PASS  
  48. 1 point
    I just answered this question. My Score PASS  
  49. 1 point
    DPruden

    Blood Bank Software

    Don't let the Beaker/Epic people tell you that only one day of training is sufficient for SafeTrace Tx. And ask to have the Beaker training and Tx training environments interfaced because the steps are much different when the information is interfaced as opposed to being just typed into Tx. Also, have someone verify the ADT/visit setup, when we went live, Epic would send a "discharge/transfer" notice across the interface whenever the patients were moved, to OR or radiology, for example. then Tx would discharge the patient and inactivate the sample, not the most ideal scenario when a patient is going to OR... We didn't see it during the validation because the test patients stayed nicely in their rooms the whole time!
  50. 1 point
    We also weigh the bags as we do the confirmation testing. The form the military uses requires that the volume infused be put on there in the post transfusion data section. Most of the time it is wrong as the nurses don't pay attention to the volume written on the form and use the volume from the pump which includes the saline to prime the line or the put 1 unit there. Kristine
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