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Everything posted by StevenB
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Not that I'm aware of, Scott. The words "only" and "all" would tend to make me say No.
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Ideally it is great to rule-out with at least one homozygous expression, but it is not always practical. The anti-K scenario is a prime example as discussed, but for those of you who insist on a homozygous cross-out: Do you really delay an identification of an anti-D and a potential transfusion, just to rule-out anti-E and anti-C? Most hospitals do not have access to r'r' or r"r" cells, so would you insist that the sample be sent to a reference laboratory for resolution? Ruling-out with heterozygous examples is an acceptable practice when the situation warrants it. Obviously, one should look at the "big picture" and if you are seeing reactivity consistently with only a homozygous expression of a certain antigen, then you wouldn't want to ignore that and rule-out on only a heterozygous expression (or 3 for that matter). My advice though: When doing a heterozygous cross-out make sure you are using a technique that is considered an enhancement for the antibody in question and if in doubt, either call your local reference laboratory for advice or ship it to them for resolution.
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A titre of 512 is not due to a standard dose of RhiG, no matter how recent....straight from the vial perhaps, but not from the vein. I agree with Malcolm; this seems more like a secondary response.
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Our first experience with Darzalex was with a patient who was receiving an "experimental drug" for MM. The tech ran ton of cells, 4 of which were cord cells. All 4 cord cells reacted similarly to the other cells tested. I've read somewhere where it is thought that anti-CD38 didn't react with cord cells, but we don't support that position. In regards to the .2M DTT treatment of cord cells not having an impact on Kell Sys. antigens, I've never come across any literature that would support that position.
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In regards to frequency, if the titer is less than 16 we recommend performing titers every 4 weeks after 18-20 weeks gestation, then every 2 weeks at the 34th week. As usual, Malcolm is spot on!
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Fight to keep your 10 days at a minimum! There is no scientific basis to move the expiration to the 3 day standard for the untransfused, non-pregnant patient. Personally, even 10-14 days is too short!
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This is directly from the AABB recommendations: Consequences of current practice Current practice for testing and interpreting Rh typing results appears to be highly successful in preventing alloimmunization to the D blood group antigen and Rh hemolytic disease of the fetus/newborn.4 However, there are unwarranted consequences associated with the practice of avoiding detection of weak D phenotypes, including unnecessary injections of Rh immune globulin and transfusion of Rh-negative red blood cells – always in short supply – when Rh-positive red blood cells could be transfused safely. If all pregnant women in the United States with a weak D phenotype were identified and their RHD genotype determined, an estimated 13,360 pregnant women who are currently managed as Rh-negative could be managed as Rh-positive, avoiding 24,700 injections of Rh immune globulin annually.1 Recommendation of the Work Group RHD genotyping is recommended whenever a weak D phenotype is detected by routine Rh blood typing of pregnant women and other females of childbearing potential. The Work Group rates this as strong recommendation, based on high-quality evidence from observational studies (1A).5 The Work Group also considered a recommendation to standardize routine laboratory methods for Rh typing that would increase detection of all patients with D variant phenotypes, including partial D, as well as weak D phenotypes. While desirable, such a recommendation is technically complex, likely controversial, and would divert the focus from our advocacy for phasing-in RHD genotyping when a pregnant woman’s routine Rh typing detects a serologic weak D phenotype. The immediate benefit of determining the RHD genotype of pregnant women with a weak D phenotype will be fewer unnecessary injections of Rh immune globulin. It's common for hospital blood banks to treat potential mothers who type Rh (D) positive at the weak D phase of testing as Rh negative. It's not uncommon to hear stories similar to yours where a patient has been told one time they are D- and then another time, D+. If you want to get a better handle on your D typing, request that your hospital sends it out for molecular testing. It can be expensive...ballpark $300...but it is the only way to determine whether or not you truly need Rh immune globulin.
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That is for the "uncrossmatched patient" with "known antibodies". It makes no reference to the antibody identification whats so ever. Of course, that's just my interpretation of how it is written. Until we see it written in Standards that the antibody identification process can be skipped in lieu of giving phenotype/genotype matched units, we will continue to try to meet the Standard's requirements as they are currently written. As mentioned earlier, there are exceptions....WAA/sickle cell...but I do not believe the DARA patient issue has risen to their level of difficulty or need. In regards to your reference labs recommendation.... This would be a great topic to discuss over a beer or two. Unfortunately that's not possible! Have a great weekend Scott.
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I have the AABB bulletin (Association Bulletin #16-02) sitting on the desk next to me. Here is the direct quote regarding antibody identification: "AFTER a patient begins taking anti-CD3: ABO/RhD typing can be performed normally For antibody detection (screening) and identification, dithiothreitol (DTT)-treated cells can be used to eliminate the interference. Because DTT treatment destroys Kell antigens, K negative units should be provided unless the patient is known to be K positive Antibodies against other DTT sensitive blood group antigens (anti-k and anti-Yta, anti-Doa/Dob, etc) will not be detectable when the antibody screen with DTT treated cells is performed; such antibodies are encountered infrequently, however." You will notice that is does not say; antibody screening or identification is not necessary if phenotype units are given. It goes on to state: "Crossmatch For patients with a negative antibody screen using DTT treated cells, an electronic or immediate spin crossmatch with ABO/RhD compatible, K matched units may be performed. For patients with known alloantibodies, phenotypically or genotypically matched RBC units may be provided. Some clinically significant antibodies may be missed with the use of uncrossmatched phenotypically or genotypically matched units, although this will occur infrequently." There were other bullet points, but not significant to this discussion. Again note, that under the "Crossmatch" section, it does not state that phenotype matched units can be used in lieu of performing an antibody identification. It does however state that for patients with known alloantibodies, matched units may be provided in the uncrossmatched patient. Warm auto cases, sickle cell cases can be an exception. Usually though, the exception for WAA patients should occur when the frequency of transfusion is so often that it make no sense to do an antibody ID every 4th or 5th day when nothing has changed. We will recommend that the ID be extended out a 2-3 weeks in these situations, or be performed if a change in DAT, or antibody reactivity is noted...or if a patient has a reaction. DARA patients can not be compared to sickle cell patients who have demonstrated the propensity for developing alloantibodies, frequently need transfusions and when in crisis, usually need blood STAT. The DARA patients that we have seen have been stable, not requiring blood on a STAT basis. The work-up to resolve a DARA is relatively easy and can be turned-out within 3-4 hrs of receiving the sample. Every sample so far has resulted in the recommendation of giving K- units. Simple, straight forward, complies with AABB standards and does not waste a potentially valuable resource depending on the patient's phenotype.
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I do not believe giving phenotype matched units allows you to ignore the reactivity that you are observing that may or may not be due to DARA. I'm not aware of any standard that allows a blood bank to do that. In addition, giving phenotype matched units can be a waste of a valuable resource. If a patient needed E-, K-, Fy(a-), that's approximately 1 in 5...no problem. If they needed c-, E-, K- S- Jk(a-) now you are looking at approximately 1 in 50. That can take time, raise the cost and remove from inventory a valuable resource for patients who actually have antibodies. Again, I'm not aware of any standard that allows a blood bank to ignore reactivity that is observed at 37C. Specifically, AABB standard 5.14.3.1 states: "When clinically significant antibodies are detected, additional testing shall be performed." Section 5.14.3.3 goes on to state: "In patients with previously identified clinically significant antibodies, methods of testing shall be those that identify additional clinically significant antibodies." No mention of just giving phenotype matched units. Under section 5.15 "Selection of Compatible Blood and Blood Components for Transfusion", there is no mention of using phenotype matched blood in lieu of performing an antibody investigation. Needless to say, lol.... I'm not an advocate for just giving phenotype matched units.
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I didn't want to hijack the thread (Elution Studies) that prompted this one.... I couldn't help but notice the number of responses that stated an eluate would be made out to three months in the patient who was transfused within that time period or pregnant during said time frame. If any of you have any statistics that support this practice, I'd love to see them. I found a study where eluates were being performed out to one month on patients with positive DATs and in that instance, the authors reported only a 0.6% rate of finding an antibody that was not already detected in the patient's serum/plasma. In following their parameters, it cost them $9000+ to find that one sample and concluded that the benefit vs cost was not justified. The Technical Manual references Judd et al. (The evaluation of a positive direct antiglobulin test (autocontrol) in pretransfusion testing revisited. Transfusion 1986;26:220-4) when it states: "For transfusion reactions, newly developed antibodies that are initially detectable only in the eluate are usually detectable in the serum after about 14-21 days." In this day and age of Gel and Solid Phase testing, I find it hard to believe that antibodies are being detected ONLY in the eluate beyond the one month mark at a rate that would justifiy the cost of having a policy that has you performing them out to three months. Even using the one month mark is pretty generous in my opinion. We perform eluates if the patient has been transfused within the last 14 days, or is suspected of experiencing a transfusion reaction. We also perform eluates in suspected HDFN cases and in other scenarios where we deem it may be beneficial. That could include a patient who had been transfused say....two months prior, but only if the clinical situation warranted it; doing it "routinely" would not be considered. Just as there is no single best test method for identifying antibodies, I'm sure our practice is not fool proof. But I also believe that finding that rare situation where an antibody can only be detected in the eluate and not in the serum 2.5 months post transfusion does not justify the cost the other 99.4% of the time that these eluates provide information that was already obtained by testing the patient's serum/plasma. If someone has some stats to suggest otherwise, like I said earlier, I'd love to see them.
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Lol....great question Malcolm! I know the MI for PeG specifically states to run an initial spin test prior to adding PeG to the test, so we are stuck. Immucor's LISS does not, yet we run the first panel at initial spin, prior to adding the LISS. Habit I guess. We do consider it to be a "control" for the reverse type results which helps as we see rouleaux all too often with the plasma testing or that pesky marauding anti-M at IS. I can think of a number of "what ifs", but they happen so rarely it's not worth the conversation.
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Just want to reemphasize this: The reactivity you see at 4C can not be compared to what you see at room temp...regardless of what the Technical Manual says. It's at least a 16C change in the test parameter...without additional testing, I'm not sure how you can justify saying the reactions at both phases are due to the same antibody. Thinking on it...the only way I would ever consider reactivity at RT and 4C to be caused by the same antibody would be if I performed a cold autoadsorption and the reactivity disappeared in both test phases. Needless to say, lol, I'm not too fond of the 4C screen. The 4C incubation for enhancing weak reverse reactions is a good technique as long as you include your control cells. The 4C screen....I'm not sure I have used that test in over a couple of decades, if ever.
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Technically, its not "necessary" to do either.... But to answer your question: No. A patient who has developed anti-E has a high chance a having been exposed to the c antigen. That is why "some practitioners" recommend typing for c, and if the patient is negative, giving c- and E- units even if the anti-c is not present. This practice is not a requirement! The same is not true for a patient who has anti-c; the chance of being exposed to the E antigen are less, so this situation is not treated in the same manner.
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Question for you dbarding13: When confronted with an IS incompatible crossmatch and your ECHO screen is negative, are you performing any IS testing in tubes with screen cells and the autocontrol? The patient's reverse type will provide you some information as long as the patient is group A, B or AB (you would obviously have a tube or two that are nonreactive). If the patient is group O however, the reverse type can not be depended on as a "control" for your IS crossmatch. In the case of a group O patient, an incompatible crossmatch could be due to anything; rouleaux, cold auto, low inc., high inc., newly formed clincially significant antibody and so on. My point is, testing screen cells and an autocontrol at initial spin can be very helpful in deciding what the issue may be. Without these, a tech is only blindly guessing at what is causing the incompatibility at IS. In the example you presented, I find it interesting that the rouleaux was not seen in the reverse typing. In my experience, it is not uncommon for rouleaux to demonstrate variable "reactivity" from cell to cell. Nice call on having the tech do a saline replacement! It's a simple and quick procedure that will often clear up your IS issues. In regards to a "cold screen"; all that will tell you is that you have an antibody that reacts at 4C. It does not tell you that the same antibody is responsible for the room temperature reactivity.
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We are using Immucor's cells. They are decent in tube, so I would assume they would be slightly better in Gel...this is blood banking though and assumptions are not always correct!
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Good Morning Malcolm,
My boss asked me an interesting question yesterday and I wanted to pick your brain about it. The question was, once an anti-M is determined to be clinically insignificant, is there a need to prove that again in future samples?
I told her that I believe it was. In my experience, I've learned that what may apply to one patient does not mean that another patient would not react differently. So... just because an anti-M is determined to be insignificant at a certain point in time, does not mean it there isn't a possibility of it converting in the future to a significant antibody and this could vary from patient to patient. Basically, I'm on the side of not making an assumption.
This resulted in my pondering what other labs are doing and it is difficult to find specific info regarding this scenario. There is plenty of articles on determining the clinical significance of anti-M, but not on the frequency of doing so for previously identified insignificant anti-M.
Anyway, I thought it would be interesting to see how this was treated under your guidance.
Steve
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No problem Steve.
The policy was changed because so many of our hospitals were using gCAT that, as you say, it was causing cross-matching issues at the hospitals. According to the BCSH Guidelines, if there are no clinically significant antibodies present, they could cross-match by "immediate spin" technique or by electronic issue. However, so many hospital Chief Biomedical Scientists were too scared to do this, or let their staff do it, that we found we were having to cross-match loads of units for them (for which we did not have sufficient staff), and so our Testing Department started to M type more units (but, as explained above, not enough)!
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Malcolm, do you have references close at hand for anti-M in pregnancy? We have an OB patient with an anti-M that reacts in gel but not a pre-warmed saline tube technique that we use to determine significance. The OB/GYN is anxious and wants to order titers even though we recommend against it. Also, I'd love a reference on the Japanese issue with anti-M HDFN if you have the time.
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Sorry to take a bit of time answering Mabel. We are having our place decorated, and are also having it valued by three different estate agents and, to cap it all, I am having my car repaired! Never a dull moment!
As far as papers about anti-M in pregnancy are concerned, there are not many because, as Geoff Daniels writes, HDFN caused by anti-M is rare (and few people publish when an antibody is found not to be clinically significant, unless the antibody itself is rare, and not much is known about it), but Geoff does caution that HDFN, when caused by anti-M, can be quite severe., the papers he quotes are as follows:
Stone B, Marsh WL. Haemolytic disease of the newborn caused by anti-M. Brit J Haematol 1959; 5: 344-347.
Macpherson CR, Zartman ER. Anti-M antibody as a cause of intrauterine death. A follow-up. Am J CLin Path 1965; 43: 544-547.
Yoshida Y, Yoshida H, Tatsumi K, Asoh T, Hoshino T, Matsumoto H. Successful antibody elimination in severe M-incompatible pregnancy. New Eng J Med 1981; 305: 460-461.
Duguid JKM, Bromilow IM, Entwistle GD, Wilkinson R. Haemolytic disease of the newborn due to anti-M. Vox Sang 1995; 68: 195-196.
Furukawa K, Nakajima T, Kogure T, Yazaki K, Yoshida M, Fukaishi T, Ibuki Y, Igarashi M. Example of a woman with multiple intrauterine deaths due to anti-M who delivered a live child after plasmapheresis. Exp Clin Immunogenet 1993; 10: 161-167.
Kanra T, Yuce K, Ozcebe OI. Hydrops fetalis and intrauterine deaths due to anti-M. Acta Obstet Gynecol Scand 1996; 75: 415-417.
Hinchliffe RF, Nolan B, Vora AJ, Stamps R. Neonatal pure red cell aplasia due to anti-M. Arch Dis Child Fetal Neonatal Ed 2006; 91: F467-F468.
Wikman A, Edner A, Gryfelt G, Jonsson B, Henter J-I. Fatal hemolytic anemia and intruterine death caused by anti-M immunization. Transfusion 2007; 47: 911-917.
There are two papers concerning anti-M in the Japanese population are as follows (the first quoted by Geoff in his book; the second by a group of us in a BSH Guideline).
Yasuda H, Nollet K, Ohto H. A review of hemolytic disease of the fetus and newborn due to MN incompatibility in Japan. Vox Sang 2009; 97 (Suppl.1): 125 (Abstract).
Yasuda H, Ohto H, Nollet KE, Kawabata K, Saito S, Yagi Y, Neggishi Y, Ishida A. Hemolytic disease of the fetus and newborn with late-onset anemia due to anti-M: a case report and review of the Japanese literature. Transfusion Medicine Reviews 2014; 28: 1-6.
Klein and Anstee in Mollison's Blood Transfusion in Clinical Medicine 12th edition, do not see anti-M causing HDFN as common enough even to mention it!
This was a bit of a "rush job" in the end, so I hope it is of some use, but, if not, please get back to me.
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Am I missing something? "....if the Weak D test is negative, we report the patient to be Rh Positive." Just checking. I agree with Malcolm: A patient is either Rh Positive or Rh Negative. If you want to report it as Rh Positive at the weak D phase of testing, well...Ok, but the patient is still just Rh Positive.
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Immediate spin crossmatch when patient reverse is weak?
StevenB replied to richj's topic in Transfusion Services
Sounds reasonable to me. -
Multiple Myeloma Therapeutic agent Darzalex interfering with testing
StevenB replied to ElinF's topic in Transfusion Services
Technically, if the patient had not been transfused/pregnant within the three months PRIOR TO that last work-up, then that last work-up stands. Without any stimulus, there is no reason for new antibody development. I agree with John though; I'd really like to know that I could rely on the patient accurately giving you their "history". And sure enough, "Standards" is of little help. It states, paraphrasing, that pretransfusion testing shall include testing for unexpected antibodies. Well, under your scenario, that is a "pretransfusion" test regardless of the time frame. However, if the patient had been transfused or pregnant prior to that last work-up, even if that sample was antibody negative, a new sample should be tested... you won't find that particular scenario though in Standards. It's timeline is transfused or pregnant within 3 months of your pretransfusion testing on the sample you just had drawn. I've noticed though that hospitals impose upon themselves rather strict standards when it comes to how long pretransfusion testing is good for. In today's world, that's probably not a bad thing. -
Positive Autocontrol in gel, negative DAT
StevenB replied to CMCDCHI's topic in Transfusion Services
First and foremost...if you are going to go back and do a DAT because the AC came up positive, make sure you do it with a freshly made cell suspension. Also, if taking that step and you have the reagents, test with polyspecific (PS) and IgG at the same time since you suspect it will be positive. If you only test with PS and it comes up positive, you'd have to make ANOTHER fresh suspension to test with IgG if you were going to do that. The 10-12 minutes it takes to do the PS test is too long for cells to sit in suspension for an accurate IgG DAT. -
@Malcolm: Trust me, I sure wasn't questioning you or your laboratory as I'm sure they are, were, in very fine hands! @Terry: Guilty...we use "that" term. Not too fond of it myself though as it begs the question "What does that mean?" Perhaps it's time to "stir the pot".
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Hey Connie, Hopefully Malcolm chimes in because I believe we have slightly different opinions.... Our IRL rarely performs the prewarm technique and we see all kinds of blood bank problems. Our reasons to prewarm are limited to: 1. Determine the clinical significance of certain antibodies; M, N, P1, A1. 2. Eliminate reactivity due to the presence of a cold autoantibody. The patient's autocontrol must react at initial spin and the panel must demonstrate similar reactivity. If the patient has a positive DAT with complement, even better. Prewarming a recently transfused patient just is not done in our lab. Prewarming reactivity that is seen at AHG and it is being difficult to ID is not done. Neither are ever recommended to our customers. My concern with blood bank techs who rotate in is that through no fault of their own, they lack experience. I believe that in a pinch, this leads to decisions made off of vague recollections....stray, junkie reactions, no pattern that can be made out; must be a cold antibody so I'm going to prewarm to get rid of the problem. And if its good for the panel, well it must be good for the crossmatch. Reactivity at AHG, especially if you are using heavy-chain specific anti-IgG, should never be treated this way. My recommendation; develop strict criteria for when it is acceptable to prewarm and hold your techs to it. If they want to do something outside of that criteria, then it should probably be sent to a reference laboratory.
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Definitely no reason to apologize, Dr. Pepper. Anytime I hear or read about using the prewarm technique I tend to go on full alert....can't help it. It's the reference tech in me, lol. We see all too often the technique being used for the wrong reasons, so I have this almost "knee jerk" reaction to the topic. Baritone/Bass here...as I've gotten older my "ear" is not what it used to be....maybe the back of the choir is a good spot for me too!
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I apologize...didn't mean to hijack this thread.
