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You were right about "although I have my doubts about that being a coincidence." It was not a coincidence. The Sanger sequencing on this lady indicated that the patient is cisAB.01/O.01. In Geoff Daniel's Human Blood Group text book, page 43, described that sera from cis AB people almost always contain weak anti-B. This is a great learning case indeed! Have anybody tried testing acidified anti-B with known cisAB cells? I am wondering if acidified anti-B would be non-reactive with cisAB in addition to A(B)?

Not sure how I missed this discussion when it first came out but here's my 2 cents worth. It is the physicians responsibility to inform the patients of ALL risk / benefits of every aspect of their treatment to include transfusions of any and all blood products! Granted, this is not always possible due to the situation but that does not absolve the physician of the responsibility! In no way should this responsibility ever be dumped on anyone else.

This is how we treat it. I have no way of verifying that there wasn't a verbal order from the physician to transfuse. We do have the physician order to transfuse on their checklist as well, and there have been nurses who just checked it and went about their transfusion without an order. I have to explain several times a year that it is the Dr.'s responsibility to order what he wants, Lab's job is to prepare what the Dr. orders, and the RN's responsibility to carry out the physician's orders. Not always popular, but we can't babysit everyone.

Thanks for that SMILLER. The bit about the Duffy null promoter means that, although your patient has the FYB gene, the Fy(b) antigen will not be expressed on his red cells, because the GATA-1 mutation, present in a homozygous state, prevents the Fyb antigen from being expressed on the red cells - but only the red cells. It will be expressed on other tissues throughout the body, and so this individual should not make an anti-Fy3, even though he is phenotypically Fy(a-b-) as far as red cell grouping is concerned. NICE CASE! The Fy(a-b-) phenotype in the Black Populations.pptx

Results of our reference lab testing on this patient makes him out to be a partial-D, specifically DAU-0. (Nothing about an anti-LW, which is where I was going.) They note that "patients with a partial RHD*DAU0 allele have not been reported to make anti-D, therefor, this patient's reported anti-D is most likely autoimmune." The Genotype is: RHD*DAU0-ce(48C) / RHD*03N.01-ceS. Also they found that the patient is homozygous for the "Duffy null promoter FY*02N.01-67c SNP". Whatever that is. The report seems very comprehensive with lots of information, including references. Scott

I think you need to demonstrate in Day of Use/Daily QC that the Anti-IgG Gel card reacts properly with positive and negative control, not only in the Indirect Antiglobulin Test (indirect agglutination with 37C incubation), but also in the Direct Antiglobulin Test (direct agglutination without incubation).

Wow! things must come in a bundle. This week, we just had a case with a broadly specific antibody, non reactive with K0 cells. K-k-Kpa-Kpb- and SNP genotyping predicted a presence of KEL gene. We are on the same page with you on our patient as well, in the process of sequencing.. It will be very interesting to see the sequencing results. Please keep us posted when your sequencing is done. Our patient is a bleeder, so we gave one Ko unit. yike!!

We phone once. When a nurse signs out the blood (electronic) we have a place where they must confirm the consent form and the physician's order to transfuse is on the chart.

with our ordering scenario, the MD can provide the order to transfuse w the orders for components. I do not f/u on orders, we do not have access to the MD order set. The only time I call is to the OR. Everything is electronic.

In the UK, we have this (relatively new) saying, "Why give two, when one will do?" This is NOT for someone who is bleeding out, of course, but for your "Average Joe" who needs a transfusion. It is predetermined what Hb level the patient needs, and a second (or subsequent) unit will not be released unless the patient's Hb has been checked. If the Hb has reached the predetermined level, the unit will not be released. This is not something that is decided by the Consultants at the Hospital; this is something that is decided by the Chief Medical Officer (nobody above him/her except the Minister for Health)!

In Massachusetts, it's the physicians. We audit a small percentage of transfusions every month, and consent in one of the things we look for. We've stopped "letters from the committee" as they are ignored. We report No Consent directly to Patient Safety/Risk Management. The hospital lawyers then contact individual MD and their chiefs. This is also reviewed at Medical Executive meetings. Very rarely now do we miss a consent. The higher up the food chain you report, the better the results.

We very rarely transfuse neonates (like 3 times in the last 4 years). Because of the rarity, we no longer stock a quad unit. We have gotten approval to give the baby the freshest O= on the shelf until the quad unit can get here from the blood center. Here is my question for others like us. When you get an emergency request for blood for a neonate, do you take the time to aliquot for the nursery or do you issue the entire unit and let the nursery physicians aliquot what they need?

At the beginning of the testing process, ProVue warns the user with a disclaimer displayed onscreen that hemolysis, icterus and turbidity (wbcs, lipemia) may interfere with reading of a sample. ProVue takes an image of the gel well and does a gray-scale analysis. The presence of turbidity, hemolysis and icterus would darken the image and prevent analysis due to lack of contrast. Byfaith was asking if her current criteria is too restrictive and for options for sample rejection criteria when using automated gel testing. My suggestion was to let the machine determine sample acceptability. Using a visual color chart comparision process that was probably developed for manual tube testing ignores the machine's capability to do sample rejection that is more consistent and appropriate for the machine.

Transfusion reaction workup is a whole 'nother animal. If I get a post-transfusion specimen that is hemolyzed, the first thing I do is ask the phleb if the draw was difficult. If it was, I send up someone else to obtain a new specimen. If we can't get a clean specimen, then that information is part of the documentation and taken into consideration with the interpretation of results.

Oh, I agree Malcolm. And we do accept slightly or even moderately hemolyzed samples in our lab, depending on the test. My point was, in the case of a possible transfusion reaction, when one has to document pre- and post- appearance of the plasma, it is completely pointless if the pre- specimen is hemolyzed to begin with. Anyway, this thread seems to be more concerned with automated ananlyzer requirements regarding hemolysis. I have found a few papers online, but it seems like they are only verifying that analyzers only begin have problems with at least moderate amounts of hemolysis. Not being experienced at all with what Byfaith is working with, I would guess that if the manufacturer doesn't have a problem with lesser hemolysis, they may be nothing to worry about. Scott

Hi Blood Bankers, This question may have been brought up in the past, but I did not do a proper search of the forums to see if it has. My Question: As Blood Bankers, how do you make sure that the Nursing Orders to Transfuse (or Administer) Blood Products are followed - for example...Physician orders Products to be crossmatched but not transfused...Nurse sees that blood is ready (or receives a phone call from Blood Bank that they are ready), does not check the Administer orders and comes down and is issued the product and hangs it. Or second scenario...Blood is ordered to be Administered (and of course is crossmatched). Nurse never comes down to pick it up from the Blood Bank. We do not call nursing a second time - once is our practice to call when the blood is ready (plus they can see it in the EMR on their side). Thank you.

True, Scott, but I learned a long time ago the difference between talking to my coworkers/director and communicating with those outside the lab. My director still freaks out when I tell her that, but I try to remember to mention that those weren't the "official" words I used. I still take offense to the physicians who want to blame lab for their failure to order tests and the nurses failing to follow instructions, though. I have learned never to respond in the heat of the moment if it isn't absolutely necessary.

The Echo won't like a specimen w/ hemolysis at 3-4+ when graded. That's actually quite a lot of hemolysis, so the specimens we reject for hemolysis are few and far between. The majority of our hemolyzed specimens tend to come from IV starts collected by nurses - they are 'supposed' to be saving us time by collecting specimens that way.

There is older literature referring to the concept of hemolysis as a positive reaction interpretation. I believe this is relavant only to tube testing. There is also the fact that using EDTA samples complement does not come into play and therefore no hemolysis of test cells? I believe our cutoff is random, going along with our chemistry laboratory cutoff.

LOL! I have the same problem with many of these articles! (More than you and others here I think!) Scott

I thoroughly agree! I read a paper on the subject once (Wagner FF, Ladewig B, Angert KS, Heymann GA, Eicher NI, Flegel WA. The DAU allele cluster of the RHD gene. Blood 2002; 100: 306-311, doi: 10.1182/blood-2002-01-0320) that purported to explain it all, but I warn you, it took me about 5 days to read, nearly boiled my brain, and I STILL don't understand it! Mind you, that says more about my ability to digest the paper, rather than the way the authors explained the subject!!!!!!!!!!

Thank you for your comment, John. My statement is also not popular with my Laboratory Director, but it is true none the less.

Ortho gel is known for picking up weaker D antigens than some tube reagents. I know that Quotient/Alba anti-D blend reacts more like the Ortho gel but the Immucor Gammaclone doesn't pick up those (mostly) weak D types 1 & 2 at IS. They will show up positive at AHG phase with Immucor. John Judd published a paper, which many follow, of considering anything 2+ or weaker in gel as Rh negative. I assume if you take the tube testing through AHG you will get a positive. Doing that will help troubleshoot the situation. None of this probably has much to do with the transfusion reactions. Rh typing of weak and atypical D antigens is a complicated mess both serologically and the terminology. If these are young females, we try to send them for molecular D typing.

Before I answered the question I wanted to wait and see what other people had to say. BankerGirl, thank you for your last sentence. It is a philosophy I had followed all of my career. I understand the argument that everyone is responsible for the patient's well being but at some point you have to draw the line and make everyone responsible for their piece of the process.

I'll assume you are doing Gel testing manually. I think you are wise to convert routine ABO/Rh and Antibody screen from tube testing to Gel testing. To QC the antibody screen test using Surgiscreen and Anti-IgG Gel card, you need a positive and negative control cell for each screen cell vial. This can be accomplished in one (1) Anti-IgG Gel card. To QC the A/B/D Monoclonal and Reverse Grouping card, you will need to test each reagent in the gel card with positive an negative controls (this will require a minimum of two cards). You can QC the two (2) Buffered Gel columns with anti-A + A1 cells, anti-A + B cells, anti-B + A1 cells, and anti-B + B cells using the same two A/B/D Monoclonal and Reverse Grouping cards. You could use the A/B/D Gel card to confirm all donor unit types or you could use the A/B Gel card for non-group O Rh positive units, the Anti-A,B Gel card for all group O Rh positive units, and use the A/B/D Gel card for all units labeled Rh Negative. All these cards would require Day of Use QC. You could use the A/B/D Monoclonal and Reverse Grouping Gel card or the A/B/D Monoclonal Grouping card for Cord Blood testing. These cards will not detect all weak D's. You will have to run Weak D testing on all Cord Bloods initially classified as Rh Negative. There are other options based on your workload.

I believe "the philosophy of not needing a transfusion at all if only one unit is needed" has changed since the transfusion triggers have decreased. I would like to institute a hgb prior to each Red Cell transfusion order.

Nursing orders to transfuse are just that - NURSING orders. The blood bank does the testing required for the product orders received and makes sure blood products are available and/or ready. If the RN/courier appears at the window to pick up a product and we have a valid product order, we will issue the product. It is very frustrating when the lab gets blamed when the nursing staff cannot follow/clarify a physician order.

FIRST SCENARIO: We have Epic as HIS and it has a module called BPAM which allows patient/unit bedside scanning. When we receive order to Prepare product we complete the order and it available for nursing to see that it is ready in the EMR. When nursing is ready to Transfuse they must "release" the Transfuse order in Epic. A copy of the released Transfuse order that includes patient id'ing information and the component and any special requirements. If we don't get the released Transfuse order we don't issue the unit MAINLY because, if they didn't do the release correctly they will not be able to scan the unit into the EMR at the bedside hence delaying the transfusion and possibly wasting the unit. SECOND SCENARIO: We frequently get Prepare orders but the unit is never transfused. That is not an issue for us since it doesn't affect our inventory in any way. We do mainly computer assisted crossmatches so we don't actually "crossmatch" the unit to the patient until the do the release Transfusion order (see above). The only crossmatches we do at time of Prepare order are those patients who don't qualify for computer assisted crossmatch i.e. have antibodies. If there was an issue as you described above I would write up a Safety/QA report and as long as you were following SOP then the onus for transfusion errors is on nursing not blood bank especially if you cannot see the orders.

My sense of the "advantages" of lower hemoglobin levels is not that patients thrive because of lower hgbs, but rather that, in many cases, they can thrive with fewer transfusions. Scott

If you read the paper carefully, the major difference in outcomes is reoperation and other complications clearly unrelated to transfusion triggers. Poor choice of endpoints and data analysis and totally non-credible conclusion regarding clinical outcomes in my view. The immense body of data showing that restrictive transfusion is not only safer but likely superior tells us this is a small pilot study with little to no real meaning for clinical practice. Cannot imagine what the reviewers were thinking when they let them publish this with these conclusions in the current form.

We've seen one of those patients with the antibody who had the severe anaphylactic reaction - impending sense of doom, etc., just like the books say. Fortunately the nurse was very attentive when the transfusion was started and caught it immediately. My advice is to instruct the nurses to watch very closely if she is transfused and make sure they know how to recognize a reaction if it occurs.

might be worth checking to see if she actually has antibodies to IgA

I also remember when the general philosophy was, if you really needed only 1 unit, you really didn't need any, but that was before the time of "evidence-based transfusion". As a Biomedical Scientist, rather than a Doctor, I always thought that a single unit transfusion (in an adult of course, rather than a baby) was an exercise in the production of alloantibodies, however, the work done by people to show that, not only can people survive on lower levels of haemoglobin than used to be thought, but that people actually thrive at these lower levels of haemoglobin, and spend shorter periods in hospital and get fewer post-operative infections, has convinced me (and thousands of other people) of the value of the single unit transfusion (and, as a side issue, it helps conserve the inventory).

Most patients with IgA deficiency and even with anti-IgA do not have anaphylactic or allergic reactions. Unless she has a history of anaphylaxis/atopy I wouldn't worry. In an hemorrhagic emergency, just transfuse and, as always, have some epinephrine on hand for reactions. It's well established now that most anaphylactic reactions happen in atopic patients and IgA deficiency has nothing to do with it, in general. See work by Gerald Sandler, et al. on the subject or listen to the Blood Bank Guy podcast by Sandler. Be happy, don't worry.

Today, We performed Kell antigen phenotyping, revealing k-, Kpb-, Jsb- (genotypically predicted as positive using SNP typing). Now, I believed his phenotype is Ko. I consider further genotyping using Sanger sequencing. Thank you for your help. Matthew Kim

Hello, Scott, I have a few questions about this case. 1) What is the eluate result that "matched the original antibody ID"? Is it panagglutination or anti-D in eluate? 2) How many sources of anti-D did you use to type your patient? We use up to 3 or 4 sources in this lab if we have such problem in this lab. Here are the things that I usually do to figure out if anti-D is that of auto- or allo- .. 1) exclude the possibility of RhoGm or IVIG adminstration 2) Perform D typing on the patient's red cells using different sources of anti-D. (we usually have 4 or 5 sources). If D reactivity is found variable positive and negative reactions with different clones, perform genomic testing to exclude partial/variant D antigen. 3) If the patient is elderly male and recently transfused with D+ blood (or if you see mixed field in the D typing), perform cell separation by density centrifugation, perform D typing and auto control using retic-rich cells. 4) If the patient is DAT positive, perform EGA or CDP treatment, test EGA, CDP treated cells with plasma and eluate. 5) Lastly, test plasma and/or eluate (wherever you are seeing anti-D) with DTT-treated red cells and cord cells to exclude or confirm anti-LW. Please let me know if there is anything else to add to this list. Hope this is helpful.

Geoff Daniels, in his book Human Blood Groups (3rd edition, 2013, Wiley-Blackwell) quotes three cases in the literature where an acquired-B antigen has been detected in apparently healthy individuals, although the first reference he quotes suggests that there have been others. It could be that, if your patient does turn out to have the acquired-B phenotype, she is another, and that the pregnancy is purely coincidental (although I have my doubts about that being a coincidence). Anyway, the references Geoff quotes, if you want to read them, are: Lanset S, Ropartz C. A second example of acquired B-like antigen in a healthy person. Vox Sang 1971; 20: 82-84. Herron R, Young D, Clark M, Smith D S, Giles C M, Poole J, Liew Y W. A specific antibody for cells with acquired B antigen. Transfusion 1982; 22: 525-527. Kline W E, Sullivan C M, Bowman R J, Linden M. Acquired B antigen and polyagglutination in an apparently healthy blood donor. Rev Franc Transfus Immuno-Hemat 1982; 25: 119-126.

The military does use "walking" donors - other soldiers who have been tested within a time frame, and are available for donation. Field hospitals are definitely much more sophisticated now than even 10 yrs ago. Field hospitals do have plasma and platelets as well as red cells available. TXA (tranexamic acid) is being used extensively in urban trauma centers. Recombinant activated FVIIa (NovoSeven)is less in vogue at the moment due to many bleeding episodes. Many of our trauma surgeons are ex-military - or active army reserve - and they are big advocates for simulated whole blood. Some of our trauma surgeons will be publishing soon on experience with simulated WB being almost as good as WB. They know nothing is as good as fresh WB, but understand that's an unrealistic goal.

If there isn't, there should be. As I have said many times on this site, I have a huge respect for nurses, but they cannot be expected to keep up to date with all of the latest reasons why a transfusion is, or is not the best or safest treatment for a particular patient, with a particular condition. It is equally difficult for a doctor to keep up-to-date, but it is easier to keep the Consultant Physician/Surgeon abreast of such things, via the Haematologist, and for him/her to cascade this "news" to their staff, and these more junior doctors would also have the knowledge (or should have the knowledge) to answer any of the patient's questions on the subject honestly.