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There is some truth in that, and especially from his perspective. However I have found that surgeons are not the best when it comes to understanding Transfusion Medicine.

consult with pathologist and keep in mind If you absolutely have to give incompatible plasma the ideal is to give it while patient is actively bleeding. If possible give RBCs that will be compatible with patient and the plasma so in your case O and as the bleeding is beginning to come under control start giving ABO compatible plasma to "top them off". The idea is that as long as patient is actively bleeding give them the incompatible product which is then being bled out onto the floor or wherever. Once bleeding is under control give the good stuff to help dilute the incompatible out and leave them with the most compatible antigen/antibody combinations possible.

Considering the push to using Low Titre O Whole Blood for MTP and trauma's, i'd say the benefit outweighs the risk. I have personally seen two incidents where a panicked Blood Banker accidentally issued O FFP in emergency release situations. In both cases, the patients turned out to be incompatible blood types (one A one B). Guess what, there was no adverse effect whatsoever in either case. No sign of hemolysis or transfusion reaction weeks later.

There was a prominent trauma surgeon who said, "Patients die from the blood they don't get, not the blood they do get".

The size of the patient can be a factor in how much incompatible plasma you can safely give, but in an MTP you are poring the blood products in, and often it is poring right back out. The comment on giving platelets is well founded.

I think it depends on what is going on. Look at the history of liver transplants. When they started, pts were getting upwards of 400u rbc. The first 20 and last 20 were abo compatible. in between it was whatever was available. I've seen massive transfusions where the patient was mistyped, receiving 20+u incompatible rbcs. Everything was fine for a few days - until the dilution factor was overcome by the pt's own immune system coming back on line. Patient doesn't survive that. Maybe, if you have to go with significant ABO incompatible plasma (O) you could switch the pt to O rbcs to reduce hemolytic activity. Have to remember the ABO abs are going to be diluted by the volumes of other solutions which are usually being infused at the same time. If the need is for coag factors, pharmacy should be able to provide recombinant products. It's a tough nut.

One possibility is state regulations on who can do what testing and the decision to train someone has been taken out of their hands. Now I'm going to get on my soap box and please don't take this too personally. There is a very big difference between training and teaching. Over the many years I have trained more people in blood bank than I care to remember. Every one of them had the basic knowledge and understanding of what was going on in the testing and knew at least one way of doing the testing. I was training them to do it our way, not teaching them the principles and background of the testing. It is simple enough to train some one to add A and B to tube C, spin for 15 seconds, shake the tube and see if it clumps but that is not teaching them anything about the testing or what to do if it doesn't work as expected. With out the basic knowledge behind the testing and processes you would find it nearly impossible to pass the BB test. I am curious, just exactly what have you been doing in the Blood Bank for the past few years? I know organizations that will allow only MT/CLS registered staff work in the Blood Bank and exclude even MLTs. My suggestion to you would be to find a program that fits your needs and complete at least the MLT level education. Another option would be to find a facility that still offers internships if there are any. They are set up to provide the training and education you are requesting from your current employer. I'm afraid this is probably not the response you were hoping for.

A few things as far as human reagents. Firstly, you never know what else may be in them in terms of antibodies directed against low prevalence antigens, because there is absolutely no way that the producer has the ability to test for all such specificities (I can remember once a human-derived anti-D reagent produced at one of the places I worked, also had a Gm antibody in it that we didn't know about. It is highly unlikely that this would have caused too many problems, but there is, nevertheless, a small chance that this could have caused a false positive). Secondly, you never know what else may be in them in terms of viruses, some of which may, as yet, be unknown to us (remember, HIV, used not to be known). This is a danger to the producer and the person using the reagent, rather than the patient. Thirdly, the avidity of human reagents is, in general, pretty poor (particularly anti-D). A few things concerning monoclonal reagents. Some of them cross-react with other specificities (although not many), but, famously, monoclonal anti-D reagents will react with the I and i antigens if used straight from the fridge. They have to be blended by experts to ensure that the desired epitopes are detected, but certain Partial D types (e.g. Partial D Type VI) are not detected (unless required). They are very specific and very avid (both of which are greatly to be desired). Virally, they are almost certainly sterile. Hope that helps.

And in this vein - look at all the ABO incompatible plts we are forced to give (esp when you can only get group O)

I am enormously honoured to announce that I am going to be awarded the Gold Medal of the British Blood Transfusion Society at their Annual Scientific Meeting in Brighton this year. It is awarded to an individual for their exceptional and long standing services to the Society and to the practice of blood transfusion in the UK. Sorry if this sounds egocentric, but I am very excited.

Well jnadeau, be it on your head! You might receive insulting posts from others on the site now! Unfortunately, the photographs of me actually receiving the gold medal and glass plaque were not of great quality, but this is one taken at the Institute of Biomedical Science soon afterwards. Even here, my hair and beard look a bit like I have just poked my fingers into an electrical socket, my tie has gone awry and, these days, a wide angle lens is required on all occasions, but here it is in all its glory!

We use it during a computer downtime when the transfusion is needed before the computers come back up. Then once the computers come back up the units are retroactivity computer xm/dispensed

Another strategy, which works for ABO incompatible kidney transplants in some cases, is a combination of immunosuppressive drug therapy, IVIgG and plasma exchange. If it works for ABO, one would guess that it could work for Inb (or anything else, for that matter). One also guesses that the antibody might be wholly or largely IgM if it only causes HTR and not HDN. If that were the case, plasma exchange could be particularly effective.

Report as Rh Indeterminate and treat as Rh+ for RHIG coverage of the Mom

Will sure do! This look so good because it is not a real-life case that I just worked on. (cough cough)

We had situations like you describe a few years back. Now checking the Blood Bank (and hospital) armbands are part of the "time-out" check-off before the patient is strapped to the table. The ID info on the bands are recorded so it is available at all times during the procedure. Scott

Does the O.R ever tell you that the Pt's armband is "inaccessible" because it is "under the patient and contained within the sterile field"? We use an armband system for our BB patients and we get told that occasionally when we need to transfuse in O.R. and they didn't get the armband number before they covered up the pt. The RN usually winds up crawling under the pt's table. What does your O.R do in that case? Especially since they are having to do a barcode read of that band? We use coolers for our O.R. deliveries (one pt per room) and I never want to even discuss the introduction of an O.R. refrigerator. Anything giving in the O.R. is documented in the anesthesiologist"s records, which are also part of the electronic record.

Thank you for answering in such an explanatory way, John and Scott. Nothing more needs to be added, in my opinion. Many folks just don't have an understanding of the education level required for our jobs as Medical Laboratory Scientists.

If I understand the question, I think that you could say that any negative reverse reaction on the patient's ABO typing would serve as a negative control--however, this would not be good enough for O patients. For a positive control, you would likewise be stuck on AB patients. But I do not think that patient specimens are regulated as "QC-able" materials in the case of a IS XM. Regardless, I would think that the "pos/neg" QC regulations are concerned with validating reagent reactivity and system integrity, and not so much with one patient's specimen reacting with another's RBCS. Scott

I just answered this question. My Score PASS  

I just answered this question. My Score PASS  

I didn't know that! This is something I will always have to remember!

A gentleman and a scholar (and a natural comedian). Thanks for sharing your knowledge in such an understandable way through the years - and now with this pic I can point to my reference! Congrats again

Sadly Neil, it is not the case that anti-Inb is wholly or largely IgM; indeed, it is almost always IgG. It is thought that Indian Blood Group System antibodies do not cause HDFN because they bind to CD44 on foetal monocytes and macrophages and, therefore, have a blocking effect on FcγR1. This being so, or likely to be so, plasma exchange is likely to be less effective that might be thought, because of rebound from the extra vascular spaces.

I work in cardiac surgery unit.It is very simple for us.We have schedules with the patients every day and we know every case in particular.Every unit of blood is labeled with the pacient's ID,ABO/Rh group,crossmatch number,the name of lab worker who performed the crossmatch and also the date of the test. We have 3 OR's and every time they need units of blood they call in our unit(which is only 2 floor distance) and we transport the units to them.They perform Bedside ABO/D test before every transfusion!All the dates from the blood unit are transcripted in patient's chart manually (we do not have a computer scan for that). So far everything works great. I am from east Europe country.

Congratulations!! You have been a wonderful resource for all on this site, thank you for sharing! Cheers!

If at all possible, they would have to consult with our pathologist. Then beyond that, the physician in charge of the case would have to provide documentation that it is an emergent situation and that they are aware that they are transfusing incompatible product. Having said that, it seems like it would be a really bad idea. Giving A plasma to an unknown is one thing, but O plasma? Scott

Will you please post a picture receiving the medal - then when I quote you I can show them my reference! Congrats Malcolm!

Our hospital only did the minimum for years and was never sited. However, a few years ago it seems like the CAP standard changed to read that all reagents must be tested with positives and negatives. Or maybe I REALLY read the wording closely. So I redesigned my QC with pos and neg for all reagents. And we do check the A2 cells everyday. I know if I left that off, my people would forget to do QC on the rare occasion they actually needed to use the cells. I try to stay ahead of the issue. I will say, I was inspecting a hospital about 2 years ago and I asked the person in charge of the BB about the negatives he wasn't doing. He pushed back really hard so I called CAP to get a ruling. CAP said doing only positives was OK and she sounded exasperated that I would ask such a question. I got the feeling she thought I was reading it too closely. I didn't change my QC after that call and I still feel better about proving over and above what is the minimum necessary to prove the reagents work. No one can ding me for not doing enough. The reagent use is minimal and I don't feel I am wasting reagents.

I just answered this question. My Score PASS  

We also have a communication log. It doesn't have to be anything fancy, ours is just a spiral bound notebook. We also give verbal report to the oncoming shift. This isn't fool proof, but it helps.

Could the Daily/Day of Use QC for the ABO Plasma Grouping Cells ( A1 and B ) be considered a positive and negative control for the saline crossmatch? In both cases these tests use patient serum/plasma added to donor red cells, the only difference being that the ABO Plasma Grouping cells are stored in solution designed to maintain agglutinability while the donor cells are stored in a solution designed to maintain oxygen transport.

Nursing is required to call Blood Bank and also to order Request to Investigate Suspected Adverse Reaction to Blood Transfusion in their computer. The computer request is sent to Meditech (Lab and BB computer) to order Transfusion Reaction Investigation. Blood sample is collected ( and blood container with Transfusion form) and routed to BB for DAT and Visual Inspection. Clerical Check is done comparing information on blood container label, transfusion form and pretransfusion blood sample for any discrepancies. This process is documented as the STAT Investigation. An EXTENDED Investigation (repeat Type and Screen, Crossmatch, chemistries, etc.) is done only if clerical discrepancies, serological discrepancies or Visual Inspection are noted.

We also use a communication log that others are referencing here. Each tech is required to read the communication log since the last shift they worked EVERY DAY as one of the first things they do as they enter the Transfusion Service. We have been doing it for years, and it has now become second-nature. Anything that has to be handed off must be recorded by the outgoing staff, and anything else to speak of (patient using frequent products or an OR or MTP that used a lot) is also helpful. We also instituted a huddle board (dry-erase board at the end of the room) and do a standing huddle around 3pm everyday when we have the most staff and are usually the busiest. Even the Transfusion Service MD on-call participates in the huddle and it has helped out with our team communication!

No, it is not just you.

That seems wrong on several levels, or is it me?

This could be due to anti c IgM in nature. I have seen this many time especially in pregnant lady.

Thank you all for your response. I just realized I asked if you would order a fetal screen, but it should be a KLEI if they are weak D +.

We report the newborn to be Rh Indeterminate, with a comment that the newborn is treated as if Rh Positive for purposes of determining the mother's RhIg candidacy. Additionally, the newborn may be tested in 4-6 months to determine the baby's true Rh type.

In other words, who accredits the accrediting agencies? There you go Malcolm living in that imaginary perfect world.

I have NO idea who are HFAP, but I would say that, whoever they may be, they are complete idiots. Your way of treating the patients as D Negative until proven otherwise (i.e. the patient is D Positive or is Weak D Type 1, 2 or 3) is EXACTLY what is suggested by people who actually know about the subject on both sides of the Atlantic (Daniels G. Variants of RhD – current testing and clinical consequences. British Journal of Haematology 2013; 161: 461-470, and Sandler SG, Flegel WA, Westhoff CM, Denomme GA, Delaney M, Keller MA, Johnson ST, Katz L, Queenan JT, Vassallo RR, Simon CD. It’s time to phase in RHD genotyping for patients with a serological weak D phenotype. Transfusion 2015; 55: 680-689). I have, as I said above, no idea whether this was an HFAP ruling, or the ruling of a rogue inspector from HFAP, but, either way, I would be appealing against the citation, or changing the organisation who inspects my laboratory, if the appeal is rejected. From my point-of-view (and I have a bit of experience) you have done no wrong, but the inspector/inspectors have not got a clue about the Rh Blood Group System, and, in particular, the vagaries of the RHD gene. My own wife is D Negative, and if this lot forced her to be assigned as D Positive on such minimal reactions, I would be suing immediately. Sorry about the rant!

I concur with the autoantibody conclusion. However, unless you've neglected to tell the forum important details about this case, this work-up should have stopped at a negative antibody screen (in cards). I'm more concerned about why are you doing lots of extra work - especially an enzyme panel. And, why, oh, why are you using a "primitive", "insensitive" tube test when the super-sensitive card tests are negative /compatible? If this is a "normal" work-up, I believe your testing algorithm needs attention.

I remember John Judd once advising me to titrate an anti-M suspected to have an IgG fraction and not worry about separating the IgG from the IgM unless the titer became significant. Then we could titrate it after destroying the IgM if need be to see what the true IgG titer was. It never exceeded something like 8 so we never had to send it out for additional testing. These seems something like that--drawing a line of what is safe to save the cost of extra testing. Only do the additional testing when it is no longer safe to avoid it. You would have to determine how you will turn it out so as to not overly confuse the OB/perinatologist. "Titer against c, E, Fya, Jkb and S positive cell = 8"? Then next time when it is 16 with a cell of that phenotype, you would repeat separate titrations and results would be "titer against c & E positive cell = 8 & titer against Fya, Jkb and S positive cell = 4"? Or do you then go to separate cells for all of them but the E & c? Or turn it out as 16 and they quit using titers to monitor? I can see some logic to moving to ultrasound monitoring as soon as the cumulative titer is above 16 or so but we also like to watch how titers change over time to help us guess which antigens baby is positive for. If you already tested amniocytes for antigens that would be moot but if you have only serology to go on you could miss some clues. We titrate E & c together because they are likely to be inherited together and separate E+, c- cells are hard to find. It also depends on if you can reliably find the same phenotype of cells for the next titration (we don't have the perfect world of using the same specific donor cell for the entire pregnancy). Maybe it also matters if you know dad's phenotype/genotype. If he is R2r then baby could be c+ E- but not if he is R2R2. Sorry to ramble on; surely someone with more experience in this than I can answer with something more substantive but I've enjoyed speculating.

I have been CAP and AABB for 30 years, and I only run pos QC,except both pos and neg for anti D. Never had a problem.

Mabel was kind enough to share this sample with our lab as we had not had the pleasure of seeing one of these. The sample was limited and it technically was not a referral, so my work was centered on getting to know anti-CD47. The patient forward typed as an A with no issues (I've heard the forward type can at times be affected), but reverse typed as an O, with 2+ reactivity in the A1 and A2 reverse cells. The patient typed Rh positive; no reactivity noted in the Rh control. The DAT was micro positive with poly specific AHG, heavy-chain IgG (HC) and C3, but was not interpret-able due to a micro positive saline control. Warm washing x4 with 37C saline resolved the positive saline control and still demonstrated micro reactions in the previously mentioned AHG sources. Interestingly, the reactivity was actually slightly stronger than the initial testing. Initial antibody testing was 2+ reactive in saline at initial spin, 3+ in saline at 37C spin (post 30 minute incubation) and 3-4+ reactive in saline at IAT with HC IgG, 3-4+ reactive in PEG at IAT (4+ reactions with the Rh negative cells tested as compared to 3+ reactivity with Rh positive cells; consistent with reports in literature), and 4+ reactive with papain treated cells (carryover reactivity was noted as a "no spin read" was 3+ and agglutination was noted prior to the addition of HC AHG). Testing with Immucor's murine monoclonal IgG Gamma Clone in PEG at IAT was macro negative, micro positive. Alloadsorption x2 (using 2 volumes of cells to one volume of plasma) onto papain-treated R1R1 and rr cells of known phenotypes (we usually do R1, R2 and r cells, but with the limited sample I dropped the R2 adsorption) removed the initial spin reactivity and confirmed the patient was group A. Alloadsorptions x3 were 1+ reactive in saline at 37C, and 3+ reactive at IAT using the HC IgG. x4 adsorptions yielded the same results. Out of curiosity, I did run a D-- cell with the x4 and it was nonreactive at 37C, but 2+ reactive at IAT. For fun, I performed titration studies on both the R1 and rr x4 adsorptions (saline, 60 minutes 37C incubation). Macro reactivity at 37C was noted at 1:32 in both samples, but technically they had a titer of 4 (1st observed 1+ reaction). At IAT, both samples had a titer of 16,384.... AFTER 4 adsorptions! A recent report in IMMUNOHEMATOLOGY stated that using equal volume (cells:plasma) adsorptions onto papain-treated cells x3 and x4 resulted in "the majority" of the samples being nonreactive in saline at initial spin and in PEG at IAT. Lastly, I did perform EGA treatment of the patient's red cells to see its affect on the positive DAT. The micro reactivity was removed following a 1min. 30sec treatment of the patient's cells, but since the sample was way beyond the manufacturer's specimen recommendation, I'm not totally confident in the observed results. Net result: It looks like alloadsorptions will be needed to resolve any observed ABO discrepancies due to reverse cell issues and PEG testing with Immucor's murine monoclonal Gamma Clone, with a macro only read, would resolve any the issue of detecting underlying alloantibodies. Thanks much Mabel for sharing this sample with us!

We do not have units in a fridge in OR (or anywhere else for that matter besides the BB). Our BB is just down the hall from OR, so our OR units are kept in the BB until needed for a specific patient Then they are issued in a cooler. Presumably the correct ID and read-back is done in the OR for each unit. Scott

I have a question about the "newborn card". I am not familiar with this card, so forgive me if this is the case. Does this card contain IgG, and is it incubated at 37 prior to centrifugation? And when you perform the testing in tube, do you incubate and carry it through AHG phase? This is how we detect weak D.

The site was giving @Malcolm Needs a spot of bother, so I have taken the liberty of uploading some spectacular images for him.

DTT SOP.pdf This procedure is based on the HemoBioscience SOP and the AABB SOP. Works for us. Prior threads on this topic have indicated that the DTT treated cells will not last long, so we do this only at need.

What? You don't already have one? Just kidding... CONGRATS! IT MAKES US ALL HERE VERY HAPPY! WE KNOW THAT THEY APPRECIATE YOU OVER THERE! (here too!) Scott