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Can I just point out here that no one serological test, or even combination of tests will detect all weak / variant Ds . And that includes women who test D+ but actually have a partial D and may make anti-D antibodies. It is SO important to know your reagents, and know what your anti-D reagents will and will not detect

When I first joined the wonderful world of blood transfusion, with particular reference to blood group serology, at the International Blood Group Reference Laboratory, when it was in London, my mentors were Dr Carolyn Giles and Joyce Poole. In those days, yes, we did use microscopes (albeit with very little magnification) and, given that we were using human-derived antisera, and the fact that I was anxious not to miss anything, I often got Joyce to check my sightings down the microscope. These were invariably "kissing cells", as you suggest, and Joyce christened them "Malcolm weaks", a term which, I understand, is still used in the Red Cell Reference Department, when there is actually no agglutination present at all! By the time I retired, I NEVER used a microscope for red cell reactions (of course, for Kleihauers and the like), but not for agglutination, unless I was training someone, and showed them the typical "mixed-field" agglutination seen with anti-Sda (I hate not being able to use subscript and superscript on herre any more) and Lutheran antibodies.

I am a worker from/in the UK, but if TRM.40780 says, "Maternal RhIG candidacy assessment must include the identification of weak-D phenotype newborns", that is exactly what it means. It doesn't say "should" instead of "must", and it doesn't say, "until you give up because you are bored, because you have never found one"! Yes, such types are rare, but they do happen, and they can cause the mother to produce an anti-D (of sorts). These antibodies are not usually particularly clinically significant in terms of further pregnancies - but the word "usually" is the important one in that sentence. The only thing I would say is, WHEN you do detect a newborn who tests as weak-D positive, don't forget to test the mother too; she may also express the same weak-D type (but, depending upon your laboratory's policy, may not have been tested as expressing this type during the pregnancy), and, if she does, she doesn't need the anti-D immunoglobulin (which, remember, is a human-derived blood product, which may contain a novel blood-borne virus type about which we know nothing - YET).

Patients with sickle trait do not have sickle crises at all, except in very rare cases when they become seriously hypoxic. There are rare cases reported in military personnel and athletes. It's not clear whether they are sickle crises in some cases or just similar symptoms seen in non-sickle cell patients. These are truly rare cases, and usually at higher stress than an altitude of 8,000 feet, which really isn't terribly high. No personal experience. In extreme circumstances, patients heterozygous for S may be slightly more susceptible to symptoms like mountain sickness, just like everyone else. Don't know for sure. They have lower hematocrits and this may be one factor. Distinguishing between sickle cell symptoms and mountain sickness may be difficult for some clinicians. Lots of people get sick at altitude, especially if they exert themselves or make the ascent rapidly, or are dehydrated. I would guess that is what happened to this group. There is no need for hemoglobin S negative units for routine transfusions to non-sickle cell, hemoglobin homozygous patients.

I can't refresh your memory, but I do know of a case of anti-Vel in the UK that caused a fatal transfusion reaction. The DAT was positive by anti-complement only, and the anti-Vel itself could only be detected in a clotted sample, not in an EDTA sample.

A magnification aid is optional for N-Hance. It could be an agglutination viewer, rather than a microscope.

Do keep us updated. I am sure we are all looking forward to news of a healthy baby

As a neophyte blood banker we read everything under the scope (early 70s - it was SOP). Then took a job and worked w a very experienced blood banker (she was on a first name basis w Laurie Marsh, the Moulds' , and more of the NY blood ctr crew). I'd ask her to look at weak agglutination (probably your kissing cells) - her response was if I wanted to call it positive - go ahead. she wouldn't. Weaned myself off the scope after that. I think all new BBers go thru that. I also liked exlimey's statement about "playing" with different types of enhancements. I still do. For me, that's the interesting stuff in BB. Like those DAT cards I rec'd. Wish I could get them in the USA.

I don't believe that an optical aid necessarily refers to a microscope. In my pre-retirement years we used the agglutination viewer when an optical aid was required. Example: https://www.fishersci.com/shop/products/fisherbrand-tube-agglutination-viewer-5-watt-bulb-w-magnifying-mirror/22363560

This is going back donkey's years, but when we used to adsorb raw AHG with human red cells to get rid of the xenoantibodies that reacted like anti-A and anti-B, we used the last supernatant to dilute an aliquot of a previous lot of AHG, and then saw if the AHG still worked. If it did, then the red cells were washed sufficiently free of human protein, which, otherwise, would have inhibited the AHG.

Strange. The Direct Antiglobulin Test has been around since 1946, and this is the first time that I have heard that IgG antibodies will NEVER cause agglutination to the naked eye. IgG ABO antibodies cause agglutination visible to the naked eye all the time, as do many examples of IgG anti-M and other specificities. Sorry, but I rather think you could be wrong here.

One thing I discovered in my many years as a Transfusion Service Supervisor is that inertia is the most powerful force in the Universe! Trying to initiate change, especially in blood banking can be extremely difficult, often impossible. Pick your battles carefully and make sure they are worth fighting. Good luck.

Just curious, but why even have a card catalog at all? That was the first thing I got rid of when we computerized my last blood bank. It took about a year, if I remember correctly, to move all the old info from the paper records into the computer. One thing we did was research each patient that we had not seen in over a year to see if they were deceased or assumed they were if over 100 years old and not seen for a certain period of time. It made no sense to fill space in the computer with patients who were obviously no longer with us.

Weekly ultrasounds and nst thru biweekly appts. Most recent ultrasound showed no signs of hydrops or any other issues thankfully, aside from 1.7 MoM, next day another ultrasound MoM dropped to 1.3. Could need IUT Between now (32 weeks) and 34 weeks depending on how these numbers change, after that will just induce if needed, will be induced before 37 weeks for sure at Mfm hospital with nicu. Re-ran titer - 1:256 (said they don’t dilute further beyond this). Given it was negative at 13 weeks, they have no idea how it happened given it was previously negative and no reason for it to have ever been positive. MFM said I’m only the second he’s ever had to have this in a first pregnancy. Doc said lab that ran the original bloodwork has changed their procedures bc of this case, so that is good!

People have long used expired antisera and panels. You just need to run controls. Which brings one to the question....what are appropriate controls? That has never been clearly defined. Some people antigen type the cells tested for the antigen(s) for which they are using the cell (i.e. if using it to rule-out Anti-E, they type it for E to make sure it is still reactive). I was taught a variation on the theme. That is, to run a Positive Control Cell, which is a cell that is positive for the suspected/ known antibody and which reacts then at the same strength. For example, let's say you suspect the patient has Anti-Jka (that is what another panel seems to indicate) but you need to run a cell on another panel to rule-out Anti-E (so a Jka-E+ cell).....your control cell would be a cell that is Jka positive and it should then react at the same strength as the Jka positive cells you have run on another panel. So, a couple of possible options.....again, CAP just says controls have to be run, but does not clarify what those controls should be. Brenda Hutson, MT(ASCP)SBB

We retype the units as they come in because like CSP0102, I have personally found units mislabeled at the blood center, so better safe than sorry I like to say.

Certainly the blood supplied by the NHSBT that what is on the label on the outside is GUARANTEED to be what is actually in the bag, and so no retyping is required. I THINK the same applies in Scotland, Wales and Northern Ireland, although am happy to be corrected. As all such "kills" would be reported to our regulatory authorities, and published in the annual Serious Hazards of Transfusion (SHOT) Report, I can say for certain that no "kills" have been reported for many, many years!

Since I personally retyped a unit that was labeled wrong I would be very uncomfortable with not retyping.

The "Swiss Army Knife" approach to serological problem solving used to be fun. Having the ability to tinker with a variety of test methods and come up with your own conclusions was one of the addictive parts of immunohematology. Alas, that is no longer viable in today's era of validate everything and demonstrate competency several times a year. I used a lot of words to say: "If you don't use it, get rid of it".

You have NEVER seen a baby who is Weak D Positive. There is no such thing as anti-Weak D! May I suggest that you read Stratton F. A new Rh allelomorph. Nature 1946; 158: 25-26, followed closely by Race RR, Sanger R, Lawler SD. The Rh antigen Du. Ann Eugen (Camb) 1948; 14: 171-184, which will explain why there is no such thing as anti-Weak D. I appreciate that CAP seem to be incapable of using correct terminology, but that does not mean that we should all descend to their levels of incompetence. Sorry for the "vent", but this wrong terminology has gone on now for 72 years; six years more (embarrassingly) than I have been alive! I'm sorry if this sounds like a personal RANT against you. YorkshireExile; it is certainly not meant as such. It is just a general rant against people who use poor nomenclature because they don't learn even the basic history of their own specialist subject - and that includes the people who SUPPOSEDLY make sure the rest of us "follow the rules"!

It is not the gel test that does not detect Partial DVI, it is the monoclonal anti-D blend in the gel that you use that does not detect those four Partial DVI types.

We have this with Epic and it does save time in an emergency or MTP. Also we don't have to worry about the paperwork, it is right in the EMR. We still ask for the call since we are the ones that are usually ordering the Emergency transfusion.

The answer is a bit more complicated. If there is no target for %S, there is no need to test for hemoglobin S in donor blood. In other words, if the transfusion is purely for anemia, not treatment of acute chest syndrome or prevention of stroke, there is usually no target %S being used by the treating physician. The reason for testing for S in the donor is not the risk to the patient, but because transfusing S containing blood can confuse the calculation of % S overall. It's probably unnecessary because the %S contribution of a single unit of S heterozygous red cells in an exchange transfusion or red cell apheresis is very small. S hemoglobin in a red cell that is from a heterozygous donor does not contribute to sickling complications. This is well known because individuals who are heterozygous for S do not have complications of sickle cell disease. Thus while it is traditional to test for hemoglobin S in donor blood for sickle cell recipients, this is probably unnecessary unless the treating physician is trying to achieve a specific %S, as in stroke prevention.

I was also thinking about 'why not drop the unit retesting' after all of the donor centers went to computerized donor labeling/retesting and I hadn't seen a labeling error in years (you did use to see a very few go by) and then realized that with so many places going to computerized "compatible unit release" - the retesting done by the receiving facility is the only chance they get to check that the RBCs in the unit do indeed match the label on the bag. Without, at least, an Immediate Spin crossmatch check of the unit vs. the pt - there would be NO other physical check done if unit retesting was dropped. So there we go, the inspection agencies will want the unit recheck for forever! If the UK's figures were studied and accepted by the FDA/CMS/AABB, etc. - we might eventually see a change, but it probably won't be soon. (my 2 cents )

I would certainly think in terms of a full crossmatch, BUT using a clotted sample, just in case. That experience in the UK, although not my own, shook me up a bit!

'Liquid Plasma' is never frozen so there's no need to thaw it therefore the outdate is not changed. 'Thawed Plasma' is the 5 Day product which results from Thawing Frozen Plasma (in all it's various forms, FFP, FP24, etc.). Note: When Frozen Plasma is thawed, it is assigned a 24hr outdate. You can extend that outdate to 5 Days IF you label it 'Thawed Plasma'. e.g. Frozen FFP is thawed to Fresh Frozen Plasma (24h outdate). You can leave it that way or change it to 'Thawed Plasma' (no FFP designation) and assign a 5 Day outdate to it. Most hospitals, if they go that route, just label it 'Thawed Plasma' with a 5 Day outdate immediately after it's thawed. (One Step vs Two Steps) Note: I'm using USA FDA rules, I don't know what they do in other countries.

Hi, I am currently Co-lead of blood bank of a medium sized hospital in central IL. While I have been a generalist MLT (with blood banking) for 14 years, I am currently going back for my bachelors and will be shopping for an SBB program. I guess I finally decided what I wanted to be when I grew up Looking forward to learning and sharing here.

First of all, please do not worry. IF you do have anti-D antibodies, and they are real antibodies, this is only one of a number of tests that the doctors will do during your pregnancy to make sure everything is going OK with your baby. What they should do is recheck your blood for anti-D levels now and again in about 4 weeks' time to see if there is any change. It will show anti-D because of the Rhogam, but the important thing is to see whether the level increases significantly over time. Also, even now, if it is very high (VERY unlikely) then that would indicate it's real anti-D as opposed to the Rhogam. Ultrasound is a good idea. It is usually done anyway during pregnancy, but it will also show if something is happening that they need to react to.

Thank you Malcolm and David for sharing your experience with me.

The requirement to perform a donor retype also plays into whether or not the LIS is used for electronic compatibility testing. AABB 5.16.2.4 The system contains logic to alert the user to discrepancies between the donor ABO group and Rh type on the unit label and those determined by blood group confirmatory tests and to ABO incompatibility between the recipient and the donor unit. * *FDA Guidance for Industry: Computer Crossmatch"

There were time when we would use NISS, rather than LISS, when the auto-antibody was really strong. Remember, before LISS, NISS was what we used all the time, and not everyone who received blood in those days keeled over and died as a result!

NicolePCanada - I agree with both Ward_X and Malcolm's comments. There are definitely situations (patient groups, diagnoses) where a less sensitive methodology like LISS-IAT can be useful to work around "junk" that may be detected in Gel, Solid Phase or PEG test systems. But...they should be employed only by operators who understand the consequences of such actions, AND have the support of their medical staff.

NicolePCanada, I agree entirely with Ward_X, but with the caveat that workers must remain competent in the method.

Protein problem patients, especially a cancer population, maybe?

Anti-D is an antibody directed against the D antigen of the Rh Blood Group System. Anti-S is an antibody directed against the S antigen of the MNS Blood Group System. Anti-D has often caused severe haemolytic disease of the foetus and newborn. Anti-S, on the other hand, although it has caused severe haemolytic disease of the foetus and newborn, it only does so in VERY rare cases. These days, with the vast improvement in foetal medicine, neither antibody should cause real problems to either the mother or the baby. Antibodies to antigens other than ABO in the circulation are not that rare. About 3% of patients in hospitals have antibodies, although the number falls in donors. I am not going to say that blood transfusion laboratories do not make mistakes (everybody makes mistakes), but it is still highly unusual, and to assume that this situation is due to a laboratory error, before all other avenues have been explored, is highly insulting to the intelligence and professionalism of the people who work in these laboratories.

We use COBE 2991s, and use protein dipsticks to test the supernatant. The positive control is diluted plasma and we dilute it to get a level of 30, the negative control is saline, and the samples are collected from the wasteline after the washing is done. The washed sample should test for negative or trace protein, following Standard 5.7.4.6, which lists that washed cells should be prepared in a way that removes almost all of the plasma. We don't look at the crit for these. There are some other threads on here that also discuss washed QC -- I would also search for those!

We run old control and new cells plus new control (even if it's the same lot#) and old cells. Results should be as expected.

I highly recommend having a separate product build for convalescent plasma - enough so that it clearly distinguishes the order from a routine thawed plasma product. If you don't, beware of the possibility that a random donor plasma can be substituted for convalescent plasma especially if you don't have a lot of COVID19 patients receiving this product.

True Joanne, it is very fast, but one of my points about this is that, when a baby is found to have a Weak or Partial D (such as Partial DVI), it would be good practice to test the mother for Weak or Partial D expression, if this has not already been done, because she may be the source of the mutant gene leading to the baby's Weak or Partial D type. If she is the source, then it is a moot point, to say the least, as to whether she should or should not be exposed to a human-derived blood product that may, for all we know, be harbouring novel virus that may be transfusion-transmitted. AT the very least, she should have the risk, albeit very low, explained to her before she is given the anti-D immunoglobulin.

To keep or not to Keep, that is the question. My answer is to review the guidelines for your accrediting agency and follow their rules. I personally keep them for approximately 2 years because that is about how long it takes to fill a storage box. Once filled, I send to an offsite storage for another 2 years then they are destroyed.

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I think that your institution may develop whatever means they feel appropriate for emergency release. The only caveat I have is that the MD who is ordering is documented on the request. Many times computer generated orders only have the attending who is in the system. Definitely keep the phone call.

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I couldn't agree more. That's why I mentioned so many caveats.

Run some panel cells; negative, heterozygous and homozygous.

Yes, but the validation does not have to be exhaustive and unreasonable. All you need to do is prove that it works as advertised in your lab.

Yes, you should do at least a small parallel study using the old and the new. Your director will have to decide on how many would be acceptable and define acceptability criteria prior to implementation. I would summarize and have them sign-off before placing it into use.

I'd say that you have to consider the capabilities of your staff. I do ask my techs to use the microscope for DATs. They are all generalists and their time in blood bank is limited. Some of them shake too hard, in spite of my best efforts to fix that problem. They use a mirror, but some don't use a mirror well. So, in order to not miss weak positive reactions they use the scope with a tube roller. We also have a definition for microscopic agglutination (right out of the Technical Manual) that says it is a clump of 4-5 cells (though I do tell them that they should be cautious with this - if tests look suspicious, check them out, don't blindly ignore what you see). When I train, I stress the difference between a clump of cells that are friendly/kissing and a clump of cells that 'love each other' (agglutination). They do very well - false positives are rare. I don't see a lot of unnecessary work being done.

I will quote (one of my favourite quotes) from Issitt Peter D and Anstee David J. Applied Blood Group Serology. 4th edition, 1998, Montgomery Scientific Publications, pages 63-64 (only because I cannot get to my copies of earlier editions at the moment - as while looking for them, a large number of my text books almost knocked me sideways, as they fell off the top of my wardrobe, and my wife nearly "brained" me too for making our bedroom look a mess!). "Reading Methods for In Vitro Tests. Now that most routine tests are carried through to an antiglobulin reading the question of how to read them does not often arise. They are usually read macroscopically in order that the cells and serum are left in the tube for progression of the test. A few cells may, of course, be removed and examined microscopically at any stage if this type of reading is required. However, one of us (PDI) has believed for years that routine use of the microscope in the blood bank creates far more problems than it solves. Almost any cell suspension, including those in which washed cells have never been exposed to antibody, if examined carefully enough under the microscope will be found to contain a few small clumps of red cells. Thus, while reading aids such as mirrors or hand lenses are acceptable, routine use of the microscope is not condoned. This reasoning also applies to the reading of antiglobulin tests. Again if agglutination cannot be seen with the naked eye, a hand lens, a convex mirror, or the type of microscope in which the contents of the tube are viewed while still inside the tube by placing the tube itself on the microscope slide, IT IS NOT THERE. Were it not for special tests, such as those in which mixed-field reactions may have occurred or when a small percentage of fetal cells might be present in a maternal sample, the microscope should be banned from the blood bank. Enzyme tests for agglutination or following conversion to antiglobulin reading, should NEVER be read microscopically." Several things should be noted about this quote. Firstly, there is NO distinction here between the indirect and direct antiglobulin test. Peter Issitt (see PDI, although I happen to know that Dave Anstee agrees with him) talks about reading antiglobulin tests. Secondly, this quote was originally written well before 1998. Since that time, there have been huge steps made in improving the sensitivity of tests within blood transfusion and blood group serology (often at the expense of specificity, and certainly at the expense of making diagnosis from the results of these tests straightforward - see the introduction of the term "delayed serological transfusion reaction", when there is laboratory evidence of a transfusion reaction, but no clinical evidence of a "delayed haemolytic transfusion reaction" (Petz LD and Garratty G. Immune Hemolytic Anemias, 2nd edition, Churchill-Livingstone, 2004). Thirdly, both Peter Issitt (1986) and Dave Anstee (1997) have been awarded the AABB Emily Cooley Memorial Award and Lectureship (amongst numerous other international awards - Dave was the President of the British Blood Transfusion Society, the Kenneth Goldsmith Award in 1985 and the James Blundell Award in 2003; these two are far from idiots! Lastly though, looking down a microscope is no panacea to detecting a transfusion reaction. I would draw your attention to Sachs UJH, Röder L, Santoso S, Bein G. Does a negative direct antiglobulin test exclude warm autoimmune haemolytic anaemia? A prospective study of 504 cases. British Journal of Haematology 2006; 132: 651-661. This paper talks about the production of de novo antibodies and anamnestic antibody production post-transfusion, as well as WAIHA. It comprehensively debunks the fallacy that a mixed-field reaction can, in all cases, be detected by the use of a microscope. So, perhaps the question should be, if the DAT is negative to the naked eye, should we perform an elution in each case? I REALLY, REALLY hope that nobody (seriously) answers YES to that suggestion (believe me, it was made with my tongue very firmly in my cheek)! Sorry about the rant!

Well, if you follow Petz and Garratty, the "bible" of auto-immune haemolytic anaemias, first of all performing a titre is a total waste of time as, although most clinically significant "cold" auto-antibodies are high titre, this is by no means a universal n, and so, if you ignore an antibody because it is low titre, you could be in trouble (more to the point, your patient could be in trouble). Secondly, determining the specificity of the antibody is even more of a waste of time. If it is an auto-anti-I, are you going to give adult ii blood? No. If it is an auto-anti-H, are you going to give Oh blood? No. If it is an auto-anti-HI are you going to give blood from a donor who is OhAND an adult ii? Well, if you can find such a donor anywhere in the world, you are a better serologist than anyone who has yet existed. Is the thermal amplitude useful? You bet your bottom dollar it is! The human body will never reach 4oC or 22oC, so performing tests at those temperatures is a waste of time, BUT, the extremities (fingers, toes ears, nose, etc) can go down as far as 30oC., and this is why Petz and Garratty recommend that tests are performed STRICTLY at 30oC, as, if the antibody reacts at 30oC or above, it is clinically significant as an auto-antibody. Tests at 37oC are only really useful if you are cross-matching blood for the patient, in order to see if there are any clinically significant alloantibodies present in the plasma.