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Over my many years I have come to realize that inertia is the most powerful, driving force in the universe and the most difficult to over come!!!

Does acquiring more good blood banking staff count?

Have you considered that your patient could be a particularly low-grade weak D, a partial D of some kind (such as an RoHar), which would explain the anti-D in the eluate as a result of the RhoGam, or that what you are detecting in the eluate is not an anti-D, but is an anti-LW? I also assume that the last wash is totally negative? Sorry to ask this.

Not only is it quicker to issue 2-4 LTOWB, it is also easier for rapid infusion. The products are supposed to be infused through blood warmers rapidly. This is important to avoid that "lethal triad" of hypothermia, coagulopathy, and acidosis in traumatic bleeds. Whole blood has been shown in studies to be more effective than components in these cases as they can be given quicker and through only one iv access. With 4/4/1, you need at least two lines and possibly more than one rapid infusion pump.

We would rarely perform an eluate on the baby's red cells unless there are clinical (as opposed to laboratory) signs of HDFN. In other words, an elution is not considered to be a "reflex test", just because the baby has a positive DAT.

If you have any, you could try D Negative Cord or Neonatal red cells, which express the LW antigen comparatively strongly (certainly compared with adult D Negative red cells).

While the Ogata-Matuhasi phenomenon has been recognised since the early 1960's, it is, that notwithstanding, a very rare phenomenon to actually come across in practice. With all due respect to you Bet'naSBB, if you "see this quite a bit", I would be a bit worried as to why.

There is an AABB standard that your facility has to have a policy on how many out of group PLASMA transfusions are allowed. This very broadly encompasses LTOWB. It's 5.15.4. That said, our level 1 adult center will give 4u of LTOWB once MTP is activated, then switch to component therapy, of which our packs consist of 4 reds and 4 type A liquid plasma. Obviously, we end up transfusing incompatible plasma on occasion to B and AB patients with our normal process. Once we have a patient type we switch to type compatible plasma of course. Our policies state this, but there is no maximum number we have defined of how many units we'll give, as sometimes we don't ever get a sample until much later than we'd like, which means we're giving A plasma for a bit. We capped our LTOWB at 4 units, mostly due to inventory constraint when we started this program, but also to ensure we weren't overloading patients with too much O plasma if they weren't type O! Our supplier has a low titer cut off of 256. I track all of the patients who have gotten our WB, including their native blood type, and we are monitoring for issues, but have had none yet. I have heard of programs that will give up to 8 units of LTOWB per patient.

With respect to RBCs. If the patient has unidentified antibodies (as the title states) then NO. If you have identified the antibodies but can not confirm the patient’s antigens (as your question states) and the AHG crossmatch is compatible with units negative for the antigens that the patient has antibodies to then yes, though there are some/many possible caveats. Hope that is not too convoluted. It would help us if you give more details. Can you please explain what you mean by filters as in this context it is a little concerning to me.

What eluate kit do you use? If you use one with a "working wash" - try repeating your eluate, washing with normal saline instead...........usually takes care of it. We see this quite a bit - especially with Rh's and K's. Our Medical Director refers to it as the "Ogata Phenomenon" https://www.bbguy.org/education/glossary/glm06/

How about a "Del" ? Fits the description perfectly. One the other hand, "twice in the last few days" is worrying. While not impossible, it's highly unlikely that a facility would encounter more than one of these anomalies (zebras) in such a short period. I assume Malcolm's question regarding the Last Wash is an allusion to some laboratory artifact - bad technique, bad reagents, etc.

I just replaced mine last month. I used to use deionized water on the old one until I read this (taken directly from the Helmer manual):

Yes John, With higher dose anti-D immunoglobulin, the DAT of a D Positive baby is quite often positive. In the UK it is now quite common to give a dose of 1, 500 IU of anti-D immunoglobulin at 28 weeks of gestation and, as a result, many babies have a positive DAT, but I have never heard of clinically significant HDFN as a result, Physiological jaundice is also quite common in newborns, whether the mother was given anti-D immunoglobulin or not, and whether the baby is D Positive or D Negative.

That standard is addressed here as the 4 max WB and as outlined within MTP and emergency release policy. A previous facility I worked at used WB for MTP until they ran out or were able to complete the Type and screen +ABOconf. Then XM PRBCs/FFP/PLT/CRYO rounds. The time frame there was per MTP, with unknown blood type. Tricky thing at my current facility is that WB is first two rounds of MTP regardless of current testing or blood type, so theoretically they could qualify for WB again with a new MTP activation, or under a new admission per se. Maybe I'm thinking about this too hard, but the SOP I'm working with seems a little thin and hasty. Why give uncrossed Opos WB to a patient you know is Apos (current T&S) just because they're initiating MTP? Only thing I can figure is that it's quicker to issue 2-4 units of WB versus a 4/4/1/ or a 6/6/1 MTP round.

Just to clarify is it safe to give blood components to patients before identifying the antigens present without having to use filters juliedel23

Oh, sorry. Yes. Low titer anti-A and anti-B, group O Whole blood. This is probably a question for the lvl 1 trauma centers. Or alternatively, does anyone have maximum out of group limits for emergency release? And if so, what's the time frame on that?

I guess low titre anti-A and anti-B. We don't have any whole blood. The usual major haemorrhage pack provided is 4 red cells and 4 FFP for transfusion in 1:1 ratio. During the TT motorcycle road racing we keep a box of 2 O neg red cells and 2 group A FFP for immediate use. This hopefully gives us time to test a sample and issue group specific if further units are required.

For your facility in the UK - this may be common practice and I can only speak for OUR facility - but we have to do eluates on ALL our pos cord DAT's...... We didn't have a Labor and Delivery unit for many many years - so I can't say this is being done "because it's always been done this way" this time... Our L&D opened up maybe 4-5 years ago.

I would upgrade both of my blood storage refrigerators to the Helmer i-series and set them up for downloading temps so less paper trail. I would bring in a new Echo (ours is upgraded, but old). I would remodel Blood Bank (knock out a wall) to give us a little more room and a more ergonomically friendly space to work, maybe add another spot to flex to workspace for MTP events and for our students. Actually, I want a whole new Blood Bank with more room and windows! I don't want much really............

Thanks everyone for your replies and comments. Yes to Malcolm, the last wash was negative. The Elution kit we use is from Gamma, the Elu-kit. One correction though, I only had one eluate recover the anti-D, the other one was a warm auto. We no longer stock the DTT, I wish we did, so I am not able to confirm if it is anti -LW. I really suspect it is.

Given that red cells are, in themselves, a blood component, the answer has to be no.

Careful, now. You're bordering on "spatial discrimination".

We offer RhIgG to Rh negative patients who are female and <50 years old who receive Rh pos products, whether plasma or platelets.

How is the tap water? You could get a water filter to remove any/most of the mineral content

Understood. There are many things laboratories do because they've "always done it". Those in the decision-making roles probably saw a "bad case" somewhere along the way and it stuck in their brains. I will concede that there are a smattering of cases of Lewis antibody-mediated transfusion issues to reference, but most workers consider them an insignificant nuisance.

@exlimey if a Lewis antibody is identified - we type the patient...... it's just how our protocols are written. The only time we would be required to provide Lewis antigen matched units would be if the antibody demonstrates hemolysis at AHG otherwise just XM compatible. Do I know why? not really - I've just been doing what I was told......for almost 35 years.

Those are theoretical constructs. The data suggest fresh isn't best if there are more infections as there have been in randomized trials of fresh vs. average storage period. More study needed, but the data are more important than the dogma. Infection is the most common cause of morbidity and mortality in all hospital patients, including newborns.

Sickle trait cells do not sickle under physiologic conditions compatible with life. Purely a theoretical construct. Oxygen transport is also normal under physiologic conditions compatible with life. The evidence that sickle trait cells present any risks to any patient through transfusion is exactly zero. Patients with sickle trait rarely, if ever, have any problems attributable to sickle trait. The epidemiologic evidence is likewise weak, if not zero.

We drain ours weekly and then wipe it out clean. Then there is this clean bath "shampoo" we use. to clean and rinse it out with. Then we squirt like 3 mLs of the shampoo into the refilled thawer and run it for through an 18 minute cycle. This usually keeps it nice and clean.

Here is our titer worksheet. We do a lot of prenatal titers for our Maternal-Fetal Center (high risk pregnancies). TO-300F01 Antibody Titration Worksheet.docx

We only type for the specific antigen but we do perform an Rh phenotype when we find a clinically significant antibody. I used to have all the relevant antisera but, as was defined so succinctly by Malcolm's bean counters, it was too expensive.

When I was working in the Reference Laboratory at the NHSBT and, come to that, when I was working for a short time in a Hospital Blood Bank, we would ALWAYS test for the C, c, E and e antigens, together with the K antigen, both for patients and donors, and we would also test for the antithetical antigen, as well as the cognate antigen (in other words, as in your example, the Jk(a) and the Jk(b) antigen. We ALWAYS did this, except when the grouping reagent was exceedingly rare (e.g. anti-Dib) or the antibody AND the antigen were extremely rare (e.g. anti-Kpc). The reason we did this, particularly in the NHSBT Reference Laboratory, was because we wanted to identify very rare phenotypes, such as Kp(a+b-), or even rarer (in most cases), null phenotypes, but there was also a paper that showed that people who were transfusion dependent, such as sicklers and thal patients tend, once they have made an initial atypical antibody (particularly anti-C, anti-c, anti-E, anti-e or anti-K) to make all sorts of specificities (I'll try to look up the paper and get back to you on here). Other papers comparing their findings actually agreed with them. I say ALWAYS, but then, of course, the Bean Counters, who know nothing about Blood Group Serology, or about Patient Requirements, and care even less, came along, and we were banned from doing this as, apparently, IT COST TOO MUCH MONEY, except in special circumstances, such as patients from the Black populations, where we were privileged to be able to test for both Fya AND Fyb, in case they were Fy(a-b-) - and, of course, most of those who were found to be Fy(a-b-) had the FYB gene, so would very rarely produce an anti-Fy3, as they were homozygous for the GATA1 gene mutation. Unfortunately, what these "suits" seem to forget, despite counting beans for a living, is that, if the patient goes on to produce other, clinically significant, atypical alloantibodies, they will occupy a hospital bed for longer while suitable blood is identified, including, sometimes, cryopreserved units, ALL OF WHICH IS FAR MORE EXPENSIVE THAN THE INITIAL TYPING WAS IN THE FIRST PLACE - but what do we professionals know! RANT OVER!!!!!!!!!!!!!!!!

We require a type and antibody screen on the neonate and transfuse according to any demonstrating antibody. Rh positive infants born to mothers who received antepartum RhIG usually have positive DAT with anti-D eluted from cord red cells. The majority of these infants don't require transfusion in my experience.

Just curious but does the baby have a positive DAT due to the RhIG? Is the anti:D demonstrable in the baby?

This is also what we do and it works well for us.