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Frequency of Antibody Identification


SRTECH

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Malcolm, #3 of dmpollock's post indicates that, as is required by the AABB in the US, all units of blood set up the a patient with a known antibody will have to be AHG cross matched. This, in a sense, could give any number of additional "antibody screening cells". If any of them are incompatible/positive then a full antibody identification regimen must be undertaken to determine why the unit(s) are incompatible. I suggest you read the paper referenced at the end of the post if you have not. In my previous life this is the regimen we followed and there were no adverse consequences resulting from it that I am aware of.

Once again I must state that much of what we practiced was driven by where our individual fears lay. There was a time when minor side crossmatching was the norm and every time 2 cells bumped into each other microscopically extensive antibody ID had to be undertaken. DATs and or Auto controls were performed on every patient every time. Over the years the pendulum of paranoia has swung to the other side based on studies, economic pressures, simply more science based information. Will it swing back, maybe, but for many it never moved and never will. I guess I'll just have to keep watching to see where it goes.

So much for my philosophical soap box for a Monday moring. :blahblah::faint:

Yes, I know John, and I do thoroughly agree with you about things like the minor cross-match, but, that notwithstanding, what I say in post 11 (and what Auntie-D iterates in post 25) is true. The antigens on the cells being used for cross-matching may not be at their optimum (take the Duffy antigens, for example, that are well-known to "go off" on storage), and the antigens on the units are an unknown as far as "homozygosity and heterozygosity" (and I know that is wrong, as those terms are only used for genes, not for antigens - but I think you know what I mean), and, if the antibody is just forming and is weak, truely incompatible units may actually be apparently compatible, and cause, at the very least, a secondary response, which could cause a delayed haemolytic transfusion reaction, leading to renal failure.

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When we adopted the approach suggested by John Judd, I called Univ of Michigan and confirmed that that was their practice at the time. We have transfused 45,000 units since then without any problem. Univ of Michigan practices have always been based on good data.

Many things are "possible," but that doesn't mean they will happen. I think it is improbable that a patient will have a "delayed haemolytic transfusion reaction, leading to renal failure" due to an antibody undetectable with a coombs crossmatch.

We had one patient with an antibody to a low frequency antigen. Often the antibody screen was negative. One in a while the screen was strongly positive with one cell and the panel would often have a single cell reactive. If we worry about preventing everything that might happen, we should perform a panel and full crossmatch on every patient so we don't miss something like an anti-Wra.

In front of me is the antigen profile for our three-cell antibody screen. It doesn't have a homozygous cell for K which is probably the most commonly formed antibody. Does this mean we should find a homozygous K cell and screen every patient with that so that we don't miss an anti-K that only reacts with homozygous cells? If the concerns posted in this thread were valid, we should be seeing more problems with delayed transfusion reactions caused by anti-K.

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No, I am not talking about antigen/antibody reactions that do not frequently show dosage, such as K and anti-K. I am talking about MNS, Duffy and Kidd antigens and antibodies which frequently do.

If you look at over ten years of data collected by the haemovigilence SHOT scheme within the UK (that has won awards within Europe), you will see that the most frequent antigen/antibody reaction that has caused delayed haemolytic transfusion reactions, coupled with some degree of renal failure, has been anti-Jka that has been missed with pre-transfusion testing. I would be amazed if the same were not true throughout the world.

All I am saying is that the screening cells MUST cover any such antigen/antibody groups with cells that exhibit "homozygous" antigen expression, or that a mini panel to cover these antigen/antibody groups should be performed; not necessarily a full panel.

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This is an entirely unsatisfactory practice - units for crossmatch are treated for optimal oxygen carrying capacity, screening/antibody cells for optimal antigen life. A unit of blood may not have sufficient reactive antigen sites to allow reaction in vitro to occur. They are perfectly capable of illiciting an immune response though.

Pretty strong statement considering it flies in the face of major university studies on this side of the pond! Apparently you focus on what could be a problem while others chose to focus on what has been proven to be a problem. We shall have to agree to disagree on this subject. :cries:

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Pretty strong statement considering it flies in the face of major university studies on this side of the pond! Apparently you focus on what could be a problem while others chose to focus on what has been proven to be a problem. We shall have to agree to disagree on this subject. :cries:

To be honest - I'd rather not be in a position where I prove something is a problem. The practice you descibe would not be permitted in the UK without full validation on each donor and timeframe first - evidence based medicine as you describe.

Just because it is done that way in the US doesn't mean that the rest of the world is wrong - check out data on opportunistic baloon ablation of narrowed renal arteries in patients with both CHD and CKD. The US has led the way with doing this and many have followed suit. There has recently been a multi-centre, worldwide study showing that the practice increases morbidity and mortality.

Until I see evidence of the stability of antigen sites on sagm donor cells I will continue to use panel cells treated for optimal antigen stability. I do not wish to risk the prozone effect.

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One side of the equation is generally missing from discussions of this type: the patient's need for transfusion. There are times when a patient actually needs a transfusion, and delaying it contributes to morbidity and mortality.

Hospitals vary in policies, patient population, resources, etc., so the best practice will vary. Often the circumstances are such that performing extra workups will delay blood availability for the patient with the antibody problem. In many cases it also delays blood availability for other patients because the time spent on the antibody delays completion of other work.

If there were some way to measure this, I would not be surprised if we found more aggregate harm to the overall patient population caused by delays in transfusion vs. the benefit of finding a rare case where an antibody undetectable by Coombs crossmatch causes harm.

I suspect that programs such as SHOT and Biovigilance are biased in doing a better job of detecting an adverse transfusion event, but do a poor job of measuring adverse effects of delay or failure to transfuse.

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I suspect that programs such as SHOT and Biovigilance are biased in doing a better job of detecting an adverse transfusion event, but do a poor job of measuring adverse effects of delay or failure to transfuse.

Actually, SHOT have been collecting this very information - we now include a review of cases where transfusion is inappropriate and unnecessary as well as those where there is significant harm to the patient resulting from a failure to transfuse, or a delay in transfusion for whatever cause.

I completely agree that we have to balance the clinical need for transfusion with trying to demonstrate 100% compatibility, and that comes down to an informed clinical decision based on consideration of the relative risks involved.

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To be honest - I'd rather not be in a position where I prove something is a problem. The practice you descibe would not be permitted in the UK without full validation on each donor and timeframe first - evidence based medicine as you describe.

Just because it is done that way in the US doesn't mean that the rest of the world is wrong - check out data on opportunistic baloon ablation of narrowed renal arteries in patients with both CHD and CKD. The US has led the way with doing this and many have followed suit. There has recently been a multi-centre, worldwide study showing that the practice increases morbidity and mortality.

Until I see evidence of the stability of antigen sites on sagm donor cells I will continue to use panel cells treated for optimal antigen stability. I do not wish to risk the prozone effect.

I believe that if you review my posts you will have a difficult time finding anyplace I indicate that someone's practice is wrong. It was not I who used the phrase; "This is an entirely unsatisfactory practice." You are certainly welcome to not follow the practice or even discount the major university studies which brought it into play but to make such a statement.... well enough said. :disbelief

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Hi All,

I apologize if someone has already listed these in another thread, but does anyone have a list of references for the studies (or better, a pdf) conducted by the Univ of Michigan, etc. about the frequency of antibody identification? I tried to search for the article cited earlier in this thread on Medline, DynaMed, and PubMed to no avail. I'd love to learn more about what those researching this has found!

Annadele

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no one has mentioned anything about the cost to the patient!! all these ab id's every 3 days would really be expensive!!

Not as costly as a transfusion reaction with a new antibody...

That being said our samples in the UK are valid for 7 days unless the patient has been transfused within the last month.

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I don't understand the controversy. A simple rule out panel, in most cases, is easy to perform and can often be done with less than 6 cells including the screen cells. We can all sleep easy that way.:confused::confused::confused:

I agree. We treat AB patients the same as all PTs as far as time interval between workups. We rule out. And we rule in with 1 homozygous of ea AB.

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I agree with Jayinsat. We do a selected cell panel with every new specimen. I didn't see anyone mention an autocontrol. We would always run one with each selected cell panel. We never have to ID the antibody again..maybe just check for reactivity in low freq's like Jka. Anything less than that would lead to sleepless nights...

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We confirm or rule out, with 1 homozygous select cell, all CS old AB. For 1 I like to know what was showing last time and 2 it tells gives us heads up they might have got blood somewhere else. This did happen when all of a sudden a CS AB showed up where we were giving ag neg for years. Also increased red cell destruction (delayed Trxx?). Turns out she went to Atlanta to visit her daughter. Needed blood. They did not see that AB but found a new one we did not. By calling them we both got our records UTD. Better and safer for the patient.

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Today I had a patient with a known Warm Auto with an underlying E,c and Jka. I ran my 3 screening cells, and 3 additional R1R1 cells that were Jka negative, all in tube with NHANCE because GEL and Solid Phase (ECHO) shows pan-agglutination. The screen cells were positive, proving the reactivity of the antibodies and the 3 additional cells, being all negative, proved nothing else had emerged. This took me less than an hour to do from arrival of the sample to completion of the crossmatch.:cool:

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Today I had a patient with a known Warm Auto with an underlying E,c and Jka. I ran my 3 screening cells, and 3 additional R1R1 cells that were Jka negative, all in tube with NHANCE because GEL and Solid Phase (ECHO) shows pan-agglutination. The screen cells were positive, proving the reactivity of the antibodies and the 3 additional cells, being all negative, proved nothing else had emerged. This took me less than an hour to do from arrival of the sample to completion of the crossmatch.:cool:

Better safe than sorry :)

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My question does dot really relate to this thread, but for lack of knowing where to place it, I am placing it here. LOL When performing a T/S and an antibody is detected and identified, we automatically screen for 2 units og antigen negative blood to the corresponding antibody, as I am sure most do. My question....do you charge for this screening or do you have a doc place an order it first? In my opinion, for what it is or isn't worth, it is the same as performing an antibody panel automatically when you get a positive antibody screen withpout a doc's order. Is anyone charging for these antigen screens?????

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