Adsorptions, or Phenotypically Matched

[Brenda K Hutson]

Just wondering how many of you transfuse Warm Auto patients with

Pheno-Matched RBCs in lieu of performing subsequent work-ups (adsorption studies)?

Thanks,

Brenda Hutson, CLS(ASCP)SBB

[Malcolm Needs ☆]

I hope, if the patient has been transfused since the last work-up, none of you, but in any case, as these patients are likely to be transfusion-dependent, or are likely to become transfusion-dependent, they should, at the very least, be match for their Rh and K types.

[JOANBALONE]

We have just started doing this for some select patients. I am curious to hear what others have to say.

[David Saikin]

If they haven't been transfused we perform an autoabsorption. We give Rh phenotyped rbcs. If they have been recently transfused we send to our reference lab for alloabsorption studies.

[jill]

We do not set up phenotypically matched units for patients with a warm autoantibody.

We transfuse Rh and K matched red cells to our sickle cell patients.

[Malcolm Needs ☆]

Just curious jill. WHy not for your patients with warm auto-antibodies? Surely, they are as likely to become transfusion-dependent as your sicklers? Granted, their immune system is usually not functioning as well as a well person (often, though, the same can be said for sicklers), but it makes it so much more difficult to provide blood for them if they spring an Rh and/or a K antibody, as such patients then often go on to make other specificities.

[Joanne P. Scannell]

We are using gel which picks up warm-autoantibodies 'wonderfully'. When this is suspected, we run an OES (Ortho Enhancement) Antibody Screen. That usually effectively clears the warm-auto and we go from there.

If it doesn't clear it, we try Albumin and go from there.

If that doesn't clear it, we send samples to our local reference lab where they perform auto or differential absorptions as indicated.

We revert to antigen-negative units if this fails.

[Brenda K Hutson]

Malcolm, allow me to clarify: I am talking about complete pheno-matched (Rh, K, Kidd, Duffy and Ss; mixed feelings about M). When I mentioned this to someone locally, they brought up the issue of just matching for Rh and K; as per Sickle-Cell Protocol. But I told them they are NOT the same; that in the Sickle Cell patient, you are only matching for Rh and K, while still performing Antibody Screens (and work-ups if necessary); then matching for everything if an antibody is made. With Warm Autos, you would have no way of knowing whether the patient had made any new antibodies; so it would not be safe to only match partially if you are not doing a work-up.

So to clarify, I guess I am asking who gives "complete" pheno-matched instead of doing time-consuming, expensive adsorptions "as per your Institutional protocol" for repeating antibody ID. I used to be a "purist" (as one well-known Immunohematologist called me) in that I felt they should always be worked up. But she hated doing Differential (Allogeneic) Adsorptions and opted instead to attempt a complete phenotype the first time they got an "untransfused patient" (or you could do retic separation); likely with partial EGA treatment; then just supply pheno-matched. So, I have kind of moved in that direction and just wondered about others...since the Reference Lab my new Hospital uses, gave a little "push back" when I discussed this with them.

And what would be the "advantage" of doing the adsorption studies? You will adsorb out a High if doing a Differential Adsorption....you might catch a Low now and then....

Would love your feedback on all of that Malcolm (as well as others).

Brenda Hutson, CLS(ASCP)SBB

I hope, if the patient has been transfused since the last work-up, none of you, but in any case, as these patients are likely to be transfusion-dependent, or are likely to become transfusion-dependent, they should, at the very least, be match for their Rh and K types.

[Brenda K Hutson]

See red below...

Brenda Hutson

Just curious jill. WHy not for your patients with warm auto-antibodies? Surely, they are as likely to become transfusion-dependent as your sicklers? Granted, their immune system is usually not functioning as well as a well person intersting comment as I believe I recall Dr. Garratty stating that while people often repeat work-ups (adsorptions) less frequently on patients with Warm Autos (and I may be wrong, but sometimes I think people find ways to "rationalize" that because no one likes doing adsorptions), that these patients may be even more likely to make underlying Alloantibodies than non-Warm Auto patients(often, though, the same can be said for sicklers), but it makes it so much more difficult to provide blood for them if they spring an Rh and/or a K antibody, as such patients then often go on to make other specificities.

It took awhile for me to be convinced to switch from performing adsorptions on these patients, to giving complete pheno-matched; but there is NO WAY I would only match for Rh and K on Warm Auto patients, while not doing Adsorption studies! Again, it is a different scenario than Sickle Cell patients; you are expecting a negative screen while only matching for Rh and K.

[lacs]

Unless our patient is also a sickler, we still adsorb. We do PEG adsorption. It's only because we want to save phenotype matched units for those who truly need them, due to shortage of good red cells.

[lacs]

Somewhat related topic, does your SOP tell you to test for endpoint when adsorb using auto cells? If not, how do you know when to stop?

How long do you incubate if you test your plasma against DTT-treated red cells in tube? I want to say 30min (similar to saline) since there is no enhancement but I've not been able to find literature to say exact time.

[Malcolm Needs ☆]

Sorry Brenda, you are absolutely correct in saying that I got hold of the wrong end of the stick about full phenotyping of blood for transfusion.

That having been said, I think that George was saying that these people do make more antibodies than do others, but that this is simply related to the number of units of blood that they receive (and, indeed, studies amongst sicklers showed the same). Indeed, with sicklers, where the units had not been matched for Rh and K, it was shown that, once they had made an antibody to an Rh antigen or the K antigen, they went on to make many more specificities, whereas, where the units had been matched for Rh and K, the production of antibodies against other antigens was far less frequent.

He also pointed out that some of the "alloantibodies" identified in WAIHA patients were probably auto-antibodies that had been mis-identified because of mimicking specificity.

Whilst I would not suggest for one minute that your practice of providing fully phenotyped blood for your patients is in any way wrong, George himself has also pointed out that such a practice can make it much more difficult to provide sufficient units, from the point of view of availability.

I hope you don't mind (blowing my own trumpet a bit here maybe), but I attach an essay I put together a few years ago (that is also in the library bit of this site), where I quote George (and others) quite extensively on the subject (on or around pages 7 to 9 I think it is).

[ATTACH]612[/ATTACH][ATTACH]613[/ATTACH]

[DOGLOVER]

We send them to our reference lab, where they do an absorption and crossmatch for us. We do not require phenotypically matched except for sicklers (who interestingly make up the majority of our warm autos). Sicklers who have made an antibody get full phenotype if possibe anyway. Absorption is done every time. If we can make it go away with PRG we will do that.

Malcolm, do you know what the mechanism is of sicklers making warm autos or a reference that I can use for our antiboyd writeups in these cases? Thanks

[Malcolm Needs ☆]

Hi DOGLOVER. You could try pages 553 to 555 ofPetz and Garratty, 2nd edition of Immune Hemolytic Anemias. It's excellent.

[lyla_n]

Patient 24 y/m

b thall

DAT 3+

Antibodies: Anti K and anti E

transfusion interval shortening progressively to now approx 5 days

Current Hb 5g/dl

How can we find whether he has developed any other alloantibody?

we are currently giving him Phenotypically matched blood for Rh and Kell only.

what should be the plan?

[Malcolm Needs ☆]

The plan should be to get a sample to a Reference Laboraotory, as a matter of urgency.

[Rh-fan]

a little bit late

The first time we see a AIHA patient we absorb and try to type patient for Rh K Fy Jk Ss (Fy after EGA treatment, the others with MoAbs), if the patient is already transfused at that time we do DNA typing. The change the patient will need blood in the future is high.

If we know the typing we still absorb but will only exclude the allo antibodies tha patient can make (so sometime with 2 or even 1 absorption cell, instead of 3). SO we use the typing to wich allo antibodies can be made.

We also use use the typing in case of urgent transfusion need (weekends and nights) to give compatible for all antibodies the patient can make. At these time we only do a test for complement activating antibodies.

After absorption we always give Rh and K compatible.

Peter

[Eagle Eye]

In this case we would give phenotypically matched RBC (Rh, K, Dyffy, Kid, S,s)...we do not honor anti-M unless patient has clinically significant anti-M.

[Brenda K Hutson]

Thanks Malcolm; and thanks for the essay (which I will read; I look forward to it). And yes, I can see how that would be the primary issue; using up antigen-negative units for patients who don't really require them. For me (at least in my current position), we are not a big Hospital so this would not be a frequent request. My staff have been told that in the event our Supplier cannot provide pheno-matched at a particular time, we will have to go the adsorption route.

Thanks again,

Brenda Hutson

Sorry Brenda, you are absolutely correct in saying that I got hold of the wrong end of the stick about full phenotyping of blood for transfusion.

That having been said, I think that George was saying that these people do make more antibodies than do others, but that this is simply related to the number of units of blood that they receive (and, indeed, studies amongst sicklers showed the same). Indeed, with sicklers, where the units had not been matched for Rh and K, it was shown that, once they had made an antibody to an Rh antigen or the K antigen, they went on to make many more specificities, whereas, where the units had been matched for Rh and K, the production of antibodies against other antigens was far less frequent.

He also pointed out that some of the "alloantibodies" identified in WAIHA patients were probably auto-antibodies that had been mis-identified because of mimicking specificity.

Whilst I would not suggest for one minute that your practice of providing fully phenotyped blood for your patients is in any way wrong, George himself has also pointed out that such a practice can make it much more difficult to provide sufficient units, from the point of view of availability.

I hope you don't mind (blowing my own trumpet a bit here maybe), but I attach an essay I put together a few years ago (that is also in the library bit of this site), where I quote George (and others) quite extensively on the subject (on or around pages 7 to 9 I think it is).

[ATTACH]612[/ATTACH][ATTACH]613[/ATTACH]

[Brenda K Hutson]

Is this a Sickle Cell patient? If YES, the standard protocol is to give total pheno-matched once they have started making antibodies (to prevent them from making more; which can make transfusion difficult when a SS patient comes into the ER in Sickle Cell crisis; once had such a patient with a hemoglobin of 2.6 who had multiple antibodies, including hrB).

If not a SS patient (and even if they are), why would you not perform rule-outs for the other major alloantibodies, just as you would any other patient (i.e. panels; select cells; etc.)?

So maybe I am not sure what/why you are asking?

Brenda Hutson

Patient 24 y/m

b thall

DAT 3+

Antibodies: Anti K and anti E

transfusion interval shortening progressively to now approx 5 days

Current Hb 5g/dl

How can we find whether he has developed any other alloantibody?

we are currently giving him Phenotypically matched blood for Rh and Kell only.

what should be the plan?

[bbanker2]

We are using gel which picks up warm-autoantibodies 'wonderfully'. When this is suspected, we run an OES (Ortho Enhancement) Antibody Screen. That usually effectively clears the warm-auto and we go from there.

If it doesn't clear it, we try Albumin and go from there.

If that doesn't clear it, we send samples to our local reference lab where they perform auto or differential absorptions as indicated.

We revert to antigen-negative units if this fails.

Can someone explain what the OES is? I work in a smaller hospital and have never heard of it. We seem to have lots of Warm Autos lately....maybe this could help us!

[jill]

I agree with you. Maybe we will in time especially since we do see alot of patients with warm autoantibodies.

[jill]

OES I believe stands for Orhto Enhancenent Solution which is a low ionic strength solution. Often times warm autoantibodies

are seen to be reactive using gel, peg, and'or solid phase but do not react in a low ionic strength medium. By testing patient

plasma with it one can use it to rule out any coexisting allosntibodies. Another way to test patient plasma is by using 2 drops

of palsma with one drop od reagent red blood cell. Incubate 30-60' at 37C, wash 4X, add Anti-IgG. warm autoantibodies often

do not react using this technique.

[Brenda K Hutson]

Sorry, just now getting back to the webiste....again.

You are absolutely correct in what George Garratty believes. But I guess I am thinking that by giving complete pheno-matched, the only thing you might catch with an Alloadsorption would be a Low. But I could see the rationalization of an Autoadsorption when applicable (not as difficult as Allo; and could catch a High).

And it was also my first thought when this other Specialist said she gives Pheno-matched whenever possible because she hated doing Allogeneic Adsorptions, that one should not look for ways to get out of work-ups. HOWEVER, with cost cuts these days; plus the fact I am working in a Hospital, not a Reference Lab, it is easier to look for alternatives.

But I do also see the other side; that to do so is to take those valuable units that patients who actually "have" those Antibodies, need (but it is infrequent for us; so that is my rationalization for that one ).

Thanks,

Brenda Hutson

Sorry Brenda, you are absolutely correct in saying that I got hold of the wrong end of the stick about full phenotyping of blood for transfusion.

That having been said, I think that George was saying that these people do make more antibodies than do others, but that this is simply related to the number of units of blood that they receive (and, indeed, studies amongst sicklers showed the same). Indeed, with sicklers, where the units had not been matched for Rh and K, it was shown that, once they had made an antibody to an Rh antigen or the K antigen, they went on to make many more specificities, whereas, where the units had been matched for Rh and K, the production of antibodies against other antigens was far less frequent.

He also pointed out that some of the "alloantibodies" identified in WAIHA patients were probably auto-antibodies that had been mis-identified because of mimicking specificity.

Whilst I would not suggest for one minute that your practice of providing fully phenotyped blood for your patients is in any way wrong, George himself has also pointed out that such a practice can make it much more difficult to provide sufficient units, from the point of view of availability.

I hope you don't mind (blowing my own trumpet a bit here maybe), but I attach an essay I put together a few years ago (that is also in the library bit of this site), where I quote George (and others) quite extensively on the subject (on or around pages 7 to 9 I think it is).

[ATTACH]612[/ATTACH][ATTACH]613[/ATTACH]

[kirkaw]

We had a patient this week with a history of WAIHA. The patient had not been transfused since 2005. We sent the current specimen to the Reference Lab and they provided phenotypically matched red cells for Rh, Kidd, Duffy, Ss and K. Tube IAT crossmatches (no enhancement) were 3+. In this situation, would your institution require a conditional release to be signed by the attending physician?

Thanks,

Amelia