antibody algorithm

[JOANBALONE]

Hi everyone,

I am looking for work aids to help the blood banker resolve ABO discrepancies due to extra reactions which may be caused by allo (A1, M etc) or autoantibodies. I am thinking quick and easy, no longer than one page. We use gel for ABO/Rh and IAT. I am not looking for ways put a name to the cold antibody if I do not have to. Mainly, resolve the ABO discrepancy and provide blood for transfusion in a timely manner. Does anyone have anything that might work?

Thanks

JB

Edited November 15, 2009 by JOANBALONE

[Malcolm Needs ☆]

I'll have a go and work on one.

[Malcolm Needs ☆]

Hi JOANBALONE,

I've given it a whirl.

It is not so much an algorithm as a shopping list, but it is a start.

If it is any use to you, I will try to refine it into a proper algorithm.

:confused:

ABO Grouping Problems.doc

[RR1]

You're a star Malcolm!!!!!

Thanks XXXXXXX

[Malcolm Needs ☆]

Well, I have put on a bit of weight lately, but I still look upon myself as a mere planet!

Thanks Rashmi.

[JOANBALONE]

Hi Malcolm,

I knew I could count on you. The first 2 sections are exactly what I am looking for and the rest is great information too. I will put this info in a flow chart to help the techs resolve these type of problems.

Thanks,

JB

[Malcolm Needs ☆]

Hi Joan,

Could I be an absolute pain an suggest that, when you have made your flow chart, you post it on BBT? I suspect that it will be much more useful to fellow members than my Word document.

[JOANBALONE]

Sure I will, but it may take a few days. Thanks again Malcolm.

JB

[jcdayaz]

Hi everyone,

I am looking for work aids to help the blood banker resolve ABO discrepancies due to extra reactions which may be caused by allo (A1, M etc) or autoantibodies. I am thinking quick and easy, no longer than one page. We use gel for ABO/Rh and IAT. I am not looking for ways put a name to the cold antibody if I do not have to. Mainly, resolve the ABO discrepancy and provide blood for transfusion in a timely manner. Does anyone have anything that might work?

Thanks

JB

If the patient is A2 (or other subgroup of A) with Anti-A1, you have to identify that. They then need to be transfused with either type O blood or A1 neg blood. We go for the first option...much less time consuming. Anti-A1 is a clinically significant antibody.

[Malcolm Needs ☆]

Anti-A1 is a clinically significant antibody.

I agree that anti-A1 is a clinically significant antibody, but only in the extremely rare occasions when it reacts strictly at 37oC. IN 30 years of Blood banking, I have only come across this once.

In almost every case, the anti-A1 can be completely ignored.

[jcdayaz]

I agree that anti-A1 is a clinically significant antibody, but only in the extremely rare occasions when it reacts strictly at 37oC. IN 30 years of Blood banking, I have only come across this once.

In almost every case, the anti-A1 can be completely ignored.

I would be hesitant to EVER completely ignore an Anti-A1. I guess we both work with significantly different patient populations. In my 17 years experience, I have seen over 30 presentations of A subgroup people with Anti-A1. 10 of those A1 antibodies were hemolytic! Very scary to entertain the idea of introducing probable A1 donor blood into the system of a recipient with a hemolytic Anti-A1.

[Malcolm Needs ☆]

I would be hesitant to EVER completely ignore an Anti-A1. I guess we both work with significantly different patient populations. In my 17 years experience, I have seen over 30 presentations of A subgroup people with Anti-A1. 10 of those A1 antibodies were hemolytic! Very scary to entertain the idea of introducing probable A1 donor blood into the system of a recipient with a hemolytic Anti-A1.

I will bow to your better knowledge and greater experience on this.

However, it seems strange to me that Geoff Daniels in his book, Peter Issitt and David Anstee in their book, Harvey Klein and Dave Anstee, in the 11th edition of Mollison's Blood Transfusion in Clinical Medicine all mention that transfusion reactions due to anti-A1 are exceedingly rare (a total of 4 papers being cited, the last in the late 1970's) and Marion reid and Christine Lomas-Francis in their book also say that reactions are exceedingly rare, as are anti-A1 sera that bind complement.

Have you thought of publishing your unusual findings?

:confused::confused:

[jcdayaz]

I will bow to your better knowledge and greater experience on this.

However, it seems strange to me that Geoff Daniels in his book, Peter Issitt and David Anstee in their book, Harvey Klein and Dave Anstee, in the 11th edition of Mollison's Blood Transfusion in Clinical Medicine all mention that transfusion reactions due to anti-A1 are exceedingly rare (a total of 4 papers being cited, the last in the late 1970's) and Marion reid and Christine Lomas-Francis in their book also say that reactions are exceedingly rare, as are anti-A1 sera that bind complement.

Have you thought of publishing your unusual findings?

:confused::confused:

Sorry, my resources don't date back to the 1970's as yours apparently do so I can't reference any of the papers you referred to here.

It is true...Anti-A1 (even the hemolytic version) does not often cause transfusion reactions. It does happen, however, and I don't want to be the Blood Banker who takes that risk.

No, publishing is not an option for me right now---I don't have the time. But I am here on BBT to share what I have seen and experienced in the strange world of blood banking to hopefully help someone else.

[Malcolm Needs ☆]

Sorry, my resources don't date back to the 1970's as yours apparently do so I can't reference any of the papers you referred to here.

It is true...Anti-A1 (even the hemolytic version) does not often cause transfusion reactions. It does happen, however, and I don't want to be the Blood Banker who takes that risk.

No, publishing is not an option for me right now---I don't have the time. But I am here on BBT to share what I have seen and experienced in the strange world of blood banking to hopefully help someone else.

Well answered, and I agree wholeheartedly with the sentiments you express in your last sentence.

NOBODY can claim to have seen it all, done it all, etc and any help is always welcome.

:D

[galvania]

To jcdayaz - now I'm really curious. Can you tell us a bit more about these anti-A1 samples. I would be particularly interested to know:

1. What group were the patients (e.g. A or AB; A2 or another sub group?

2. How did you establish that they were haemolytic?

3. Did you manage to see if there was a mixture of IgG and IgM present?

4. Did anyone actually have a transfusion reaction due to the anti-A1?

5. You talk of dealing with a different patient population. Where are you based? Is this possibly one of those problems that is valid for one area of the world and not others?

Looking forward to your answers

[jcdayaz]

To jcdayaz - now I'm really curious. Can you tell us a bit more about these anti-A1 samples. I would be particularly interested to know:

1. What group were the patients (e.g. A or AB; A2 or another sub group?

2. How did you establish that they were haemolytic?

3. Did you manage to see if there was a mixture of IgG and IgM present?

4. Did anyone actually have a transfusion reaction due to the anti-A1?

5. You talk of dealing with a different patient population. Where are you based? Is this possibly one of those problems that is valid for one area of the world and not others?

Looking forward to your answers

1. Only @2 presentations of hemolysis in A2 people. Others were presumably different subgroups of A. Sorry, we didn't identify other subgroups of A besides A2specifically. We simply "assumed"(scary word to use in Blood Banking) they were "other" based on the strength of reaction in the front type.

2. We were still doing tube testing at the time....it was not hard to see hemolysis in the tube. We would see normal reaction in the anti-B tube and in the anti-A tube nothing but red/hemolyzed blood with a normal looking A front type.

3. Sorry, did not ever confirm IgG, IgM status.....

4. No Transfusion reactions....we NEVER tried to transfuse a patient with Anti-A1 with antigen positive blood. It was, and remains (3 blood banks later) against written procedure. Currently, we just automatically transfuse with type O blood---much easier.

5.I think you are on to something here....all my experiences with hemolytic Anti-A1's were when I lived in the deep South of the US-- Louisiana and Arkansas. Now I am based in Arizona and haven't seen anything in three years!! hhhmmm.. I will have to investigate this further....

My own two cents....I know the literature states Anti-A1 is not significant if it doesn't react at 37 degrees. It is hard, VERY hard to get compliance from BB staff--mainly "off shifters"--on when or when not to honor this antibody. Therefore it is prudent (for us) to have one policy in place written in no uncertain terms to transfuse all patients presenting with Anti-A1 with type O blood. We just consider it not worth the risk. Is the risk small? Most certainly. One worth heading, however (we think).

Thanks for your interest.

[Malcolm Needs ☆]

Thanks for that.

The only thing I would ask is, are the group O units tested for high titre ABO antibodies, or are they random from stock?

[jcdayaz]

Hi Malcolm,

We just pull random O's from stock and AHG crossmatch them. Do you have a different suggestion?

[Malcolm Needs ☆]

Hi Malcolm,

We just pull random O's from stock and AHG crossmatch them. Do you have a different suggestion?

Well, the thing that would concern me is that, if you are giving random group O units, some of them may well have high titre anti-A (and/or anti- in the plasma (even the plasma reduced units).

This anti-A is most certainly clinically significant, depending upon the stature of the patient receiving the blood, their secretor status and the amount of blood they are receiving. There are many papers in the literature citing quite major transfusion reactions due to passive transfusion of high titre ABO antibodies (admittedly, mostly in patients of small stature and mostly involving plasma components, but some involving red cell components).

I would be much more concerned about this, than the transfusion of A1 blood to an individual with an anti-A1, even if, as yet you have seen no overt transfusion reactions. It may be that the autologous red cells are not surviving for the usual 120 +/- 10 days, and that transfusions are having to be given more frequently than would otherwise be expected.

Does your blood supplier not label those units that have been found to be high titre ABO antibody negative; because if not, they should.

[Marilyn Plett]

I am unaware of any blood center in the US that routinely tests and labels Group O RBCs for high-titer anti-A or-B. As a reference lab, we provide over 13000 antigen-negative Adsol-RBCs annually to area hospitals. I'm guessing 90% of the RBCs are Group O and half of the designated patients are NOT group O. We have yet to hear of a problem even with children and/or sickle cell patients.

[Malcolm Needs ☆]

I am unaware of any blood center in the US that routinely tests and labels Group O RBCs for high-titer anti-A or-B. As a reference lab, we provide over 13000 antigen-negative Adsol-RBCs annually to area hospitals. I'm guessing 90% of the RBCs are Group O and half of the designated patients are NOT group O. We have yet to hear of a problem even with children and/or sickle cell patients.

Thanks Marilyn.

Without doubt, the Adsol helps, but that notwithstanding, there are still cases in the literature.

[jcdayaz]

Well, the thing that would concern me is that, if you are giving random group O units, some of them may well have high titre anti-A (and/or anti- in the plasma (even the plasma reduced units).

This anti-A is most certainly clinically significant, depending upon the stature of the patient receiving the blood, their secretor status and the amount of blood they are receiving. There are many papers in the literature citing quite major transfusion reactions due to passive transfusion of high titre ABO antibodies (admittedly, mostly in patients of small stature and mostly involving plasma components, but some involving red cell components).

I would be much more concerned about this, than the transfusion of A1 blood to an individual with an anti-A1, even if, as yet you have seen no overt transfusion reactions. It may be that the autologous red cells are not surviving for the usual 120 +/- 10 days, and that transfusions are having to be given more frequently than would otherwise be expected.

Does your blood supplier not label those units that have been found to be high titre ABO antibody negative; because if not, they should.

Thanks for your suggestions.

I, like Marilyn, have never seen any blood supplier in the US that labels high titer Anti-A and/or Anti-B type O units. Your point is certainly valid and one worth considering.

Were you referring to whole blood? Our packed cell units have very little plasma from the donor left in them--but most certainly still some. We use only leukoreduced packed cell units for red cell replacement.

[Malcolm Needs ☆]

I will check this with my Consultant on Monday, but I have a feeling there was a recent case involving a red cell pack in the UK that was both leukodepleted and was suspended in SAG-M (our version of Adsol).

Don't fret about this over the weekend, in case I am wrong (again!).

[jcdayaz]

I will check this with my Consultant on Monday, but I have a feeling there was a recent case involving a red cell pack in the UK that was both leukodepleted and was suspended in SAG-M (our version of Adsol).

Don't fret about this over the weekend, in case I am wrong (again!).

Whoa...scary thought!

[Malcolm Needs ☆]

Oh I don't know; my Consultant isn't that scary really!!!!!!!!!!!!!!!!!!!!!!!

:giggle::giggle: