I am puzzled with current patient with warm auto with transfusion need.  May I ask for your expertise?

 

Patient:

Transfused biweekly for last three years. Gave molecular tested phenotypically matched units. (all significant ag)

Rapid acid elution: all pos.

alloadsorption: no alloantibody present.

Autocontrol pos.

DAT: Anti-IgG pos, Anti-C3 neg.

 

I found out that there are quite of few units are actually completely gel XM compatible for this patient.  I thought that you can't find compatible units for true warm auto. Or I am wrong. I think I did hear someone say sometime you get lucky to have compatible unit for "weak warm auto."  Well I am happy that we have compatible units. But can someone please explain this "weak warm auto" to me and why there are compatible units? How do you know it is not high freq ab with DAT+

 

Thank you in advance,

 

P.S. this patient once had transfusion reaction. (pulse, temp, bp, bilirubin)

 

Richmond.

This is one of the most difficult problems to sort out in blood transfusion Richmond!

 

Certainly, you can get compatible units in the cross-match if most of the auto-antibody is on the patient's red cells and very little of it is free in the plasma.  What strength reactions are you getting in the panel by IAT?

 

Also, what is the underlying disease and what is the patient's ethnicity?

 

The transfusion reaction you describe certainly sounds genuine, because of the raised bilirubin, otherwise I would have thought along the lines of a non-haemolytic febrile transfusion reaction.

 

Could you give us a little more detail (as questions above) and then I'll have a go (but don't guarantee to solve your problem!).

Thank you Malcolm. 

The patient is causasian and has chronic Gi bleeding issue (oh well.) Ab screen rxn and x/m reaction are 1+. Like I indicated before, some gel X/M ( about 15 %)  are completely compatible looking. And so does one of screen cell. Completely negative. And yes, very recent rapid acid elution is all positive as it has been last three years. One day the patient was transfused with 2+ completely phenotype matched units,  the patient had a transfusion rxn.  Usually we give 1+ completely x/m unit, but I choose that unit because it was expiring.  Then two weeks later I found out that there are some compatible units.  But they were only Rh, K matched units.  I gave the units (of course after informing a pathologist.) over completely phenotype matched yet incompatible units. The patient was fine.

 

I have not been in transfusion service too long.

How often do you see warm auto with completely negative x/m?

Hi richmond,

 

Thanks for the reply.

 

From the reactions you report (weak reactions by gel IAT and 15% of cross-matched units being compatible), I would say that it is most unlikely that this patient has an antibody directed against a high prevalence antigen.  Were this the case, I would expect compatibility with only 1% of units (or, a great deal fewer, depending upon the specificity).

 

I would suspect that the patient may have been stimulated to produce the auto-antibody by bacterial infiltration into his circulation as a result of his chronic GI bleeds, and may well be on antibiotics to counter this.

 

Under such circumstances, we would generally give only Rh and K matched blood (well, and ABO matched, of course!), rather than match for other antigens.

 

I also just wonder if the reaction the patient underwent was as a result of all of the "biochemical nasties" released during storage of the unit, which, you say, was near its expiry, together with the (probable) low level systemic bacterial infection being just sufficient to "tip them over the top" into a reaction, and probably had little or nothing to do with a red cell antibody.

 

Where I work is a Reference Laboratory, and so we see many cases of WAIHA a year (too many!!!!!!) and, of those, I would estimate that a good 10 to 20 give compatible units by gel technology IAT, and a lot more that give reactions by this technology, give compatibility by pre-warmed, warm-washed LISS tube IAT at 37oC.  Note though, that almost all of these give quite strong reactions by gel technology using papain-treated red cells - which explains your reactions with the eluate.

 

I hope that helps a bit.

I used to work in a reference lab and we would intentionally crossmatch with LISS because of the chance of getting a compatible XM in patients with WAIHAs.  Maybe it is not the best inventory management, but I would always prefer to give XM compatible units, even if incompatible units would expire first.  Even if it is just for piece of mind.  

 

We did have one patient who had an anti-Coa that appeared for a long time to be a WAIHA.  His DAT was positive due to reaction with the Co(a+) donor cells.  It took several reports of possible transfusion reactions to figure out that this was an example of an antibody to a high-incidence antigen.  I believe it was finally figured out by doing what Malcolm alluded to:  they tested the donor with several rare antigen-negative cells based on the patient's ethnicity.

One could have a combination of problems--a weak warm auto plus a tendency to react with a constituent of the gel diluent present in prediluted reagent cells, but not in the diluent used in making up cell suspensions for crossmatches. The main difference in these diluents in the US is the presence of antibiotics in the diluent of pre-diluted cells.  I wouldn't expect one screen cell to be negative in this case though.  Sometimes "gel junk" does seem to be worse with, say, D pos cells--almost as though the antibiotic complexes with the cell membrane better on D pos cells or something.  Or how about Dombrock?

Is he receiving transfusions bi-weekly because of his chronic GI bleed or because of his warm auto?  I sort of think someone ought to be looking at the underlying problem here and deal with it rather than just keep filling him up with blood!

Thank you ALL for your responses.

 

The patient has continued to receive blds ( unfortunately " his symptoms are consistent with his diagonosis and receiving bld is only way he can extend his life ") and he is doing very well with those gel x/m compatible units. 

 

Maybe that one time transfusion rxn was due to "biochemical nasties" like Malcolm suggested.

 

In addition, I have one more question.

 

Suppose the patient is Dob negative with all the symptoms, rxns, current pt's conditions that I have provided. Would you send out the specimen to a reference lab to see if the patient has anti-Dob? Assuming that you already did some of testings that you would never get compensated for. And cost of testing for anti-Dob won't be compensated. (I remember reading something like cost of testing should be justified by clinical significance of testing.)

 

Thank you in advance,

Richmond.

It is a bit difficult for me to answer this, because all our costs are via the NHS (Government - or, to be cynical, the tax payers!), but both anti-Doa and anti-Dob have been implicated in transfusion reactions (albeit, rarely).

 

The real problem is that "grouping grade" anti-Doa and anti-Dob are extremely rare, even for Reference Laboratories.  It may be that they have to genotype for the DOA and DOB.  That may prove to be very expensive; but it may also prove life saving.

It is a bit difficult for me to answer this, because all our costs are via the NHS (Government - or, to be cynical, the tax payers!), but both anti-Doa and anti-Dob have been implicated in transfusion reactions (albeit, rarely).

 

The real problem is that "grouping grade" anti-Doa and anti-Dob are extremely rare, even for Reference Laboratories.  It may be that they have to genotype for the DOA and DOB.  That may prove to be very expensive; but it may also prove life saving.

Removed

Edited June 3, 201510 yr by RollSlow10

The odds are huge, but the antibody does exist!  We had a pregnant lady with anti-In^b last year (who, incidentally, seemed to travel between about 9 of our hospitals during her pregnancy, which complicated things somewhat, as we only had 2 units of compatible In(b-) blood in the UK at the time).

 

What is the ethnicity of your patient?

Under such circumstances, we would generally give only Rh and K matched blood (well, and ABO matched, of course!), rather than match for other antigens.

 

Malcolm, I am so glad that you added the ABO comment there. ::Whew!!!::