~20 y/o AAF. O Positive.

Positive antibody screen 3-cell screen. All cells positive. First panel (Ortho A panel) all cells positive but autocontrol negative. All testing in gel.

Ortho B panel has some rule outs and some positive cells.

Immucor resolve 3% panel cells converted to gel, we get a few more rule outs and positive cells.

We identify anti-Fy(a), anti-K, anti-C and some antibody of undetermined specificity in the patient's plasma.

 

We get history from the patient, they had been transfused 5 days before. We call the transfusing hospital. They had identified anti-Fy(a) and anti-K and transfused 4 Fy(a) and K neg units.

 

We do tube testing and find that the anti-C reacts at both immediate-spin and 37C.

DAT panel

Polyspecific: 1+

Monospecific IgG: 0*

anti-C3: 1+

sal ctrl: 0

 

An eluate is performed and anti-Fy(a) and anti-K are identified from the panel. 2 Fy(a)/K-neg C+ panel cells react 1+ but 3 others do not. One Fy(a)/K/C-neg cell that reacts in the plasma and has been reacting in various other patients reacted in the eluate.

 

Patient has high fever (102-103F+), hemoglobinuria and generalized body ache. Patient's plasma was grossly icteric, LDH and Bili both high. Reportedly the patient experienced severe flank pain during the transfusion itself but was discharged that same day.

 

Patient's hgb has plummeted since admission.

Sorry to be an idiot, but what is AAF?

Guessing AAF is African American Female.

Is she a sickler?

Anna

I'm just wondering if she is having an episode of hyperhaemolysis, particularly as her Hb is plummiting.  If her Hb goes below her pre-transfusion Hb, I would be extremely worried that this might be the case, as further transfusion is contraindicated, except in extremis, in which case she may also require cover with IVIG and steroids.

I apologize Malcolm, in retrospect I can see how that is a USA-centric acronym. And yes, african american female.

 

 No, no mention of sickle cell disease. No sickle cells seen in diff. Not sure if she has the trait.

 

The patient has chronic anemia due to dysfunctional uterine bleeding, previously on hormone therapy but off the therapy in order to become pregnant. From physician/nurse documentation I'm not sure how much of her current hgb trend is related to the reaction itself or bleeding.

 

Does anyone have an explanation for why the patient had anti-Fy(a) and anti-K in her eluate when the patient had not been transfused any Fy(a)/K-pos blood? One of our senior technologists was describing how in the early phases of a transfusion reaction of this kind, non-specific antibody will get pulled into the mix and be able to be eluted with gel methodology. I think this is the case and I trust their experience and knowledge, but does anyone have an explanation for why/how it happens?

 

The patient has been ordered for transfusion of one RBC, for which we are acquiring common antigen-matched blood.

Always disheartening to see a young woman with dysfunctional uterine bleeding getting frequent transfusions, and to see this type of severe reaction. Seems like there has to be a better way to control that type of bleeding without just transfusing them everytime they come into the Emergency Department.

Has she also received plasma products or platelets? That might have contained antibodies? Or could the bleeding actually be due to the missed abortion of a Fya+, K+ foetus?

No problem about the "AAF" acronym.  I should have able to work out that one myself!

 

Yes, there are occasions when you can elute antibodies that "should not be present".  We had one patient who we followed for years.  He was K-, with anti-K, and so was transfused with K- blood for years and years, and yet, we could still elute "anti-K" from his red cells.  WHY is a different matter all together!

 

I agree with both Terri and Anna (as I almost always do, in both cases!).

By the way, just because the patient is not a sickle cell patient, hyperhaemolysis is not ruled out, but bleeding is much more likely.

A new specimen was submitted on the evening shift that I posted the case study, to accomodate a request to transfuse one RBC unit. The reaction strength was significantly increased and there was new reactivity compared to the initial specimen. With this specimen, only panel cells that matched the patient's common phenotype were negative.

 

So far that we can tell the patient phenotypes C-E+c+e+K-k+Fya-Fyb-Jka+Jkb-S+.  MN & Lewis phenotypes were not performed and little s antisera is on backorder.

 

One unit was ordered from the reference lab and arrived C-K-Fya-Fyb-Jkb-s-. The unit was compatible in gel and in LISS crossmatch.

 

Patient was transfused yesterday afternoon. Later that evening a transfusion reaction workup was submitted. Patient had developed new onset dark brown/red urine, rigors, and dyspnea 6 hours post transfusion. Post transfusion workup revealed that the crossmatch with the transfused unit was now incompatible. A sample has been sent to our reference lab for additional testing.

Malcom would you be willing to re-post your presentation of hyperhemolytic syndrome?

This is looking more and more like a hyperhaemolysis. But I am wondering also, is she on antibiotics? Is she having a severe drug-induced haemolytic reaction?

I agree Anna (or, just possibly, an anti-Jsb???????????).

  Why the other abs in eluate when pt received ag neg rbcs:  Matahasi-Ogata phenomenon is my guess.

A new specimen was submitted on the evening shift that I posted the case study, to accomodate a request to transfuse one RBC unit. The reaction strength was significantly increased and there was new reactivity compared to the initial specimen. With this specimen, only panel cells that matched the patient's common phenotype were negative.

 

So far that we can tell the patient phenotypes C-E+c+e+K-k+Fya-Fyb-Jka+Jkb-S+.  MN & Lewis phenotypes were not performed and little s antisera is on backorder.

 

One unit was ordered from the reference lab and arrived C-K-Fya-Fyb-Jkb-s-. The unit was compatible in gel and in LISS crossmatch.

 

Patient was transfused yesterday afternoon. Later that evening a transfusion reaction workup was submitted. Patient had developed new onset dark brown/red urine, rigors, and dyspnea 6 hours post transfusion. Post transfusion workup revealed that the crossmatch with the transfused unit was now incompatible. A sample has been sent to our reference lab for additional testing.

I think it is antibdies caused hemolysis. This or those antibodies has not been detected. Maybe because they are disappear so soon, such as Kidd antibodies, or the technique is not suitable to detect it. My suggestion is 1.use serum instead of plasma to detect 2. use different temperature 3. gel , tube coombs, Polybrene , peg and other technique

David, would you be willing to share with us what is  Matahasi-Ogata phenomenon? Thank you in advance.

I agree that using serum, instead of plasma, may help. I do know of cases of clinically significant anti-Vel that only react with serum (but, don't forget, your AHG will have to have an element of anti-complement).

So we had a genotype performed and it turns out the patient has an e-variant. C-e-K-Fya-Jkb- RBCs are all compatible in gel/LISS. Haven't transfused the patient again at this time.

If the patient is haemolysing after each transfusion, and has an e-variant, it sounds like you could have an anti-HrS or an anti-HrB lurking there.

NASTY!

Still waiting on the finalized, reviewed report from the reference laboratories for both the genotype and the antibody interpretation. This has been very interesting to review in real time.

~20 y/o AAF. O Positive.

Positive antibody screen 3-cell screen. All cells positive. First panel (Ortho A panel) all cells positive but autocontrol negative. All testing in gel.

Ortho B panel has some rule outs and some positive cells.

Immucor resolve 3% panel cells converted to gel, we get a few more rule outs and positive cells.

We identify anti-Fy(a), anti-K, anti-C and some antibody of undetermined specificity in the patient's plasma.

 

We get history from the patient, they had been transfused 5 days before. We call the transfusing hospital. They had identified anti-Fy(a) and anti-K and transfused 4 Fy(a) and K neg units.

 

We do tube testing and find that the anti-C reacts at both immediate-spin and 37C.

DAT panel

Polyspecific: 1+

Monospecific IgG: 0*

anti-C3: 1+

sal ctrl: 0

 

An eluate is performed and anti-Fy(a) and anti-K are identified from the panel. 2 Fy(a)/K-neg C+ panel cells react 1+ but 3 others do not. One Fy(a)/K/C-neg cell that reacts in the plasma and has been reacting in various other patients reacted in the eluate.

 

Patient has high fever (102-103F+), hemoglobinuria and generalized body ache. Patient's plasma was grossly icteric, LDH and Bili both high. Reportedly the patient experienced severe flank pain during the transfusion itself but was discharged that same day.

 

Patient's hgb has plummeted since admission.

It is possible that you are witnessing the development of a new antibody whereby the patient was sensitized by the transfusion received 5 days prior. The additional reactivity (IS and 37C) would be caused by a higher concentration of IgM class antibody which is normally the first immune protein produced follow by the IgG class upon persistent exposure of the immune system to the non-self protein (aka antigen) and may account for the increased reactivity noted in the second specimen.

Hi Ronald,

I think that the chances are that it was not a de novo anti-C, but, judging from the number of panel cells that were positive, against those that were negative, something like an anti-Sla (or a Knops/McCoy type antibody of some sort). Most White donors are Sl(a+), whilst some Black donors are not (same applies to patients, of course!).

It is likely that the C+ panel cells were derived from white donors (likely, but not by any means definite) and so they are also highly likely to be Sl(a+). It still could be a case of hyperhaemolysis, and this extra antibody is a clinically insignificant "red herring".

Of course, this is all speculation, but it does sound like a CR-related antibody!

  Why the other abs in eluate when pt received ag neg rbcs:  Matahasi-Ogata phenomenon is my guess.

HI David, The correct spelling is : Matuhasi-Ogata phenomenon.

I realize I never came back to this post. The reference laboratory we sent the workup to determined this was anti-hrS/hrB.