David Saikin

Your current system is only comparing paper results. Why have you not just entered data directly into the BBIS? I have never understood copying paper results into the BBIS after the fact/at the end of shift/etc. I have seen major errors during inspections when this has been policy.
Your BBIS has truth tables and you should get an exception report and also be able to print out a copy of all work performed (not just the interps). Nothing will prevent someone from incorrect data entry, but your system will alert them (and you) if the truth tables are violated - should evoke some investigation before results are validated. Your system is your safeguard, that is why you validate its functionality before you go live.

I'm opposed to it. A few Joint Commission inspectors have mentioned to me over the years that they have removed many from ORs and they were glad to hear we didn't have one.
I agree that if this is a done deal, to try to have continuous monitoring on the equipment with temp indicators on the units. Having an electronic method to monitor the temp of that equipment would be preferable to taking manual temps every day.

My experience with OR refig is similar to those above. In the OR - that staff took daily temps; we did the maintenance and alarm checks. I STRONGLY recommend a temp monitor on each bag signed out to the OR. The staff there will remove the blood for the case and then return it. Unless you monitor closely your products will be compromised and you will not even be aware. Our OR staff insisted they never took the blood out - ALL of our monitors were ALWAYS converted. Your Medical Director will need to take a firm stand on this issue. Another anomaly I encountered was: at night, if we sent for extra blood, it was always brought to the OR ref and not the Blood Bank. I found surgical residents taking blood from the boxes and transfusing it when there was labeled, crossmatched product in their ref. Their comments were: "We know you got that blood for this pt." Can't believe we did not kill anyone.
Good luck and be firm.

I think the original question is about trauma to the mother.  The rosette has nothing to do with a KB in this scenario . . . the rosette only looks for Rh+ cells while the KB looks for fetal hgb . . . as Terri and I have said,  the docs are looking for fetal cells in the mother indicating the placental circulation has been compromised and therefore complications to the pregnancy may occur.

Hi Richard,
There are three possibilities (from what you say).
The first is, of course, that the lady has, at some time in her life, received a transfusion from an E+ donor.
The second is, as you quite correctly say, a naturally occurring anti-E (a very common finding).
It could be that the lady is pregnant through another male and is too worried to admit this, but I have doubts about this, as it is highly unusual to detect an Rh antibody in a first pregnancy by a different male partner (and you would probably have your nose broken if you suggested this!!!!!!!!!!!!!!!!!!!).
I would suspect that the titre is quite low (am I correct?) in either case.
I have grave doubts about an E variant (although, of course, these do exist) as they are very, very rare.

I only run an auto ct if I am doing an ab id.  Not run routinely.

I agree too - Least incompatible is like saying someone is "a little pregnant"!

I agree too - Least incompatible is like saying someone is "a little pregnant"!

I agree too - Least incompatible is like saying someone is "a little pregnant"!

I agree too - Least incompatible is like saying someone is "a little pregnant"!

Problem is, giving 'least incompatible' just makes the tech feel better.  Patient-wise, grade of compatibility doesn't always correspond to clinical significance (that's a whole 'nother conversation).
 
Knowing that, if we have a patient whose auto antibody cannot be either removed (e.g. autoabsorption or differential absorption) or circumvented by other methods (e.g. less sensitive method, prewarming, etc.) so we can see 'what is under there', then we transfuse antigen-negative for the antigens that the patient does not possess.  In other words, we avoid potential antibodies/antibody formation and we 'ignore' auto-antibodies.
 
I say 'ignore' in semi-quote because if the patient is overtly hemolyzing (not all are fulminent), then it may be best to transfuse antigen-negative for the so named auto-antibody.
 
If we had this patient ... if we can't clear away the auto-antibody, we'd give antigen 'identical'.  (Noticing comments above, give E-neg only if he/she is E-neg.)  If he/she is in an acute hemolysis situation (i.e. rapidly hemolyizing and dropping hct, severely low hct) then we'd consider giving e-neg RBCs.

I agree wholeheartedly with Joanne Croke about the "least incompatible" issue. I'm not a fan and no longer use the term here. We either give compatible units, or make our physician sign for incompatible.

whenever I have an "auto" anything I transfuse Rh phenotype specific rbcs (or recommend this when it is a referral).  Anytime I have NOT done this, I invariably see the Rh abs that the pt would develop.   I don't know how valid this is but it seems that once a pt is in the autoab mode, they tend to be more inclined to be sensitized. 

whenever I have an "auto" anything I transfuse Rh phenotype specific rbcs (or recommend this when it is a referral).  Anytime I have NOT done this, I invariably see the Rh abs that the pt would develop.   I don't know how valid this is but it seems that once a pt is in the autoab mode, they tend to be more inclined to be sensitized. 

whenever I have an "auto" anything I transfuse Rh phenotype specific rbcs (or recommend this when it is a referral).  Anytime I have NOT done this, I invariably see the Rh abs that the pt would develop.   I don't know how valid this is but it seems that once a pt is in the autoab mode, they tend to be more inclined to be sensitized. 

So true ... the reagent antibiotic antibody issue has been around for years, too.  This is covered by my 'interferring substance' interpretation. 
 
I guess I'm taking the attitude 'I'm looking for clinically significant antibodies.'  All the rest is academically interesting but doesn't change how we choose the units from the refrigerator.

Maybe I'm taking the simplistic approach but when we see mixed cell reactivity, we consider the 3 reasons given by the manufacturer for causing such results ...
1. Mixed population - this is not the case for screening/panel cells so that out.
2. Cold Agglutinin - you investigated that and got negative results so no cold agglutinin there.
3. Rouleaux - I'll assume you checked that out as well and found none otherwise you would have said differently. n.b. Logic tells us that rouleaux should be seen with all cells, but experience tells us that it doesn't always happen that way.
 
In addition, the premise for reactivity in gel is essentially that the cells that are 'not smooth' don't make it to the bottom.  Anything that causes the surface to be 'rough' causes a 'positive result'.  Irregular shape (e.g. sickle, acanthrocytes), abnormal immunoglobulin coating, etc. etc. so those things need to be added to that list.  (Keeping in mind that reagent cells are aged.)
 
Also, gel is acidic, so we see more Anti-M than we did with tube testing.  I'll assume you checked that out.
 
Anti-Pr ... aren't all human cells Pr positive?  However, if I remember correctly, isn't Anti-Pr also enhanced by acidity?  Again, your patient doesn't have a cold agglutinin.
 
Gel is also great at picking up HLA/HTLA antibodies.
 
Currently, with no cold agglutinin demonstrated, no rouleaux and a negative DAT, and 'some pos with some neg results', we'd run the antibody screen with OES (Ortho's version of LISS/Albumin) and if that is negative, call it 'HLA/HTLA Antibodies' and move on with our lives.
 
P.S. We do have two active patients right now who's plasma reacts with everything in gel ... negative DAT, no cold agglutinin, no rouleaux and totally negative with tube testing ... calling it 'interferring substance with the method' as we'll never know what is causing this .. meds? abnormal proteins?
 
 

Our nurses bring a copy of our blood component request form with each pick up.  We keep these on file and they are also used by the Medical Director in evaluating appropriateness of transfusions.

Hi David,
Unless they have performed thermal amplitude tests, which, of course, they may have done for all I know, I can't see that they can say it is a clinically insignificant panagglutinin. If the antibody is detectable at 30oC or above, then it is clinically significant, whatever the specificity.
In this particular case, however, I am a little worried about the specificity - not from the transfusion point-of-view - but from the patient outcome point-of-view. As the antibody/antigen reaction is destroyed by the action of proteolytic enzymes, it is unlikely to be either an auto-anti-I or an auto-anti-HI, but sounds more like an auto-anti-Pr, which, as far as I am aware, foretells a worse prognosis for the patient than does an auto-anti-I or auto-anti-HI.
Of course, from this distance, I could be talking complete rubbish!

First of all, heartiest congratulations on passing your exam.
 
I think that that the patient is Fy(a-).
 
I also think, however, that the anti-Fya also contains another antibody, probably directed against a low prevalence antigen, which is expressed on the patient's red cells, but not expressed on the Fy(a+b-), the Fy(a+b+) or the Fy(a-b-) reagent red cells.
 
Hence, when the elution is performed, the eluate reacts with the patient's red cells, but not the Fy(a+b-) or Fy(a+b+) reagent red cells.
 
Did I pass?

I don't know about others but gel is the not the end-all, be-all in antibody studies.  For instance, if I am doing an warm auto - I have never been able to absorb all the warm ab out of the specimen if I test in gel.  I always go with a PeG autoabsorption and do my studies in tubes rather than gel.  I don't think I am going to miss any signficant allosensitization using tubes for this scenario.  I still have referrals that use tubes and 22% albumin or LISS routinely, I like to be able to reproduce their results using the modalities that they use (when necessary).  Sometmes gel is just way too sensitive and if I back off the sensitivity I can get a clear cut result. I feel the same way about the capture technology - sometimes it is way too sensitive.  Tube testing, I believe, is still the standard of care regardless of what the vendors are saying or even that the majority of users use the newer technologies.  I also do NOT run all specs in the cold - only if the studies indicate a likely cold reacting moiety.

I don't know about others but gel is the not the end-all, be-all in antibody studies.  For instance, if I am doing an warm auto - I have never been able to absorb all the warm ab out of the specimen if I test in gel.  I always go with a PeG autoabsorption and do my studies in tubes rather than gel.  I don't think I am going to miss any signficant allosensitization using tubes for this scenario.  I still have referrals that use tubes and 22% albumin or LISS routinely, I like to be able to reproduce their results using the modalities that they use (when necessary).  Sometmes gel is just way too sensitive and if I back off the sensitivity I can get a clear cut result. I feel the same way about the capture technology - sometimes it is way too sensitive.  Tube testing, I believe, is still the standard of care regardless of what the vendors are saying or even that the majority of users use the newer technologies.  I also do NOT run all specs in the cold - only if the studies indicate a likely cold reacting moiety.

I think you need to do some molecular biology.  I guess you have a weak A subgroup.  Most peculiar that it's coming up with the lectin and not the clones, but that could be something to do with the formulation of the reagents.  There might be some potentiators in the lectin that aren't present in the clones, or the pH could be different etc etc. I agree with Malcolm that you need to test with human anti-A - tube technique.  Use an excess of anti-A (if reagents aren't available, use group B plasma) and incubate at 4°C and (separately) at RT.  That should give you some answers

Only about 25% of A2B individuals will have an anti-A1 detected by routine ABO testing methods.

According to Peter Issitt's book Applied Blood Group Serology (paraphased):  Between 1 and 8% of A2 individuals produce Anti-A1, and approximately 22 and 35% of A2B individuals produce Anti-A1.
 
So, it is very typical to not find Anti-A1 in the plasma of A2B patients.
 
 
Donna