catchmenow51

I vaguely remember a study in the early 80's showing 25Gy, 30Gy and 35Gy, with the recommendation that 30Gy might be a tad better than 25Gy at getting complete inactivation in all products. But my memory fades me today -- actually, it faded years ago, but I forgot when ...

I want to preface the following remarks by saying that I am, or at least spent over 35 years, a blood banker in various capacities.  I am one of you. 
Blood bankers, with good reason, can generally be described as untrusting to the point of paranoia.  No one can do the job as well as we can and that includes other blood bankers.  I have never known one of us who would willingly trust a sample drawn at another facility.  It's hard enough to trust our own phlebotomy staff!  I don't even want to get into nurse draws!  We are this way because we understand the potential dangers and in all honesty most of this comes from a true concern for patients we never personally see.  I had one staff member quit a blood bank day shift to work as a generalist on the night shift because she was convinced that the use of the new automated analyzer would result in the death of all of her patients because she would not personally be doing the testing.  Granted that's a little extreme but it is an example.  
So to answer the original question of this thread, I am fairly confident you will find little or no support for "using a blood bank sample drawn and tested from another facility".

It seems to me that you have covered all bases Mabel.
There is a telling sentence in Reid ME, Lomas-Francis C, Olsson ML.  The Blood Group Antigen FactsBook.  3rd edition, 2012, Academic Press (page 419), which states, "Experts agree that anti-Yta are often benign and antigen-negative blood may not need to be transfused."
Certainly in the cases I have seen over the years, I have never had to give Yt(a-) typed blood (although, because of the geography of England (it's a lot smaller than the USA!), such blood could easily be obtained from the National Frozen Blood Bank, and/or from "tame" donors.

Don't reference labs/hospital labs use many things outside of IFU?  These things are used to aide in the identification of antibodies. They are not used solely for ID, as that would be ridiculous. Just like using expired panels, only, to ID antibodies.  Expired panels are only used to help rule in/out.  It seems that validation would be the fact that DTT works when the controls work.
 

Don't reference labs/hospital labs use many things outside of IFU?  These things are used to aide in the identification of antibodies. They are not used solely for ID, as that would be ridiculous. Just like using expired panels, only, to ID antibodies.  Expired panels are only used to help rule in/out.  It seems that validation would be the fact that DTT works when the controls work.
 

Don't reference labs/hospital labs use many things outside of IFU?  These things are used to aide in the identification of antibodies. They are not used solely for ID, as that would be ridiculous. Just like using expired panels, only, to ID antibodies.  Expired panels are only used to help rule in/out.  It seems that validation would be the fact that DTT works when the controls work.
 

Well, in a way, yes.  They will not waste time on trying to perform alloadsorptions (as these don't work) and will probably perform genotyping from the word go, rather than trying to get a phenotype.
To be honest, the submitting hospital should give the Reference Laboratory as much information as they can about ANY patient, whether they be on ANTI-CD38 (gagpinks, they are on a monoclonal antibody - not a monoclonal antigen!!!!!!!!!!!) or not.

I try to avoid using it if at all possible.

I've seen positive autocontrols with negative DAT's, just curious if anyone has seen positive DATs with a negative autocontrol? I have always performed an autocontrol first and if the autocontrol is positive then we go to a DAT.

An auto-control and a DAT have not always given the same result in my experience!

I dont find any reason, to defer any Kell positive donor, and not eather refuse to use this blood, i think some population should be protected like children girls, women in pregnacy age, and multitransfused people like thalasemic or drepanositic ones. And of course, any person with anti Kell.
All other people can be transfused with Kell positive red blood cells.

Still liking my Helmer cell washer. Very glad we switched from the Sorval. Earlier Sorvals were great but the re-branded CW2+ was awful. The Helmer may cost more up front but it is worth it because we have no problems, no parts to buy and no hair pulling.

Has anyone had any problems with the the inside cover of the cell washer "chipping"? It looks as if the paint is chipping off and I'm wondering if it is due to the weekly bleach cycle. The cellwasher is only 3 years old. I don't remember ever having this problem with the older cellwashers, but of course, I sometimes don't remember what I had for dinner last night.

Human source commercial antisera like anti-Fyb have shown weakening antigens after DTT treatment in our hands .  Others have not found this.  We wish we could figure out why our reagent cells sometimes lose their Fyb antigens.  Donor units that we have treated have not seemed to lose reactivity.

So, the easy questions first eh Mari?????!!!!!!!!!!!!!
Personally, I think the IT guy gave you a poisoned chalice.  The reason I say this is because we can all list antibodies that are not generally considered to be clinically significant, and then, all of a sudden, one comes along amongst these specificities that has not read the appropriate text books and goes ahead and causes a clinically significant reaction.  Then what happens is that the person who said "anti-X" is not clinically significant, and this single example of anti-X turns out to be clinically significant, and you have to defend this in court.
The real problem these days is that the technologies available to us are now much more sensitive than when I started (when cross-matches were recorded on a stone slab with a hammer and chisel) and many antibodies that were not clinically significant (because we just didn't detect them with the technologies available at the time) are now readily detectable - BUT, they are not necessarily detectable at strictly 37oC, as , for example, many examples of anti-M are now detected by "IAT", even though they do not really react (in real terms) at 37oC.  The real problem comes when, for example, an anti-M genuinely DOES react at 37oC, and it is treated as clinically insignificant, electronic issue is used, and one or more of the units is M+ and the patient has a severe reaction - who answers in court?
The worrying thing is that there have been papers published over the last few years quoting an anti-Leb as causing a transfusion reaction, and an anti-P1 causing a transfusion reaction (a certain Garratty G being a co-author on this one).
I would say, therefore, that the best thing to do is to read through the relevant parts of The Blood Group Antigen FactsBook, Human Blood Groups and Mollison's Blood Transfusion in Clinical Medicine (latest editions in each case), and use their experience, rather than your own (no insult intended) as the courts would probably take the authors as "experts" should you come across any of these clinically significant "outliers".
I wish you the very best of luck!

Could be either. In my experience, PeG is a bit more sensitive than gel. When we had nebulous reactions in gel, we resorted to PeG to ID the antibody.
I think it's always valuable to remember that there is no one system that will detect all antibodies, even within the same specificity - that's just life (or maybe I should say, that's just biology).

I'm on call 24/7.  I tell them to consult the policy first.  If you try and can't find it anywhere in a policy, ask your coworkers to show you where to find the answer.  If nobody else on your shift can point you to it, THEN you call me.  Do not guess!
I get a lot more text messages than I do phone calls.  Usually they already know the answer, they are just wanting me to confirm their answer.  We have quite a few generalists on my eve and night shifts that are not very experienced with difficult BB issues, so I have no problem with them calling me.  I would much rather that than a patient gets hurt.  I feel like it's part of my job as BB Manager to support them and have them feel confident in asking for help when they need it.
I think the key to "weaning" them from calling too much is giving them really great policies (written very simply so anyone can follow them, even if they have not done the test for a while) and some good flowsheets (which I am still working on) for antibody workups, RhIg workups, etc.

My game plan with the kidds is to honor what antibody I think I see (assuming it agrees with their phenotype). Because titers with kidds are notorious for falling quickly, and their transfusion reactions can be particularly unpleasant, I always think its better to be safe than sorry.
 

We don't worry about the f unless the patient has a true anti-f. Seems kinda overkill to me, but that's just my opinion.

As a Reference Service Manager (and not yet totally driven insane; despite what Rashmi may say) I would thoroughly recommend not bothering to send in your samples from patients with antibodies directed against low-frequency antigens, and just give cross-match compatible blood!
For one thing, identifying the specificity of such an antibody (if it's not something like an anti-Wra) is like looking for a needle in a haystack.
For another, such a patient usually makes multiple specificities of antibodies directed against low-frequency antigens, and so a) we would probably never identify all those present, as we do not have access to red cells expressing every low-incidence antigen, and very often, a cell that has been identified as, for example, Li(a+) isn't, because it was identified with an anti-Lia that also had, for example, anti-Bxa in it, but we didn't know that.
Lastly, for now (as my rant muscle is running on low) the chances of you cross-matching blood, and then giving a unit that is likely to cause a clinically significant haemolytic transfusion reaction are so low as to be all but zero (just think of the number of patients who have been given blood by electronic issue, some of whom must have antibodies directed against low-incidence antigens, and some of whom have probably been given blood positive for the corresponding low-incidence antigen, and you see what I mean).
I shall now go and lie down in a darkened room!!!!!!!!!!!!!
:crazy::crazy:

Oh I see; sorry.
Well, if we have a patient who has made an anti-f (usually an R1R2), we usually say give either R1R1 or R2R2, but, if the patient has an auto-antibody and has not got anti-f, we would recommend just Rh antigen specific, and by that, I mean you could give an R1R2 patient virtually anything in the way of Rh, so I still go with what you say!!! 

I brought this up many years ago to one of the Reagent Manufacturing Companies (cannot recall now which one it was....Immucor, Gamma or Ortho....or maybe one of the ones that is no longer around).  When changes are made to Manufacturer's Inserts (and they can be as minor as a change in 1 word, which we can spend a long time searching for), it would be really nice if the Manufacturer would indicate the changes on the inserts (i.e. maybe italicize what is changed; or underline it; or highlight it......just give us a clue)!  We want to catch the significant changes, but not spend an hour reading and re-reading the insert to find the    ever-so-subtle and non-significant changes.
Thanks for listening,
Brenda Hutson, MT(ASCP)SBB

I think the patient is going to be in trouble.  At this point there is not much we could be doing differently . . . except maybe type the patient for k along with the initial K typing.  Fortunately those k/Kpb neg pts should be few and far between.

According to the AABB Association Bulletin 16-02, if you detect an actual antibody and need to do an AHG crossmatch, you can treat the K-/antigen- donor RBCs with DTT before doing the crossmatch.  If you have identified and honored all of the underlying allos, your AHG crossmatch would be compatible :-).

Although the baby seems to be doing well, it would indeed be nice if the father's cells were available to test with the eluate (and Mom's serum). Or you could have a reference lab take a look for antiboduies to low-incidence antigens. Identifying the antibody might also be helpful in managing future pregnancies which probably would have a 50% chance of the same serologic scenario. I would think that no clinical signs of HDFN are no guarentee that the next child would fare as well. And if nothing else, the ex-blood banker in me would just want to know what the darn thing is!