macarton

to save into a Word document, click PrtScn, send to clipboard,  then to put in document, click on spot you want it and right click and paste.  On the popup boxes, if you want whole screen with the pop up, hit PrtScn, then cancel, then to put in document, click on spot you want it and right click and paste.  You'll have to do some trimming then.

to save into a Word document, click PrtScn, send to clipboard,  then to put in document, click on spot you want it and right click and paste.  On the popup boxes, if you want whole screen with the pop up, hit PrtScn, then cancel, then to put in document, click on spot you want it and right click and paste.  You'll have to do some trimming then.

I agree with Malcolm

Not possible, Malcolm!  You have the 'most liked content' here!
Besides, you'll be speaking to all us blood bankers - kindred spirits, as it were.

Certainly, if that is okay with Cliff.  I have to warn you though - the presentation itself contains a photograph of me. so that might well put people off!

Thanks to a very generous invitation from the organisers (in particular Phil Hoffman, aka Dr Pepper on this site, and Maddie Josephs, Chair) I will be attending and speaking at the 69th Annual Clinical Laboratory Science Convention - Central New England (ASCLS - CNE) taking place at the Rhode Island Convention Center between May 9th and May 11th 2017.  I will be talking on Wednesday 10th May 2017, giving a lecture entitled, "An In Depth Description of the Kell Blood Group System." and then, after a well-deserved break for the delegates, and for those that can stand it, a second lecture entitled, "King Henry Viii, McLeod Syndrome, Chronic Granulomatous Disease and Kx."
Sorry if this comes across as being "big headed", but I am really excited about coming back over to the USA.    

ProVue (Automated Ortho GEL)
Erytra (Automated Grifols GEL)
Manual Ortho GEL
Manual Tube (Quotient Reagents)
Anti-A
Anti-B
A1 cells
B Cells
Anti-A
Anti-B
A1 cells
B Cells
Anti-A
Anti-B
A1 cells
B Cells
Anti-A
Anti-B
A1 cells
B Cells
4+
2+
0
0
4+
4+
0
0
4+
2+
0
0
4+
0
 (micro strong agglutination)
0
(Micro rouleaux)
2-3+ (incub RT)

If the reverse typing use the same A and B cells, then the differ between gel and tube are caused by the methods, otherwise, it maybe caused by low antibodies against B cells in tube method. To verify it, we can change to another B cells to test in tube method.
I tend to agree it looks like an ABsubgroup, on my daily use of gel, I find it is not as sensitive to detect reverse reaction as tube method, I  guess that is the cause of no reverse reaction on gel but has reaction in tube.
 
 

There is a Replace BBK Crossmatch Test routine, which can swap the IS XM mnemonic to your IAT XM test mnemonic.

That's a very good thing to keep in mind, thank you for posting that.

Hi Scott,
I'm back in the land of the living!
I think the key bit of your quote from the Technical Manual is:
"However. an eluate from the patient's red cells coated only with complement should be tested if there is clinical evidence of antibody-mediated hemolysis, for example, after transfusion.  The eluate preparation can concentrate small amounts of IgG that may not be detectable in routine testing of the patient's plasma.".
which, incidentally, is essentially what I said in an earlier post.
The other important phrase from the quote from the Technical Manual is:
"When the only coating protein is complement, the eluate is likely to be nonreactive."
The word "likely" is very important here, as it means that the eluate is not definitely going to be nonreactive.
Particularly in the case of a very weak antibody, such as one that is derived from an anamnestic response, it is not unknown for almost all of the said antibody to be sensitizing the red cells, and for very little, if any, of this antibody to be free in the plasma/serum - certainly not by normal serological techniques.  However, if an eluate is performed, and the eluate is made with less eluting fluid than normal (normally it is a 1:1 ratio with the washed packed red cells, but that ratio can be changed to, for example, two volumes of washed packed red cells to one volume of eluting fluid), then essentially, the concentration of the antibody being eluted from the red cells is doubled.
Such findings were described in Sachs UJH, Roder L, Santoso S, Bein G.  Does a negative direct antiglobulin test exclude warm autoimmune haemolytic anaemia? A prospective study of 504 cases.  British Journal of Haematology 2006; 132: 651-661.
As I have said in other, earlier threads, although this paper was designed to look at DAT Negative cases of AIHA, the authors also actually describe many cases of a delayed haemolytic transfusion reaction (possibly delayed sereological transfusion reactions) detected by eluting antibodies from the red cells of the patient, even though the DAT was negative and there was no free antibody in the plasma/serum that was detected by routine serological techniques.
So, the evidence from this is that the eluate may well be more reactive that the plasma/serum in terms of being able to identify the presence of, and elucidation of the actual antibody specificity.
You go on to say:
"And this from Malcolm: there are times when the causative antibody is an IgM.
But what is the likelihood that you are going to pick up an IgM antibody (significant or otherwise) with the anti-IgG reagents used for antibody detection?  And from an eluate no less, which I believe are notoriously weak anyway even if present?"
What I was driving at here was the fact that, if there is clinical evidence of antibody-mediated haemolysis, particularly after a transfusion, every effort should be made to identify the specificity of the antibody, to ensure that the cognate antigen is not expressed on the red cells of any units that may subsequently be transfused.  This effort may include the use of a clotted sample, rather than a sample anticoagulated with EDTA, as, of course, the EDTA would chelate the calcium, manganese and magnesium ions that are required for maximal initiation of the classical complement cascade.  In such a case, a monospecific anti-C3d reagent, or even a monospecific anti-IgM reagent, rather than a monospecific anti-IgG reagent would be used.  It was in this way that one of the red cell immunohaematology reference laboratories of the NHSBT was able to show the presence of an IgM anti-Vel in the circulation of a patient who had undergone an acute (sadly fatal) haemolytic transfusion reaction, where no IgG anti-Vel could be detected in the plasma.
The bit about the "strength" of the eluate I have dealt with above.
I am acutely aware that the ability for the normal hospital blood transfusion laboratory to be able to carry out such tests is unlikely, as they would not carry the necessary rare and expensive reagents, but in a case where there is clinical evidence of antibody-mediated haemolysis, samples should be sent to a reference laboratory for full investigation before further transfusion is attempted, unless the physician decides that withholding further transfusion is more dangerous than a possible further transfusion reaction.
Sorry for the over-long post.

We still do eluates up to three months after a transfusion, but ONLY if there are good reasons, such as a symptomatic patient.

I mail the patient a business size card with our 2 hospital logos, our contact information, patient name, antibody and blood type on it.  I also put a warning in the allergy section of our IS to call BB and why.  I also document on the BB history side of our Meditech the  date card sent and OE warning so we know not to sent another one or put the allergy warning in.

When we were converting over to Meditech 15 yrs ago, we found an issue with emergency releases if it ordered the IS Xm and we found out later the patient had an antibody. We reported it to MT and we set up a XM profile that had the IS, gel, and tube Xm in it.  All are auto NP except the IS.  If we need to result something other than the IS, we NP it and change the NP on one of the other tests to the test result we performed.  We can't do electronic Xm with the version we have, but when we upgrade to 5.66, I would think we wouldn't have issues.

I'll behind you soon I hope.  Lots of world out there for me to photograph.  Have fun.

Here's the latest news on this issue:
https://www.ascp.org/content/Newsroom/epolicy-news-October-2016#1

Att All:
 On behalf of pathologists and laboratory professionals, ASCP is urging the laboratory community and other interested individuals to Sign the Petition urging the Centers for Medicare & Medicaid Services (CMS) to reconsider its position that nursing is a biological science for purposes of performing laboratory testing. We ask that you forward this petition to all of your colleagues.
http://cqrcengage.com/ascpath/app/sign-petition?0&engagementId=239813
Here is the link to sign this important petition!
 

Horrible idea.  The existence of Lab Assistants is becoming more popular too; and their range of duties is expanding (outside of CLIA regs of course).  We are one of the only medical professions that seems to want to "dumb itself down".  Physician therapists, pharmacists, PAs, have all raised the bar for themselves by requiring higher degrees and certifications.  In my state (NY) that has licensing, some labs are trying to get around it by using foreign workers on temporary work visas; get them in and out before anyone notices.  It's getting crazy due to the shortage here, but I feel like the worst thing we could do is get more lax in who we allow to result lab tests.

ASCLS has provided feedback to CMS regarding this issue.  I'm more than a little distressed about this as a direct comment on the medical technology profession as a whole.  As an SBB, I'm qualified by education to perform as a general supervisor only for my high complexity reference laboratory and yet an RN can function as my director?  I respect every nurse I've ever come in contact with, but their education is not focused on laboratory testing to the same extent ours is.  They are part of the health care team, but they are not laboratory scientists.
I've attached the ASCLS Government Affairs Alert.
Government Affairs Alert.docx

I sincerely hope you are correct Scott.
I have the utmost respect for nurses and transfusion practitioners (many of whom started out as nurses, but neither they, nor many haematology doctors (let alone general doctors) should be allowed anywhere near a blood transfusion laboratory, without extensive training and education - something that we have been exposed to for many years.

Actually it is a blood derivative.
In the USofA blood is considered a drug by the FDA - to get better remuneration for his staff one of my previous lab mgrs had all the blood bank staff assigned to the same pay scale as the pharmacists - pretty ingenious I thought.

Hello everybody 
Google search is very good to this forum. Anytime I've had a blood bank question that needed an answer Google has always directed me here. Its great to see colleagues sharing knowledge. I like learning and there is much to learn about blood bank.
So it was only a matter of time that I joined.

And anti-Ch, anti-Rg and a few others.

For years, we have run a ficin panel on all of our work ups. Very helpful in enhancing some weak antibodies and those  that might be masked by duffy's and MNS systems.

Well David, I see your problem, but I may be able to suggest an answer.
Firstly, the anti-D seems to be quite weak (which is what made me think of my proposed answer).
Secondly, of the "common" Rh types, the R2R2 type has the highest number of D antigens per red cell (15 800 to 33 300), and so will tend to give stronger agglutination than will an R1R1 (which may explain why you are getting agglutination with all your R2R2 cells).
Thirdly, and turning to the R1R1 red cells, some of these may, of course, be R1r', rather than R1R1, and, therefore, have fewer D antigen sites per red cell (about 9 900 to 14 600, compared with 14 500 to 22 800) and, unless the donor is genotyped, or you can do an informative family study, you may never know (but remember the Cepellini effect).  In addition, the number of D antigen sites expressed on a "normal" R1R1 can vary quite a lot from one individual to another (and, indeed, from one cell to another, in the same individual).  In other words, those R1R1 red cells that react with your patient's anti-D could be near the "22 800" end of the spectrum, whilst those that do not react with this anti-D may be nearer to the "14 500" end of the spectrum.
All figures are taken from Geoff Daniels' book, Human Blood Groups.  3rd edition, 2013, Wiley-Blackwell, page 205.
I am not saying for one moment that this is the only, or the most logical explanation, but it is, at least, one explanation!