Ally

Like @Bet'naSBB said, there's really no easy answer.
My first response is ALWAYS, check with the manufacturer to see if they have documents or guidance.
Then, read the package inserts, they may have info.
Then, barring anything definitive from above, you and your medical director need to review your patient population and determine how many of each type of patient you want to test. Do you have a lot of antibody patients? Do you treat cancer patients?

We did a Plasma Exchange recently on a patient 5 days in a row with approximately 10-12 units of FFP each time.
On day 3, the band expired and we retested the new sample to find the previous antibody had disappeared.
It's a dilutional effect where the titer is dropped below detectable levels.

Happy Friday everyone! 
First off, Thank you Malcolm 😊 for that excellent PPT lecture! 👌 With your permission, I'd love to share it with my students; it's exactly the kind of content that helps bring these complex concepts to life (and mildly melt brains in the best way possible).
Speaking of melted brains… let's talk Anti-G differentiation, shall we? While I agree that differentiation isn’t necessary for transfusion purposes because in cases where anti-G is suspected, the recommendation is the same (D and C antigen-negative PRBCs); in the US Reference Lab world, it's a whole different dance. Differentiating anti-D + anti-C from anti-G is essential in alloimmunized patients with anti-D + anti-C for Rh Immune Globulin (RhIg) prophylaxis administration indication. Medical teams want to know if a patient is a candidate for RhIG, and if it's still indicated, especially to avoid future medical and legal complications. And so begins the beautiful (read: painstaking) double adsorption and elution process. 😫
 
The presence/development of a real anti-D indicates the patient does not require RhIg administration, whereas the presence of anti-G indicates the need for RhIg prophylaxis. That way, RhIG is avoided in patients with a real anti-D (although clinical correlation is recommended to guide every decision).
In this case, we saw what looked/reacted like anti-D and anti-C (1). Adsorption with R2R2 cells showed anti-C in the adsorbed serum (2) and anti-D and/or G in the adsorbing R2R2 cell eluate (3). Usually, we would stop and call anti-C and anti-D, if we have no reactions on C Ag Pos cells, but since suspected anti-G was in the mix, we routinely differentiate/separate it. The anti-D was confirmed in (4) by adsorbing the eluate containing the suspected (anti-D + anti-G) with an r'r unit. So far, so good. However, when we tried to separate the anti-G by elution of the adsorbing r′r cells, expecting a reaction on D and C antigen-positive cells (5), we got a negative result (Cue dramatic music).
I know, I know...at this point you’re probably wondering if we’re still in the Blood Bank or if we’ve accidentally wandered into theoretical physics. Trust me, my brain also wobbles when explaining G differentiation. It's the kind of thing that makes you rethink your career choices... for about 5 minutes... and then roll up your sleeves and start prepping another adsorption. 😅
A couple of housekeeping: We ficin treat our adsorbing cells, and sometimes use PEG in adsorption for efficiency. After briefly considering a career in something less chaotic, we retraced our steps. No PEG this time, 60-minute incubation, followed up with a DAT after each adsorption to check for antibody coating... and voilà: finally got the positive reaction we were looking for. The patient has anti-D, anti-C, and anti-G.
I can only think of a possible weak DAT strength pending elution, or PEG interference when used in adsorption. As always, this is Blood Bank, we know a million things can go wrong, and often do. But in the end, science (and a lot of perseverance) wins. 
Thanks again to everyone for your input, patience, your brains, and your sense of humor. And again, Malcolm, thanks for your lecture, teaching, dedication and inspiration!
I wish everyone a calm weekend. May your panels be clear, your DATs negative, and your eluates informative. 😉
 

Thank you for your exceptionally kind words DLabGirl, and by all means use the lecture as you wish.  The same goes for anyone else who might want to use it, with the proviso that you a) realise that it is a bit "long in the tooth", and b) I did mean that we, in the UK, would still look to ensure that there really is an anti-D present, before we do not recommend giving anti-D immunoglobulin.

We use our CAP samples AFTER the results have been submitted and results have been received from CAP.
We just finished assigning a BUNCH of "Internal Assessments" and "Method Comparisons" using our first batch of CAPs that we'd already received our results for.  All these count as "blinds" for the staff.  Instead of making 1 tech do the whole survey, we give each assignee one sample to do and then compare their results with those expected by CAP.  works great!
For FMH, we get two CAP "TMCAF" surveys per year.  1/2 the staff does the first and the other 1/2 the second so everyone gets a blind for FMH.

Technically, any sample you don't know the answer to is "blind" to you, so any regular patient with no history can be used for a blind blood type for example. Yes, for DAT and FMH it's harder, but we typically use the CAP samples as Bet'naSBB said, rather than try to make up samples that are not quite right.  

Sorry Neil, but I have to point out that this is not completely accurate.  Any red cell antigens that are adsorbed onto the red cell surface, rather than being an integral part of the red cell membrane remain the type of the patient, rather than the donor.  This is true of the Lewis phenotype (for instance, if the recipient was Le[a+b-], and the donor was Le[a-b+], after the transplant, the red cells will group as Le[a+b-], and not as Le[a-b+]}.  This is also true of antigens within the Chido/Rodgers Blood Group System, and certain others.

If the recipient is a Secretor, they will continue to secrete ABO substance of the original ABO type, which, of course, will also be adsorbed onto the red cell surface (as well as being in the plasma, leading to the phenomenon of "accommodation", and this is why most recipients stay with a reverse group of "AB" after an ABO mis-matched stem cell/bone marrow transplant.

SORRY TO BE A PEDANT, PARTICULARLY AS I AGREE WITH EVERYTHING ELSE YOU HAVE WRITTEN!

This may be a little outdated, it's from a prior facility.  We did a tremendous amount of transplant infusion, and this evolved over the decades I was there.
Management of Hematopoietic Progenitor Cell Transplant Recipients.docx

In the UK, the Guidelines would (quite correctly in my own opinion) NOT allow us to perform electronic issue on any sample, whatever the pathology, on a patient where the forward ABO type does not match the reverse ABO type (apart from Newborn babies).

The +s stands for strongly expressed.

The expression of the P1 antigen varies considerably from person to person, but the reaction strength with anti-P1 is an inherited trait (i.e. the strength of the expression on the red cell surface).

"I apologize for this dumb question."  BBnoob69, NO QUESTION IS A DUMB QUESTION, IF YOU DO NOT KNOW THE ANSWER.  If you don't know the answer, the dumb thing is to not ask the question in the first place.  NEVER be afraid to ask a question on here,

We have educated our multiple myeloma specialists to send a type and screen before administering the first dose of a daratumumab (Darzalex).  Our standard operating procedure is to have a panel of three cord blood cells (we have a large OB service) that is a laboratory developed test of sorts.  Cord cells do not express CD38 at interfering levels.
As it turns out we have made more of an issue of this than it warrants.  Patients who have negative antibody screens essentially never develop new antibodies to red cells after being started on daratumumab probably because it potential inhibits B cells function.  Minimal B cell function apparently yields little ability to make antibodies to red cell antigens, which are relatively weak alloantigens, especially when there is no adjuvant or inflammation in the recipient.  That said, a manufacturer is making a soluble CD38  analog that will inhibit the anti-CD38 activity and make testing easier from what I've read.  DTT treatment is also reasonable.  But the good news is that patients on this drug do not make new antibodies. There are literature references to this, and we have probably tested about 500 patients with no new alloantibodies. Mostly non-transfused patients, obviously.

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Of course, my facility is blocking the link.....
Is this a web page? Could you private message me the link please?
TIA

We were always AABB accredited.  That requires a facility representative.  That was always me.  That gave me the equivalent of individual access.  In fact, it was not possible (well everything is possible) to have an individual membership if you are also the site representative.
They do have a best practices sections, which is great.  We also have a document library here, and members here are always willing to share their ideas on topics, if not their actual SOPs, just ask. 
You do get a discount on their books like Standards and the Technical Manual.  With your membership, you also get a monthly subscription to Transfusion.
I used their mentorship program after being in the filed for over 25 years.  I got a new position, and the mentor they assigned me was wonderful.  We talked through a lot of challenging situations I was facing.
There are other sections of their site that become unlocked.
Is it worth it, that's up to you.
 

My facility is not AABB accredited, just Joint Commission and FDA, and I have an individual membership. I am the supervisor, and we are a large level 1 metropolitan trauma hospital. I have gained so much from my membership. Everything Cliff mentioned about resources is true, and I can't tell you how many times we've taken advantage of the discount on books for my pathologists (none of whom are transfusion medicine specialists). 
AABB membership also opened up all the subcommittees and sections, and I now sit on 9 subsections and lead one of them. I am also a mentor in the program Cliff mentioned above. 
I would say it's worth it for at least one year, so you can try it out and see what you get from it. Pro tip: if you love it, they do offer a 3 year membership option that knocks some of the cost down.  

I never regretted my individual AABB membership.  They can be an excellent resource, especially in your new position.  Having said that, I imagine things may have changed since my retirement.  I would suggest getting a membership, if you are not seeing the cost: benefit ratio in your favor you can always cancel or just not renew.

See my answers above.

I thought for the first time I would share one of the educational webinars we have been producing with the ISBT because it is a fascinating topic addressed by a great lecturer (Sue Johnson).
So do miss out on the opportunity to watch the recording of this ISBT educational webinar Could it be drugs? How to differentiate AIHA from DIIHA Start zoom webinar | The International Society of Blood Transfusion (ISBT)
 

Agree that if not for transfusion purposes, ABO types do not need repeating.  We don't do confirmations for potassiums or troponins either.

We do not require a confirmation when no red cell transfusions are ordered - ie - prenatal testing, or just an ABO/Rh.
Most BB LIS systems will not "allow" the selection of ABO specific red cells if there are not TWO matching examples of the ABO on file with reactions.
As an example:  Our hospital just went to a new BB LIS (under duress).  The ABO interpretations came across to the new system but NOT the actual reactions.  Because of that we've had to perform a second 
ABO on essentially EVERY patient who we get a Type and Screen on - as this is the only test that allows for the selection of red cell containing products.  We also went to a new version of EPIC at the same time as the BBLIS switch and it has somehow been set up by someone to recognize all patients who DO NOT have 2 ABO's with reactions on file and it will automatically order the 2nd ABO for us.

We use clear plastic bags to transport blood products. Blood products are not considered biohazardous. 

OMG - we evidently have a new generation of inspectors.  As Mabel said - OSHA regs.  The real pain is having to respond with a corrective action of teaching them.
 

Under OSHA, tested donor blood is not considered biohazardous.  For heaven's sake, we infuse it into patients!  It would take me some time to find the regulation, but it is in the OSHA regs.

Lewis antibodies do not cause HDFN and do not need titration.  We do not Lewis phenotype transfusions to patients with anti-Lewis antibodies, but do a manual antiglobulin crossmatch to find units that do not react. I'm sure there are rare patients whose antibodies can cause removal of Lewis positive red cells at an accelerated rate, but this is not something that needs to be considered unless the patient shows signs of hemolysis or rapid red cell removal.  Never come across this in 50 years of practice :).  But never say never in medicine.

Our policy is to give crossmatch compatible blood. Having said that, we had a patient years ago that had anti-Lea and anti-Leb who did not respond as expected to transfusion . There were no other confounding factors that we could identify. We transfused antigen negative units and the hemoglobin went up and stayed up. We have not seen the patient since. Interpret that as you wish.