WisKnow

Congratulations Malcolm! You undoubtedly deserve it.

Is anybody using cord blood cells to resolve panagglutinin due to anti-CD38 interference? Can you share your procedure? Ours is DTT. Thank you.

Does everyone need to perform unknowns even if the direct observation for the same set of tests have already been done? I mean, are unknowns supposed to be done for the same set of stuff?

So, in a tertiary transfusion service department, how much competency assessment needs to be done? If we group the tests into test systems, how many test systems would turn out to be necessary to do competency assessment on? For example, in the area of immunohematology where we do a lot of tests: antibody ID, DATs, EGA, DTT, ficin treatment, elution, ReSt adsorption, warm auto or allo adsorption, etc. Grouping these tests into a test system, does each staff still have to do ALL of these individually?

Hi all! Our SOPs are so detailed about addressing our downtime procedure to the extent that we don't get motivated anymore to even refer to them during the actual situation. There are just too much to read when we are in a hurry to process STAT samples. So, we are planning to split them according to different scenarios like when it's only the Sunquest which is down but Epic is up and vice versa or when all the computer systems have crashed and when there is power outage. Do you have SOPs that you are willing to share? Thank you!

We're also using Epic and struggling with how the doctors place their blood orders. Epic doesn't alert them even if same orders have just been placed. So they could order 8x of 2 units of RBC for example when actually, they only need 2 units. Calls will still be back and forth just because of the duplicate orders which if only the Epic alerted them would not have been placed.

Thanks Malcolm, our goal is just to save on cost. So, we are aliquoting patient's plasma, positive for anti-K, for example and give it a 1 year expiration date. This, we use for our 0.2M DTT quality control instead of the commercially available anti-K. Does anyone know if this practice is regulated by FDA or CLIA? I actually don't see any but I just want to confirm because FDA is so strict on patient's specimens and may require trackable viral results record if these specimens are to be stored as in house reagents. Not so sure though. Thanks in advance for all your inputs.

Hi there! I am wondering if any of you use patient's plasma (antibody positive) as antisera. Does FDA require results of viral testing before you can use any patient sample as in house reagent?

They will discuss this matter and other matters when you request presentation from them.

The genotype of this patient according to the results from a reference lab is A101/B101. A certain mutation makes his B subgroup so weak and variable,

Is this the 0.2M DTT that we use to treat reagent red cells in HTLA or anti-CD38 cases?

Does anti-CD47 interfere with your antibody screen and compatibility testing like the anti-CD38? Does it affect patient's DAT?

We give Rh negative apheresis only to females of child bearing age. No neonates and pediatrics are at our site.

It is the policy at our facility to give E=c= RBCs when patient has anti-E and types also as c= or if c pheno is unknown or cannot be done due to very recent transfusion, but we do not type the units for E when patient has anti-c only. In this case, we only give c= units.

Thank you Maicolm! Patient is 46 years old. Dx: Lumbar foraminal stenosis

Here is a weekend case: Patient's sample was A (forward) and backtyped as AB with provue. Tube testing was AB with forward and back typing, however it was only 1-2+ with anti-B. The weird thing was, it did not look like a mixed field. Even after 15 min. incubation at room temperature, backtyping did not change. At 4C, A1, B cell and autocontrol all came up positive. I only saw some A subgroups and A3 was mixed field. I would presume B3 would look the same. And so this case could be AB3. Is there a way to confirm it with genotyping? What is your opinion?

We give our R1R2 patients with warm autoantibody whether the warm auto is currently detected or historical with little c or little e negative RBCs whichever is available. Little c negative of course is much easier to find than e.

I am not sure if there are 0.2M DTT treated cells readily available commercially if that is what you meant. We prepare our 0.2M DTT and use it to treat the positive cells we selected for antibody workup. It's a piece of work because you have to set up 0.2M DTT quality control by picking a heterozygous E and a K+ cell, antigen type them before and after treatment with 0.2M DTT. Kell group is destroyed by it. The antibody identification is performed using the treated cells and after everything has been ruled out, we still recommend K negative unit.

Hi dot! I am not sure if there are 0.2M DTT treated cells readily available commercially if that is what you meant. We prepare our 0.2M DTT and use it to treat the positive cells we selected for antibody workup. It's a piece of work because you have to set up 0.2M DTT quality control by picking a heterozygous E and a K+ cell, antigen type them before and after treatment with 0.2M DTT. Kell group is destroyed by it. So after everything has been ruled out, we still recommend K negative unit.

Thank you Mabel! That means we will continue to use 0.2M DTT treated cells.

Does anybody know if "antigen typed" cord cells are commercially available in the U.S. for use instead of us treating our screen and panel cells with 0.2M DTT when working on multiple myeloma patients receiving Anti-CD38 or Daratumumab?

Thanks Maicolm and Scott! The only reason why we had to identify the IgM antibody and differentiate it from Non specific cold and cold auto was to document how we resolved the backtype discrepancy. We're also worried of the clinically significant IgM behaving high incidence antibodies that may be on the way like anti-Vel and anti-Tja or PP1Pk if the autocontrol is negative or cold auto is not proven.

May I mention here that the antibody screen with provue was negative. Also, the A1 reverse cell was typed for N and it was positive.

Hi All! Do you still use 4C incubation when autocontrol does not come up at room temperature and you are having 2 cells out of 16 not pointing to any of the IgM antibodies? Resolving a back type discrepancy, a forward type looked like A but had extra reactivity with anti-A1 reverse cell = 3+. Short cold panel was run and plasma was negative with autocontrol only. So, we pulled a whole panel to identify the possible antibody reacting at RT. Anti-N was initially identified . So N negative unit was used to resolve the back type. But when review was being done, it appeared that 2 cells were 3+ positive but N negative and there were no extended typing found. We could not phenotype the patient for N bec she received transfusion 7 days ago. Since the autocontrol was negative with the same phase (RT), is it safe to result it as anti-N as the backtype was resolved with N neg segments and non specific cold at RT, for reevaluation when next workup will be performed? Or chances are, autocontrol may have come up at 4C if we did that and it might have been a cold auto?

Presumed to be anti-Pr when negative against ficin pretreated cells.