jmm8427

There's a lot out there but I know Immucor has a webinar coming up Oct 31st: https://immucor.webinato.com/register

It sounds like if at that point (after throwing everything at it including DTT and papain) you don't have the rare antisera/cells and reagents to identify the antibody then you are going to have to send it out anyways and the reference lab will probably end up repeating most of that testing in order to ID the reactivity on their end. You are right, you have to consider that implementing trypsin is a big project with SOP revisions, may involve added costs, is known to have stability issues, and how often do you expect you will really need it and keep your staff competent? Will it really have any added benefit to your testing? From personal experience in a smaller reference lab with limited rare reagents as well as in a larger IRL, I would say it sounds like you may want to wait on the trypsin until you have a better inventory of rare reagents to aid in completing antibody ID?

One could argue that by doing the panel first you are being efficient and potentially saving time with antibody identification if something is detected. But by doing the screen you are saving reagent/cost. I'm not sure there is a right or wrong answer to this question?

I agree, my experience with trypsin is not good either. It took us quite a few tries to get it correct - the stability was the biggest issue. It took lots of time to figure that out

Sigma-aldrich?

We go straight for the panel, we're an IRL so I don't know if it's different between hospital and reference lab?

I totally agree! And, from personal experience, finding the people with this deeper knowledge of blood groups is getting harder and harder to find... Are you looking for a position in KY by any chance?

Good point Malcolm, and you are correct in that it is implied the candidate must have detailed blood bank knowledge with the Specialist in Blood Banking (SBB) degree requirement. I would find it extremely difficult to pass the SBB exam without this knowledge

Kentucky Blood Center is looking for a Reference Laboratory Manager for their Immunohematology Reference Laboratory (AABB IRL), see below and this link: http://kybloodcenter.org/about-us/careers/

I think the manual we have asks us to replace them on a regular basis (every 2yrs? I don't have it in front of me), we do not validate (or re-validate) after replacing

A little off topic but related to DARA: Some of my techs are reporting that hand-washing the tubes in tube testing (PeG) versus using a cell washer is more likely to give negative reactions with DARA samples. I wonder if anyone else has experienced this?

Just like tbostock we've used the packing material or cut up a sponge... if it gets soiled just throw it out and cut up more.

Thank you for speaking Malcolm! It was a pleasure to see you and the entire SCABB conference was excellent!

Where does it say to do it semi-annual? Our facility is being inspected soon, I think it'd be a good thing to know...thanks!

I agree, so annoying! I'm at a blood center and had quite a few regular platelet donors come up with anti-Wra with this screen cell lot...

http://www.indianinitiative.org/cases/ http://www.bbguy.org/ http://transfusionnews.com/ --> sign up for question of the day

I've had the same experience as Linewine99, and inspectors will look to make sure training and competency is complete if the director is working the bench

Thank you both! No, we didn't crossmatch any units but I will see what that does. And I didn't think of Pr! Out of the lab today but I'll give it a second look, thank you!

We have a troublesome patient that came in again, history of warm auto a few years ago, cold autoantibody and an antibody of undetermined (reacts majority of cells). What do you think: majority of cells reacting in gel (about 1-2 were negative; strength of reactions 1-2+) with positive autocontrol, No reactivity with PeG except autocontrol is 1+, 1-2+ reactions at room temp and 3-4+ reactions at 4C. A cold auto-I was identified based on the 4C/RT reactivity and cord testing. Ficin testing panel was negative (including autocontrol), DTT panel was reactive still. Neutralization testing was performed but cells were still reactive. A cold autoadsorption didn't work. A RESt adsorption was performed but still had partial reactivity. The plasma reactivity was able to be adsorbed out this time with allogeneic cells. The DAT was positive, no transfusion in last 3 months. The eluate was non-reactive. EGA treated cells were negative when tested with the plasma/PeG, Do you think the reactivity is due to autoantibody or is it an alloantibody? We don't think the warm auto is back but we weren't quite sure to make of all the gel reactivity and weren't quite sure what to do next, if anything. Thoughts? Thanks for the help!

We recommend matching the Rh system (CcEe) and K, hemoglobin S negative units; matching Duffy, Kidd, MNS system only if they make an antibody. (If it becomes too difficult to match exactly we do the best we can, we also attempt to molecular type them and confirm if the patient has the GATA mutation) . We're a reference lab so many of our hospitals have different policies. Some just give hemoglobin S negative, a few give C-E-K-HgbS- unless the Rh system is different and a few follow the same policy we have. The information we've looked at indicates that there is no uniform policy among institutions regarding transfusion of these patients but it is nice to hear what others are doing.

I messaged you!

I think most accredited SBB programs are probably great, it depends on you. Do you work better with an online setting and can motivate yourself to study or seek out the information you need? Or do you need to attend the class and get the interaction with the other students/teacher?

Malcolm (or anyone else), can you expand on what you said about auto-anti-Pr? Is there a reason why that foretells a worse prognosis? How would you positively identify the -Pr vs -I or -HI? Thanks for any info!

Thank you so much Malcolm!

@Kip, good question I'd like to know what everyone else thinks about that. We just had one and determined the anti-M was IgM but the doctor insists he wants to keep performing a titer in case it becomes IgG. So what was the point of having us determine the Ig classification?!