Mabel Adams

I'm resurrecting this old thread to see if anyone has updates on how you charge for TEG or ROTEM testing.

Interesting idea. Sorry, I don't have an answer for you.

We issue uncrossmatched units in our BBIS, so it prints tags for the units that resemble those for crossmatched units. Fast, easy and accurate plus the RNs can scan the units in Epic to document transfusion. We use SafeTraceTx. We have a downtime uncrossmatched blood form we can complete on paper. We keep a photocopy. See attached. Emergency Release of Blood Products (form) (20553_0).pdf

"Anti-CD36 (anti-GPIV) Frequently Interferes with Routine Red Blood Cell Antibody Testing in Patients of African Descent" is a plenary session at AABB this fall. I can't find any useful information on it through an internet search. Does anyone have any references or information on this, which I assume will be a therapy at some point.

I only wish I could know another language anywhere near as well as Yanxia knows English! She has always impressed me with her blood bank knowledge as well.

Blood bank methods aren't expected to correlate perfectly. We use their differences to avoid rouleaux, clinically insignificant, and weak warm auto reactivity so we can better detect any significant alloantibodies. No method will detect 100% of significant antibodies. I am going to tweak the above to say we can "better detect' antibodies so it works better with the next sentence and doesn't imply that we can detect "any" significant antibodies.

When TJC inspected us last year, we weren't cited but she recommended that we include in our QC policy for the lab why we don't do BB correlations. I finally got around to writing this up. Did I miss anything? Is anything in error? No published evidence or immunohematology expert supports periodic method correlations. Blood bank methods aren't expected to correlate perfectly. We use their differences to avoid rouleaux, clinically insignificant, and weak warm auto reactivity so we can detect any significant alloantibodies. No method will detect 100% of significant antibodies. If they don't correlate on a given sample, there is nothing to be done to "fix" the methods. Deviation from manufacturer's instructions violates FDA and other regulations. It would be extremely complex and probably futile to try to validate all changes that would make all specimens correlate. To select a specimen for correlation testing that is expected to correlate between methods while avoiding those that won't correlate is unscientific and a waste of resources.

Ortho MTS gel instructions say to wash if there is interference from clots, which may happen with cord blood, but it doesn't say to always wash cord cells before running a gel DAT.

Ah, I was thinking of it like anti-G, but a haplotype with D but without C is much more common than one with C without e. Also, anti-Ce isn't reacting with something made by both the C and e genes like with genes for D and C can both make G. I think.

If we have to hunt for a sample to use for this that will give consistently comparable results, we aren't testing the method, we are testing our ability to find a suitable sample. I heard that CAP will sell you one that will consistently give the same results. If we aren't going to change anything (can't recalibrate gel!) based on the answers we get (like chemistry would), then why are we doing this? I talked TJC out of it last inspection (I probably got a little heated over the stupidity of it because I had to come in the day after a concussion to meet with them, but maybe they took pity on me and didn't cite me because of my unfiltered brain). No one has been able to explain to me any meaningful takeaway from doing this comparison. If I am ever forced to do it, we will just keep copies of sample results that we run by two methods to solve a problem and make a note that they are acceptable because we expect these differences between methods. If anyone can give me a valid use for this, I would be very appreciative.

If this were the case, wouldn't she react with e+ cells as well as C+ cells? Or does anti-Ce tend to react more strongly with C than with e?

I've been accused of looking for unicorns when I hear hoofbeats!

We print bag tags on ISBT Q3Q4 label stock which we then put on manila tags and use a plastic tie to attach them to the units. This way we can use the same printers and label stock for making labels for 5-day plasma. Our nurses document in Epic or on downtime transfusion records that have space for a duplicate of the bag tag labels.

I'm over my head with this case for a Friday afternoon. Patient is a 70 yo apparently Caucasian female who was transfused in 1981 in childbirth. No transfusion since. She was in ED for a fall but has been discharged. Very limited sample volume. O pos. Appears to have anti-C reacting 1+ in gel. Reacts 1+ with another cell that is C neg and HLA pos. HLA is noted as present on 2 of the C+ cells that react but not on the other three C+ cells that react. Have negative reactions that allow ruling out all of the other usual suspects. DAT is 3+ with IgG; neg for Complement. Patient types C+, E+, c+, e+ with the e reacting quite a bit more strongly than is typical with our Ortho anti-e reagent (comes up solid 4+ at immediate spin). We have not done an eluate, partly because it seems not worth the resources because she has been discharged. I suspect a mimicking anti-C autoantibody or just Bg antibodies, but is there anything else we should be thinking about? I get confused in all of the rare Rh variants so thought I would save myself a lot of reading and ask the experts.

If we know the patient has anti-E, for us that would justify using O neg for uncrossmatched if it didn't deplete the O neg supply too much and we could screen O pos for E quickly. More so for known anti-D. Not saying anything was done wrong in this case.

We use Adsol units for small volume transfusions. We remove the plasma/additive for exchange transfusions and replace it with AB plasma. St Charles in Bend OR. Our NICU is the highest level (3, backward from trauma designations) but not that big. We have a 24 bed capacity.

If you give the same product to all patients regardless of age, blood type, gender etc. then why an extra check? Assess the risk for this product being infused improperly and compare that risk to other things that require 2-person check to see if it is anywhere near equivalent. Probably there was some historical computer system that required it and now it is "how we've always done it".

We put the unit in the incubator and this morning it shows some swirl, so we are accepting it.

Yes, I think that is probably what would be required.

In this modern world where cold storage of platelets is now accepted by FDA and almost all are pathogen-reduced, what do we do with a room temperature stored platelet that lacks swirl? Give it to a bleeding patient like cold-stored platelets? Do you reject platelets that arrive from the supplier within appropriate temperature but lacking swirl? Do you have an assessment that helps you decide they are okay to use?

Has anyone considered how to build for cold stored platelets in their BBIS? SafeTraceTx at least, has expected temperature ranges for products on return from issue or delivery so we couldn't very well lump cold stored platelets in with other platelets. I guess we could build an entirely new product class with its own temperature range. Not that we are going to get cold-stored platelets anytime soon, much as we would love the 14-day shelf life. We are too small and remote to keep a dual inventory for oncology vs. trauma patients. I'm just curious how others plan to solve this issue. After all, the driving force of our lives is keeping our computers happy, right? Now if FDA would just approve 7-day expiration for all PR platelets!

Does anyone remember the humorous/terrifying thread on here more than a decade ago of all of the insane things we had heard of? "I can't hang this plasma on my patient, it's liquid and the doctor ordered FROZEN plasma". Or, "I don't care if the plasma isn't thawed yet, I need to hang it stat! Send it up now!" "I ordered that blood culture stat and it's been 2 hours. Why don't I have a result yet?!"

I always based my judgement on the fact that the original studies to determine significant titers were done using double dose cells. Plus, nowadays, with donor eggs, the baby can be homozygous for the antigen.

Anyone else remember when the RhIG used to come with some of it in a separate vial which we had to test against the patient's cells? I guess to prove that they really were Rh negative. We definitely had to do an antibody screen with that. That was before 28-week RhIG or Fetal Screen/rosette tests.

There used to be a regulation that the birth parent not be sensitized to D to be a RhIG candidate. We trust that the baby lacking a positive DAT due to anti-D is sufficient evidence and have not done anything but the needed Fetal Screen in a couple of decades, even when we didn't do admission T&S routinely. I think key is what will we do differently with the results? If you detect anti-D, you will assume it is RhIG and give RhIG again. If the Ab screen is negative, you will give RhIG. The test doesn't change the treatment so why do it? This assumes that a strong anti-D, clearly due to sensitization, would cause the baby to have a positive DAT and therefore any needed workup would be completed for that reason.