Ensis01

As I was talking about hrB and hrS I am to blame. Bioinformatics and blood banking; a minefield of possibilities and headaches

OK playing devils advocate for fun: the anti-C and anti-e were identified as allo-antibodies, as the article reported that the patient lacked the antigens, so phenotype R2R2. If the policy was to give patient's Rh and K matched RBC, then exposure to HrB (and HrS) would have been avoided (I can not figure out the frequencies of RBC that are e neg and HrB pos and Jeff Daniels was making my head spin, again). Blood 2013; 122: 1062-1071: I like these types of paper as they empirically, and definitively show the complexity of transfusion medicine and in this case of the Rh system, which reminds me how much I have to learn. Correct me if I am wrong please, but it seems that the Bioarray assay shows genetic mutations but does not identify some antigens, for example it does not seem to separate the e antigen mosaic and identify HrB and HrS, which the newer assays can. So my question is how many cases of alloimmunization in sickle cell disease the paper describes over the 13 year period would have been avoided if our current knowledge of the Rh system was utilized? Ask the same question in 5 years time!

The way I read the article; the lab has a policy of only running the ficin panel if they cannot clearly explain the reactivity, which seems like a good idea only if the ficin panel clarifies the reactivity. The article states that this occurred frequently enough that it was cost and time effective as fewer samples were sent to their reference lab. I assume that if the ficin panel does not clarify the pattern more confusion results, as exlimey said, and they send the sample to the reference lab. So sounds a reasonable policy if the techs can interpret the results correctly. The article also used an example of identifying an anti-C and anti-e in a sickle patient; most transfusion services (several threads on this site) match Rh and K for these patients.

Rh/K for WAA and SS patients, plus neg antigens for any antibodies made. There are several papers (based on SS populations) that show matching Rh and K will effectively prevents the patient developing antibodies (with exceptions). I can not remember the papers though.

I do not know as we always phenotype using tube. You may however have issues as the IgG DAT will be more sensitive in Gel, and the MTS diluent 2 may affect the fragility of the cells (or not).

I seem to remember that the concentration of platelets in plasma is an important part of QC for the 5 day expiration, something about pH changes over time I think, which may be why platelets come as singles, doubles and triples? I would check/clarify with your blood bank/supplier. As applejw said; you are changing the environment, which may impact the functional survival of the stored platelets.

EDTA Gyycine-Acid kit. Often used in the USA instead of Gamma-Quin to dissociate IgG from red cells. It has the advantage that it is faster than Gamma-Quin but the disadvantage that it inactivates the antigens from the Kell system. DCeDCe: my advise is to follow the insert very closely i.e. to the second. If the DAT is strong you may need to do the process twice (max). Once treated the cells are often fragile and so test with little delay. If the complement DAT is also positive a higher degree of hemolysis and cell fragility occurs and so reducing the incubation time is often needed. I suggest beginning by EGA treating out of date screening cells that are K pos and k pos then test with anti-K and anti-k to see if the antigens have dissociated. Then move on to DAT positive cells with IgG only. Hope this helps.

My apologies you are correct, monoclonal reagents rule out polyagglutination in the DAT (Isset, Harmening and Daniels) and I should have said: "Therefore if the patient's Poly or anti-IgG or anti-C3b,-C3d DAT is negative; false positive results are ruled out and the saline control is not needed."

Daily QC shows that the Poly, anti-IgG, anti-C3b,-C3d, CC and CCC reagents are working correctly and negative reactions at the AHG phase show the cell washer is removing free IgG/IgM. My understanding is that the DAT negative saline control is only required when the patient has a positive poly, IgG and compliment DAT. The DAT saline control, when negative, rules out pollyagglutination (either microbial or acquired). Therefore if the patient's Poly or anti-IgG or anti-C3b,-C3d DAT is negative; pollyagglutination is ruled out and the saline control is not needed.

Agree with AMcord; we also learnt to check how and where the temperature was taken, i.e. ensure the same method and location was used before and during transfusion. We would sometimes see first temp under the armpit, second oral and so on. Catch this early and several febrile reaction workups were avoided, often enough to be worth the effort of checking the method.

Thank you

Malcom, you replied to Liz’s question that the chance of the patient developing anti-A1 was almost zero due to immunosuppression followed by accommodation. Am I correct in assuming the immunosuppression is due to the drugs transplant patients take? I had never heard of "accommodation" and my quick google search suggests that accommodation occurs when a transplanted organ has normal function despite the presence of alloantibodies. These antibodies are capable of binding to the antigen and activating compliment, but for some reason they don't. My search went on to state that accommodation is more likely if the antibodies are removed (temporarily) by plasma exchange just prior to transplant, which has resulted in several successful ABO-incompatible transplants!!!! It seems reasonable that variability in an individual’s accommodation potential exists. Is it a stretch to link accommodation to the variability in individuals forming (or not forming) antibodies. Are the ramifications known? For example if an individual has a high degree of accommodation, i.e. good for transplants and transfusion; does it mean having an immune system that may not be as effective at identifying and killing pathogens? Understanding accommodation seems useful for the immunohematology field as well as organ transplant, yet this is the first I have heard of it. If you could please provide further explanation or references I (and I would guess others) would appreciate it.

I am confused because if/when a unit of blood goes to the nursery: how does blood get into the set? How does a presumably disposable uncalibrated infusion set calculate the amount of blood to be transfused? How is the change in product code and expiry date modified and documented or is the remaining blood just wasted? How and who determines that the correct amount of blood was given? Why would these, I assume, blood specific infusion sets be in the nursery? Am I missing something?

4 hours from issue in BB LISS. As the BB generally assumes audit responsibility it removes ambiguity.

Minimum requirement is to present the patients name and MR# in writing. This ensures there is no confusion as to who the blood is for as there could be other emergent situations occurring. In this type of situation written can be on the RN's hand, glove, post-it note etc. If patients name and MR# not brought with them in a written form they call for the info, write it down and present to tech.