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I would say no as not sendng a high risk form doesn't affect the potency, safety or purity of the product. One could say not having the doctor sign the form affects the safety because perhaps they won't watch the transfusion more closely than usual but should the transfusion still be monitored ? Anyway you could always submit a deviation just to cover the BB behind, if it isn't reportable the FDA will let you know. This I know as I have filed reports that were questionable to file or not to file and received notification that it wasn't . But the non-conformance (not following the SOP) should be reported in whatever way the lab reports their errors internally.

We use PeG as our routine backup for solid phase testing. However, there is a place for LISS in our tool kit. If we have an antibody consistent with a warm auto and the patient has never been transfused, we use LISS to decrease sensitivity to get under the warm auto. If the LISS screen is negative and AHG crossmatch is compatible, we transfuse those units. We also see panreactivity in some OB and Onc patients both with solid phase and PeG. We run a solid phase panel - if panreactive, we switch to LISS following the same process we use for the warm auto.

Malcolm Needs - Thanks so much for the quick response. There's no ethnicity on the patient yet but I doubt she is Japanese by her last names (very Hispanic). We are not planning on antigen typing the red cells for M at this point since it only showed up at immediate spin. We didn't do the workup on the mom so although the other BB said they ruled M out we don't know for sure if they use the 3/3 homozygous rule that we use. You are definitely correct about the M still possibly being IgG, I do realize, thanks for correcting me. It's been a very weird year, since last July when we had our first true anti-U, then an huge increase in the number of extremely strong WAA, an anti-hrB at Christmas, and now this newborn. I hope this doesn't become standard for us but with our Hematology/Oncology clinic growing each year and all the solid organ and HPC transplants I'm sure we're only touching the surface. I miss the days when a children's hospital blood bank worried more about making smaller aliquots than dealing with rare antibodies.

Two things. Firstly, although the anti-M may be "naturally occurring", it need not necessarily be IgM. Many examples of anti-M, reacting in the cold and RT are, in fact, agglutinating IgG (a bit like ABO IgG antibodies and anti-P in the DL Test). In addition, maternal IgG antibodies are actively transported across the placenta and, as a result, the baby ends up with a higher concentration of some IgG specificities in their circulation than is in the mother at birth. As the anti-M in the baby's circulation is so weak (showing dosage), it could be that it is of maternal origin, but that it is so weak now in the mother that it is undetectable in her plasma using normal serological techniques. Secondly, some precocious babies are (rarely) known to produce their own IgM antibodies at birth (this can be proved by the babies producing an ABO antibody that cannot have come from the mother - say a group O baby with anti-B in the plasma, from a group B mother, or by looking at the Gm and/or Km types of the immunoglobulins - see, for example, Toivanen P, Hirvonen T. Iso- and heteroagglutinins in human fetal and neonatal sera. Scand J Haemat. 1969; 6: 42-48), so it could be the baby's own antibody, despite what I said above! Lastly, and this came to me as I was typing (hence a third point), is the mother of the baby of Japanese origin? The only reason I ask is that, if she is, be a bit careful, as anti-M of low titre has been known to cause a sort of delayed HDFN in this ethnicity (see Yasuda H, Ohto H, Nollet KE, Kawabata K, Saito S, Yagi Y, Neggishi Y, Ishida A. Hemolytic disease of the fetus and newborn with late-onset anemia due to anti-M: a case report and review of the Japanese literature. Transfusion Medicine Reviews 2014; 28: 1-6. doi: 10.1016/j.tmrv.2013.10.002). Incidentally, although I have seen anti-A or anti-B in a newborn's plasma, I have never seen an anti-M.

I would pull the unit from inventory and contact the supplier. They should have the resources to investigate the problem with the donor.

As a neophyte blood banker we read everything under the scope (early 70s - it was SOP). Then took a job and worked w a very experienced blood banker (she was on a first name basis w Laurie Marsh, the Moulds' , and more of the NY blood ctr crew). I'd ask her to look at weak agglutination (probably your kissing cells) - her response was if I wanted to call it positive - go ahead. she wouldn't. Weaned myself off the scope after that. I think all new BBers go thru that. I also liked exlimey's statement about "playing" with different types of enhancements. I still do. For me, that's the interesting stuff in BB. Like those DAT cards I rec'd. Wish I could get them in the USA.