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For those of who works in transfusion service laboratory and would like to learn more reference cases, I can post some mock-up cases here. If you would like me to do it, please hit the "heart" button on this post. If enough folks want to practice case studies on reference lab cases, I can post mock-up cases here weekly or so..

I know this post is like 3 years old, but just wanted to say it would be nice to see some practice case studies in transfusion medicine. Thank you.

I have experience with Grifols analyzers but am currently with Ortho. With the multitude of supply issues and delayed shippings I'm trying to see if Grifols is feasible, especially in my area. I don't know of anyone in the West-Midwest using them. Everyone I know on Grifols is east coast or west coast. Curious to know if you've experienced any supply delays, back orders, etc. The core lab is shopping for alternatives to Ortho, so I may as well too. Any feedback appreciated!

As most of you know, there is a severe blood shortage nationwide(USA). Please donate it you can. Thank you, you are heroes!

We are currently bringing in 3 techs with H1B visa sponsorship. We've had one or two at a time a few times in the past with a generally good experience. We've been so short for so long that this was a necessity.

Sadly, we did not.

It is all over the place, to be honest. It is Caucasian, rather than caucasian, It is group O, D Positive, and group A, D Positive, rather than either group O Positive or group A Positive (see the early editions of Peter Issitt's book). It is Oh (with a subscript "h"), and not "Bombay". The FUT1 gene, or, rather, the lack of a functional gene through various different genetic mutations, leads to the "Oh" phenotype, but this should NOT be called the "Bombay phenotype". Although this phenotype was first described by Bhende YM, Deshpande CK, Bhatia HM, Sanger R, Race RR, Morgan WTJ, Watkins WM. A “new” blood-group character related to the ABO system. Lancet 1952; i: 903-904. DOI: 10.1016/S0140-6736(52)92356-8, Another example of the Oh phenotype can be seen in the rare recessive condition, Leukocyte Adhesion Deficiency Type II where, to all intents and purposes, the patient will have a normal H gene, and yet the red cells are of the Oh phenotype, and anti-H can be found in the plasma. the phenotype has been identified in many different parts of the world (and is not just confined to mutations in India or even Asia (Hidalgo A, Ma S, Peired AJ, Weiss LA, Cunningham-Rundles C, Frenette PS. Insights into leukocyte adhesion deficiency type 2 from a novel mutation in the GDP-fucose transporter gene. Blood 2003; 101: 1705-1712. DOI: 10.1182/blood-2002-09-2840). The other thing is, of course, that "Bombay" no longer exists - it is now Mumbai! I APOLOGISE FOR BEING A COMPLETE PEDANT!

I'd get a few of the blood bank vending machines. One for the OR and one for the ED.

I actually pulled the package insert for our panoscreen cells from Immucor, and on page 2 the insert actually says add plasma, then cells and mix. The the next line says add potentiator, the step to do the immediate spin is no longer present. I would never have noticed this if not for this blog. There is a note that if desired the immediate spin can be performed. I do believe that I will be having a discussion with my Director and Medical Director so that I can change the procedure because if it is not needed (which in my humble opinion it is not necessary) then we need to get rid of the steps. scott

Thanks Malcolm! I looked closely at my screening cell package insert and was surprised that it no longer says to perform immediate spin. It says to perform a spin at 37C but if potentiators are used to follow their instructions. We actually use PEG instead of LISS and PEG is not supposed to be spun after incubation. I have looked at those inserts for years and never REALLY saw this wording and have no idea when these instructions changed. I knew we didn't really care about RT antibodies anymore but I thought the immediate spin was required. We have so many rules in BB and we just follow them without question. I feel like I am in an alternate universe right now.

I can only go by what I was taught. The room temperature immediate spin told us nothing, apart from the fact that there may have been a "cold reacting" antibody present, which we didn't care about and didn't want to detect, because, if it did not react at 37oC, it wouldn't be clinically significant anyway. We also performed tube testing at 37oC, using albumin as an enhancing agent, but never once did we ever detect an antibody by this method that we did not also detect by IAT, and usually, we detected it far easier by IAT, so we stopped performing that method. As far as I know, and we kept a weather eye opened just in case, this never caused even a mild transfusion reaction. In answer to Ensis01, I believe what was being detected with Kidd antibodies in those days was not so much the presence of weak agglutination, but the presence of haemolysis, as serum still had complement present that could be activated, but, with the use of EDTA anticoagulated plasma, this was no longer so, as the EDTA chelated Ca++, Mg++ and Mn++, all of which are required as cofactors at the C1qrs stage of the system. There was no reason why this haemolysis should NOT have been seen in the tube IAT when serum was used, but very few people actually looked before the addition of the saline for washing the tests before the addition of the AHG, and then, of course, no agglutination may have been seen at the end of the test, unless the AHG used was broad spectrum, including an anti-C3d.