exlimey

Hah ! Excellent point, David. I wonder how much emphasis should be put on those "microscopic" reactions, especially when the endpoint a titration is most often defined as the "last MACROscopic (or 1+) reaction"? How do the Powers-That-Be justify that little nugget ? Can you imagine resulting-out a "change in titer" based on a microscopic reaction ? Talk about piling-on to the already acknowledged confusion level.

An excellent discussion point. I think many others have similar questions and concerns. The have been several other threads on this forum with similar subject matter. As an Old Fart, I feel obliged to spout some (un-referenced) history. Most of the original work on clinical significance of antibodies in pregnancies was done in the absence of potentiators and definitely before the use of (semi)automated test systems. I think it was a "saline-IAT" using 22% albumin (BSA) as a diluent. Most of those antibodies were anti-D, for obvious reasons. There's not much out there in the literature in

Just curious.....what does the system do with those potentially immunogenic K+ units (donors) ?

I am not aware of any LICENSED anti-Cob available in the USA. The American Red Cross system uses an unlicensed version for most of its Cob phenotyping requests. I believe Cob can be determined by the HEA BeadChip process (molecular typing). If you have a patient that needs Co(b-) red cells, I think those are your two options: PHENOtyping with an unlicensed reagent or units predicted to be Co(b-) by GENOtyping.

My personal favorite Ch/Rg confirmatory test: Strong reactions with C4d-coated cells. Old school, but really cool to see.

If indeed two samples are mandated by standards, AABB or otherwise (I'm not doubting your information, lalamb), it would seem that from some of the responses here, many labs are going to have to re-tool their processes, including building such practices into their computer systems.

Ahhh.....the unanswerable question. My personal favorite: Even if the first and second tubes were collected from different patients, there's still a good chance they'll still match ABO group (~40% group O, ~40% group A, etc.). If one were a gambler, those would be good odds. But, that being said, I still think two tubes are better than one.

Forgive my ignorance, but are the above stuck to the outside of the bag, and therefore measuring/indicating the surface temperature of the blood product ? The "storage vs transport" hairball will be debated well after we're all dust.

How do you suggest measuring the "core" temperature without compromising the bag ?

This is the best thread, EVER !!!! Keep it rolling, please.

I was originally trained using an "inverted microscope" - that was a thing of beauty. The light source was above, the relatively low-powered lens below. The cells stayed in the tube and the tube could be rotated to get movement and/or a suitable thickness of liquid in which to see the cells. It was great and very easy to use (even though it had a large footprint), but as others have commented, if one looked long enough, one could always find "friendly cells". I'm not a fan of microscopic reading and I dissuade others from doing it. As I've said in the past, high level tools and techniques

Apologies. I was discussing reagents used in tubes, not gel cards.

I disagree. It is in the FDA's manufacturing requirements that DVI be detected. Unfortunately, I couldn't find a suitable CFR quote, but several of the Directions for Use I looked at from different manufacturers indicate that they detect DVI. However, I agree that strategic differential use of reagents such as these on patients vs donors can certainly help the transfusionist and/or determine the necessity for Rh Immune globulin.

Anti-D reagents are specifically formulated to detect DVI - that is REQUIRED by the FDA in the USA. It was also true of the human sera-based reagents I manufactured in the UK during the 1980s. There was a period when anti-D reagents were approved for donors or patients. The reagents used for donors were required to detect DVI, arguably the "weakest" expression of the D antigen of the known D-variant and typically that meant an antiglobulin phase was required. Those reagents formulated for patients often were not designed to detect DVI (had no IAT) and subscribed to the "it's better to tre

See....you've already got the makings of a club. You can celebrate your CEce heterozygosity together.