exlimey

You did indeed read my mind. O cells (panels) nonreactive, A cells (XMs) reactive = A2 with anti-A1.

What is the ABO group of the patient and of the crossmatched units ?

He passed peacefully in his home near Wilmington, NC.

I'm in line with the above answers. A current diagnosis would be useful, especially to give us an idea if the aforementioned blood products (platelets, plasma) may be in play. There has to be some kind of more recent stimulus.

Thanks, Sandra. As I'm sure you knew, I am aware of the answer - no way, no how are blood suppliers going to "discard" ~10% of their product. But I think it's important to consider the consequences of some of the now routine testing algorithms. No testing mean results are unknown, but once one has information, one may be required to take action. Many transfusion protocols for chronic users involve Rh (C/E) and K matching - there's another batch of donors whose (partial) phenotype is known and considered to be quite immunogenic. It goes on. I do find it interesting that your system "hides" the K+ status, but openly prints the K- attribute on the label. Another thought: If the K type of all of the patients were known, they could get the K+ units. The antigen frequencies should match up.

At that point, you could probably test the Last Wash for specificity !! You'd probably get the results you need.

I have always run the eluate and last wash in parallel, but the question did make me think. I appreciate the attempt to reduce (potentially unnecessary) work, but don't like the idea of doing two-stage testing (eluate first and then Last Wash, or the other way around). If this happens, you've lost any efficiency (and time) you believed you gained by not testing the eluate and Last Wash in parallel. However, the cautious approach to a low volume (rare) specimen may have some merit - checking the Last Wash first adds confidence that any eluate prepared from the washed cells will be more likely to be valid. The two-stage testing concept has crept into the laboratory over the last couple of decades and is completely valid for follow-up or reflex testing. But.....one of my peeves: Reagents that suggest "Immediate spin, incubate negatives". If you're running a negative control anyway and/or most of your tests will be negative (DATs with anti-Complement reagents), you'll almost always be incubating, so why bother with the Immediate Spin ? Bottom line: Do what the eluate kit manufacturer says (unless you've validated otherwise).

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 terms of controlled or organized studies regarding other specificities. There are a fair number of one-of-a-kind case studies, but most of the stuff is retrospective analysis of data. Basically, other than anti-D, nobody really knows what an antibody titer means, but as Ensis01 suggests, detecting a change in titer (increase) may be more important. In an era when basic tube shaking is going away, it only makes sense (we have no other option) to convert to the new techniques and equipment, but I suspect that it has the potential to further confuse an issue which already has enough confusion to (dis)satisfy everyone. I don't envy anyone handling this hairball. As a last thought...the high-powered potentiators (and techniques) used today don't reflect what's going on in vivo. Arguably, if one ignored the 22% BSA diluent, the saline-IAT is a better mimic of the in vivo scenario.

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 should only be employed by those who understand the limitations and consequences.

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 treat them as D-" philosophy. Today's reagents are typically qualified/licensed for patients and donors, i.e., they are formulated with the same performance characteristics. Even so, all are a blend of monoclonals (IgM/IgG) since not one single clone can detect all of the "normal variants" (a great oxymoron). Apologies for some of the antiquated terminology.

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

Good point, but we're very unlikely to make the antibody.

Sorry, John. You'll have to start your own club. Perhaps "f-negatives Rule", or something like that.

An interesting idea, but I'm not sure I want my psychological dirty laundry hung out for the world to see.