exlimey

Is this approach applied to rare units ? For example, a donor who is Kp(b-), with anti-Kpb in their circulation. Granted, such a unit would probably only go to someone who already had anti-Kpb, so technically there would be no impact (analogous to Mabel's anti-D scenario). Just curious.

It's remotely possible that Ortho use different diluents for different cells. I remember a rumor that "fresh" cells are suspended in one kind of diluent, but frozen-thawed cells are in a similar diluent with a couple of extra chemicals to compensate for the freeze-thaw process. I think that frozen-thawed (deglycerolized) cells are sometimes used in emergencies when the scheduled donor(s) don't appear.

I agree with all the previous comments. You cannot manage a transfusion reaction in a patient who has died from lack of blood. One thing to add: In the time before time......emergency release units were always O negs. However, today's practice has evolved in a risk-based manner and it is now accepted that O pos units can fulfil this function. Perhaps ironically, if the old practice had been employed in this case (use O negs), it would have been very unlikely that this patient would get a E+ unit.

Any of the major laboratory suppliers can help with lab design and furniture, for a price, of course. VWR (Avantor) and Thermo-Fisher are probably top of the list. I think that Mabel is referring to "Herman Miller" - a longtime standard for labs and offices. I think they may sell direct or through the distributors. Good luck. Designing a new space can be both fun and frustrating. Nothing can ever be perfect, compromises always have to be made.

I think you can just use basic 40% glycerol (in water). Glycerol is available from many sources. Use an equal volume of 40% glycerol to washed, packed red cells. Freeze @ -80 C is small aliquots. I don't remember the details of recovery, but it involves washing with a couple of different Saline concentrations, akin to deglycerolizing red cells for transfusion. The "Valeri Method" - see the article below. Vox Sang 2000;79(3):168-74. An experiment with glycerol-frozen red blood cells stored at -80 degrees C for up to 37 years. C R Valeri 1, G Ragno, L E Pivacek, G P Cassidy, R Srey, M Hansson-Wicher, M E Leavy

What type of freezer are you planning to use ?

Moving seems to be very common after retirement, but It would be tough to leave Bend. Beautiful city and environs. I suggest fly fishing, but I'm biased. Lots of opportunities where you live, some of the more famous waters. Lots of mental stimulation, too (although not medical), with a heavy dose of Zen.

Wow. That's bizarre. The routine retest of incoming materials detected the "transplanted" segments, only because of an Rh difference. If the transplants just happened to be the same ABO/Rh as the host - fairly good odds for an O+ to another O+, for example, it would be undetectable. I wonder how many times that's happened ? No way to know, I suppose.

This is fascinating stuff. A lot of science, learned the very hard way, with a heavy dose of art. I don't envy those having to make these calls.

Thanks. Probably an unanswerable question: How low a titer is "low enough" ? A follow-up.....can one transplant an A1 kidney into an A2 patient with anti-A1 ?

Apologies in advance for my ignorance on these matters. Are the units/products in the remote storage locations assigned to specific patients, or are they available to random patients ? If the former is true, arguably they've already been issued.

Agreed. No criticism was intended, I was just surprised at that approach. So by reading between the lines, the logic is that by transplanting a kidney from a donor with a weaker expression of A antigen (A2), the group B recipient/host is less likely to detect/reject it ? Did I get that correct ? Just curious, can one give a group A1 kidney to a group B patient who has a very low isoagglutinin titer ?

Wow. That eliminates ~80% of group A potential donors.

I agree with Malcom - not much value, if any. I, too, have done many such noninformative adsorptions. In a recently-transfused patient, there is perhaps a very remote chance that (allo)adsorptions on an eluate would reveal a "only on the cells, not in the serum yet" newly formed antibody. This might be important if the clinicians suspect faster-than-normal red cell loss, but it would be very difficult to differentiate from the typical increased red cell demise seen in patients with warm autoantibodies.

WOW ! Just, wow. I really wasn't expecting to hear this. I can't imagine the multitude of failures involved in such an event. Of course.....if one was mislabeled (or mistyped), there's probably an equally badly mislabeled partner out there somewhere.

Apologies in advance to the above for using their comments as examples. Just to stir-up a little controversy.......if we trust our Government-regulated/approved blood suppliers to have quality systems, get the correct answer and label accurately, why are in-coming Red Cell Units re-typed for ABO/Rh ? And....go......

I believe the primary action of CDP is as a mild acid, thereby eluting bound IgG (reducing DAT) and denaturation of HLA/Bg antigens (removal of "unexpected reactivity"). Perhaps the prolonged treatment time removed some of the sialic acid on the red cells and has inadvertently created cells that are easier to agglutinate, i.e., the equivalent of enzyme-treatment ?

Lots of users on this Forum are in the same place and I'm sure they have some good advice on how to approach this issue. However, I would be cautious of implementing an optional process that potentially calls into question the quality of previous work.

"Pettifogging".....an 'olde worde" that is so relevant today. Thank you for reminding me. I shall try to work it into as many conversations as possible.

Agreed....history is always a wildcard. I had a case once where there a teenaged male individual had antibodies to red cells (I can't remember the specificity) with no apparent transfusion history. Later questioning revealed that the person was part of a "Blood Brothers" group who routinely and ritually exchanged blood through self-inflicted cuts. Each to their own.

I was also thinking of a prior sensitization. A weird, barely detectable D+ phenotype may not generate a new immune response, but may be enough to reactivate the primed lymphocytes in an individual who's anti-D has faded into non-detectability. Tiny re-exposure and wham ! Nice, strong, clear-cut anti-D, apparently out of nowhere.

Reading between the lines, I believe you're saying that C+D- (r'r) panel cells are nonreactive, thereby excluding the presence of anti-C, If that's the case, and since said cells should carry the G antigen, it is very unlikely you're dealing with anti-G. Anti-LW may mimic an anti-D pattern by demonstrating reactivity only with D+ cells. It's also very remotely possible that one of the donors carries a rare form of D-antigen that is not readily detected by typical commercial reagents. However, those are very rare and their ability to stimulate an immune response is not well understood.

In this case, the Safety goons may be your very best friends. If the space you describe is really that bad, you could use the safety angle as leverage. Alternatively, modern instrumentation (including the Ortho Vision) often has very specific installation requirements (space/clearance/ventilation, etc)....that may ammunition, too.

Careful, now. You're bordering on "spatial discrimination".

How about a "Del" ? Fits the description perfectly. One the other hand, "twice in the last few days" is worrying. While not impossible, it's highly unlikely that a facility would encounter more than one of these anomalies (zebras) in such a short period. I assume Malcolm's question regarding the Last Wash is an allusion to some laboratory artifact - bad technique, bad reagents, etc.