Joanne P. Scannell

There are quite a few (too many to mention here).
Can I cite for you, NHSBT Guidelines in your search engine, followed by looking for SPN214/3 (SPN stands for specification) and up will pop a document entitled "The Clinical Significance of Blood Group Alloantibodies and the Supply of Blood for Transfusion., written by my very good friend Nicole Thornton, Head of Red Cell Reference at the International Blood Group Reference Laboratory in Filton (Bristol) in the UK.
If I tell you that the document is 22 pages long, you may understand my first sentence!

Without some sort of 'vending machine' device to control and document the in/out/in/out/transfused to whom information, just leaving O Neg RBCs in a refrigerator somewhere for nursing to take/return at will is not a good idea.  I'm not even sure if regulatory agencies will support that.
Not only that, giving O Neg to 'everyone' is not good management of resources.  We (and most hospitals in our area at) restrict the use of O Neg to Females <50yrs old.  (And even that is coming up for debate in some arenas.)
There are 'vending machines' out there that will interface with some Blood Bank Software.  Maybe someone who is using such a machine can comment on that.

I can't refresh your memory, but I do know of a case of anti-Vel in the UK that caused a fatal transfusion reaction.  The DAT was positive by anti-complement only, and the anti-Vel itself could only be detected in a clotted sample, not in an EDTA sample.

'Liquid Plasma' is never frozen so there's no need to thaw it therefore the outdate is not changed.
'Thawed Plasma' is the 5 Day product which results from Thawing Frozen Plasma (in all it's various forms, FFP, FP24, etc.).
Note: When Frozen Plasma is thawed, it is assigned a 24hr outdate.  You can extend that outdate to 5 Days IF you label it 'Thawed Plasma'.
e.g. Frozen FFP is thawed to Fresh Frozen Plasma (24h outdate).  You can leave it that way or change it to 'Thawed Plasma' (no FFP designation) and assign a 5 Day outdate to it.  Most hospitals, if they go that route, just label it 'Thawed Plasma' with a 5 Day outdate immediately after it's thawed.  (One Step vs Two Steps)
Note:  I'm using USA FDA rules, I don't know what they do in other countries.

As you see from the posts here, there are various opinions of what to do. 
Correct =The regulatory agencies do state to run some sort of controls, etc. 
You are in charge, therefore you do what you believe is best within the guidelines when there are gray areas like this.  If you believe you should change the protocol to 'QC for the Antigen', then do that.
Validation?  You have criteria, I'm sure, for the cells passing inspection for use.  I venture to say that most hospitals don't keep reagent RBCs more than a month or two past their outdate.  It would be interesting to hear about that.  If you are running QC for the tested antigen 'Day of Use', that's your validation that the cell is still working for your purpose.  (I maintain that 'validation' is needed for situations where QC is not going to be run, e.g. You validate the time a box will hold a temperature so you don't have to take the temperature every time.)
We do validate that a new panel is ok by running QC Antisera with them when they arrive.  I've had inspectors tell me I must do this and I've had inspectors tell me to stop.  Hmmm … I do what I am comfortable with, i.e. err on the side of caution.
We don't use outdated panels … too many issues. 

Certainly the blood supplied by the NHSBT that what is on the label on the outside is GUARANTEED to be what is actually in the bag, and so no retyping is required.  I THINK the same applies in Scotland, Wales and Northern Ireland, although am happy to be corrected.
As all such "kills" would be reported to our regulatory authorities, and published in the annual Serious Hazards of Transfusion (SHOT) Report, I can say for certain that no "kills" have been reported for many, many years!

Our IRL suggests we use LISS for crossmatching when we have a WAA.  Most everything else we do is in gel because we don't get enough sample being a children's hospital.  Also we do LISS antibody screens when we're dealing with an anti-M since kids get a lot of cold M antibodies.  This way we can tell if it goes all the way through AHG and requires M neg products or if not then just LISS crossmatched red cells.  When I changed to the N-HANCE it was the same time I changed our red cells for antibody screens so that made my validation simpler.  We now do method to method correlation between gel and LISS but only at a qualitative level for obvious reasons although when we did our validation we matched within 1+ an all our testing.    

When I first joined the wonderful world of blood transfusion, with particular reference to blood group serology, at the International Blood Group Reference Laboratory, when it was in London, my mentors were Dr Carolyn Giles and Joyce Poole.  In those days, yes, we did use microscopes (albeit with very little magnification) and, given that we were using human-derived antisera, and the fact that I was anxious not to miss anything, I often got Joyce to check my sightings down the microscope.  These were invariably "kissing cells", as you suggest, and Joyce christened them "Malcolm weaks", a term which, I understand, is still used in the Red Cell Reference Department, when there is actually no agglutination present at all!
By the time I retired, I NEVER used a microscope for red cell reactions (of course, for Kleihauers and the like), but not for agglutination, unless I was training someone, and showed them the typical "mixed-field" agglutination seen with anti-Sda (I hate not being able to use subscript and superscript on herre any more) and Lutheran antibodies.

I don't believe that an optical aid necessarily refers to a microscope. In my pre-retirement years we used the agglutination viewer when an optical aid was required. Example: https://www.fishersci.com/shop/products/fisherbrand-tube-agglutination-viewer-5-watt-bulb-w-magnifying-mirror/22363560

Good point ... but most MDs give the RhIg when Weak/Partial D is reported because they don't understand the situation even if we try to explain it to them.

I am a worker from/in the UK, but if TRM.40780 says, "Maternal RhIG candidacy assessment must include the identification of weak-D phenotype newborns", that is exactly what it means.  It doesn't say "should" instead of "must", and it doesn't say, "until you give up because you are bored, because you have never found one"!
Yes, such types are rare, but they do happen, and they can cause the mother to produce an anti-D (of sorts).  These antibodies are not usually particularly clinically significant in terms of further pregnancies - but the word "usually" is the important one in that sentence.
The only thing I would say is, WHEN you do detect a newborn who tests as weak-D positive, don't forget to test the mother too; she may also express the same weak-D type (but, depending upon your laboratory's policy, may not have been tested as expressing this type during the pregnancy), and, if she does, she doesn't need the anti-D immunoglobulin (which, remember, is a human-derived blood product, which may contain a novel blood-borne virus type about which we know nothing - YET).

The answer is a bit more complicated.  If there is no target for %S, there is no need to test for hemoglobin S in donor blood.  In other words, if the transfusion is purely for anemia, not treatment of acute chest syndrome or prevention of stroke, there is usually no target %S being used by the treating physician.  The reason for testing for S in the donor is not the risk to the patient, but because transfusing S containing blood can confuse the calculation of % S overall. It's probably unnecessary because the %S contribution of a single unit of S heterozygous red cells in an exchange transfusion or red cell apheresis is very small.  S hemoglobin in a red cell that is from a heterozygous donor does not contribute to sickling complications.  This is well known because individuals who are heterozygous for S do not have complications of sickle cell disease.  Thus while it is traditional to test for hemoglobin S in donor blood for sickle cell recipients, this is probably unnecessary unless the treating physician is trying to achieve a specific %S, as in stroke prevention.

We, too, encounter Anti-M often using Gel.  Apparently, Gel is just acidic enough to enhance this pest.  
Because the enhancement is more about pH than temperature, whenever we suspect Anti-M, we revert to other methods to help determine it's 'etiology'.  Prewarming Gel does not change the pH issue so we don't do that. We can't trust that negative results in prewarmed Gel are truly due to a cold Anti-M or that the positive results aren't due solely to the acidity.  (Besides, if testing is done using a Blood Analyzer (e.g. Vision, Eflexis), the cards are pre-warmed anyway.)
So, we test the plasma using Prewarmed Tube Testing (e.g. PEG which has similar sensitivity for most antibodies sans the low pH).  If positive with that, it's a Warm Anti-M. 
We also test at Room Temperature using Pooled Screening Cells.  If positive, then it's a cold Anti-M. 
If negative with both Prewarmed Tube and RT Pooled O Cells, it's 'Anti-M (Detected using Gel Only)' ... just due to the pH drop, no clinical significance. 
Likewise, positive with both, it's an Anti-M with a broad thermal amplitude.
Do what you like with the results.
PS.  Testing positive with Anti-M reagent does not mean the patient can't make Anti-M (Patient may be Mg Pos).  Someone please correct/confirm that or am I working on old reagent data?  (Like we don't see Anti-T or Aquired-B anymore because the reagents are 'purer'.)

We, too, encounter Anti-M often using Gel.  Apparently, Gel is just acidic enough to enhance this pest.  
Because the enhancement is more about pH than temperature, whenever we suspect Anti-M, we revert to other methods to help determine it's 'etiology'.  Prewarming Gel does not change the pH issue so we don't do that. We can't trust that negative results in prewarmed Gel are truly due to a cold Anti-M or that the positive results aren't due solely to the acidity.  (Besides, if testing is done using a Blood Analyzer (e.g. Vision, Eflexis), the cards are pre-warmed anyway.)
So, we test the plasma using Prewarmed Tube Testing (e.g. PEG which has similar sensitivity for most antibodies sans the low pH).  If positive with that, it's a Warm Anti-M. 
We also test at Room Temperature using Pooled Screening Cells.  If positive, then it's a cold Anti-M. 
If negative with both Prewarmed Tube and RT Pooled O Cells, it's 'Anti-M (Detected using Gel Only)' ... just due to the pH drop, no clinical significance. 
Likewise, positive with both, it's an Anti-M with a broad thermal amplitude.
Do what you like with the results.
PS.  Testing positive with Anti-M reagent does not mean the patient can't make Anti-M (Patient may be Mg Pos).  Someone please correct/confirm that or am I working on old reagent data?  (Like we don't see Anti-T or Aquired-B anymore because the reagents are 'purer'.)

Ok, I'll ask the other question that needs to be asked:  Are you SURE that the cells put into the vial for Unit #1 are from Unit#1? 
Serologically, those discrepant results don't make sense (which is why you are inquiring) so I'm looking at the mechanical issues.  Is it possible that during the heat of the moment (STAT, Uncrossmatched), the tech who retrieved the segments from the 2 units actually pulled both segments from Unit #2?  When the crossmatches were repeated manually, was a new segment taken from the unit and that's why you saw the expected incompatibility?

Ok, I'll ask the other question that needs to be asked:  Are you SURE that the cells put into the vial for Unit #1 are from Unit#1? 
Serologically, those discrepant results don't make sense (which is why you are inquiring) so I'm looking at the mechanical issues.  Is it possible that during the heat of the moment (STAT, Uncrossmatched), the tech who retrieved the segments from the 2 units actually pulled both segments from Unit #2?  When the crossmatches were repeated manually, was a new segment taken from the unit and that's why you saw the expected incompatibility?

Ok, I'll ask the other question that needs to be asked:  Are you SURE that the cells put into the vial for Unit #1 are from Unit#1? 
Serologically, those discrepant results don't make sense (which is why you are inquiring) so I'm looking at the mechanical issues.  Is it possible that during the heat of the moment (STAT, Uncrossmatched), the tech who retrieved the segments from the 2 units actually pulled both segments from Unit #2?  When the crossmatches were repeated manually, was a new segment taken from the unit and that's why you saw the expected incompatibility?

Yes, I got one of those emails 'from you' and almost answered it until I saw the grammar and thought, 'No, he wouldn't write that badly!'.  So, I decided to check with you in here to see if you did send it.  Guess you didn't!
Hoping you are well!  I haven't done much in here because it's been ridiculously busy!  And we are 'this far' away from being able to order/transfuse COVID Convalescent Plasma.  A new product ... lots of fun.

If you know this patient is A Pos and you know the discrepant backtype is due to a cold agglutinin, why are you trying to re-establish what you already know?

If you know this patient is A Pos and you know the discrepant backtype is due to a cold agglutinin, why are you trying to re-establish what you already know?

I would agree with everything you say Sandra, except that I would say any Lutheran antibody (and anti-AnWj come to that) tends to give a "stringy" mixed-field type of agglutination; not just anti-Lub.

Has the presence of anti-Sda and anti-Lub been ruled out? Both have been reported to show mixed field reactivity and both can be reactive at room temperature. Microscopic exam of reactivity in any phase would help rule out anti-Sda, and since your said it did not look like rouleaux, can it be assumed that it also did not look like an anti-Sda? That leaves possible anti-Lub.  The RBCs could be cleared of IgG and typed or an Lu(b-) RBC could be tested with serum and eluate. And, this could be an autoantibody...And then going back to a sample to blood bank for broken wrist, perhaps more going on diagnostically here, What was admission Hgb? Transfusion history is important for auto vs allo specificity. With the eluate stronger than the serum and with mf in DAT, should be concerned about possible transfused cells and this being an alloantibody.

We issue Group A Plasma (or whatever is shortest outdate as long as it is not Group O)  until we have a BB Specimen and the ABO/Rh is verified.  Then we switch to ABO compatible/specific.
The expiration date of the specimen does not apply to non RBC containing blood products, so as long as the patient is wearing the corresponding BB Band, we will issue Plasma, Platelets and/or Cryo.
I agree, the non-ABO match allogenic stem cell transplant recipients are a challenge, but as someone pointed out in an earlier post, these patients become obvious and we can deal with their 'new' blood type 'in the moment' according to our current protocol.

We purchased bins from VWR International.  They are manufactured by AKRO MILS if you want to check their website: https://akro-mils.com/
They are inexpensive and come in various colors: Red, Blue, Clear, White and many sizes.
We got Item# 75854-808 ... a case of 12 clear, 4" tall x 11.625" deep x 6.625" wide.  6 fill one of our drawers (3 in front, 3 behind them) very nicely.  If you message me, I'll tell you the price (very reasonable).
They sell dividers for them, too ... again, in the same colors.
We also use them for our reagents.
We stole the idea from Chemistry, by the way, so I can't take all the credit for this idea.

1.  We will perform an elution with a positive DAT within 3 months of a transfusion, BUT, will also perform elutions on other cases (even if the DAT is negative) if the clinical symptoms give us reasons to suspect that an elution may be of help.  Nothing in the world of blood transfusion is pure black or white.
2.  Normally, we use the acid elution technique, but will, occasionally use the Lui technique.
3.  Usually, but not exclusively, gel IAT.
4.  Full panel, as a minimum, but may include A1 and/or B cells, and others as required partner's red cells in the case of a suspected case of HDFN due to an antibody directed against a low prevalence antigen).
5.  I can't think of any - YET!!!!!!!!!!!!!!!!