GAFFER

I'm going to be blunt.  This is ridiculous!!  You have the potential of causing far more problems by removing the cubes from their protective container.  

Interesting discussion. Yes, cardboard can carry dirt and/or insects, but to imply that the presence of such on supplies like saline cubes creates a risk to patients and staff is an extreme stretch. We don't live in a  vacuum and most of us spend time outdoors with the dirt and bugs every day (potentially bringing them inside with us). A wipe with a damp paper towel should be sufficient to clean an obviously soiled outer container.
If you talk to the manufacturer of the saline, I'm sure they would argue that the outer box is not merely a convenient shipping container, but also an integral part of the product itself, designed to support the flexible primary container and get the best performance from the product. After all, they've designed in a nice little tear-out section that creates a perfect hole for the spigot/tap.

Well, unless they are K+k- and have made an anti-k!!!!!!!!!

It simply means that the P1 antigen is particularly strongly expressed on these red cell samples.  Therefore, if you come across a weak anti-P1, it may apparently react with these particular red cell samples, whilst apparently not with, for example, the third red cell sample shown in your antigram.  Although not identical to dosage, per se, it is fairly synonymous with dosage at a phenotypical level.
The strength of the expression of the P1 antigen is an inherited trait.

Still running, co-incidentally received a sample this morning here in RCI (Oh). Still log on to monitor for any new posts/offerings once a month (or so).

Still running, co-incidentally received a sample this morning here in RCI (Oh). Still log on to monitor for any new posts/offerings once a month (or so).

I agree with you that it does sound daft, but I am in the position to tell you why this is the recommendation, despite it apparently being contrary to BSH Guidelines, as I was still working when the decision was made (albeit, I don't agree with it!).
The huge majority of hospital blood transfusion laboratories now use column agglutination technology (CAT) as their "first line of attack", and many of them use the CAT that uses gel in the column, rather than glass beads.  This form of CAT is particularly adept at detecting anti-M in plasma by IAT, even though the anti-M may not actually be reacting at strictly 37oC.  There are several reasons as to why this is so, but a couple of them are that "cold" reacting IgM anti-M can sensitise red cells particularly quickly (in a matter of seconds at room temperature), but can take quite a time, even at 37oC, to dissociate back off.  This means that the anti-M is often still sensitising the red cells at the end of the incubation time and, of course, centrifugation is, in itself, a potentiator of agglutination.  In addition, the gel in the column is at a slightly low pH, and many examples of anti-M "like" a slightly acid environment to sensitise the M antigen.  This all means that this particular kind of CAT is very good at detecting anti-M, but making it appear to react at 37oC, when, actually, it doesn't.
This left the RCI Laboratories with a dilemma.  Cross-matching blood by tube at strictly 37oC takes a long time, and the RCI Laboratories are not, shall we say, over staffed!  This meant that RCI Laboratories were being stretched to breaking point by having to cross-match for samples containing anti-M, as so few hospital laboratories could now perform IAT by tube technique (particularly with the need to demonstrate competence in the technique being used).  The alternative was to test many more units for the M antigen, and to provide M Negative units to the hospitals, whether they use CAT of that type or not, so that they could perform their own cross-matching, and actually end up with compatible units.  In theory, this was great, but it left the RCI Laboratories with fewer phenotyped units with which to select for, say Fy(a-b+) for a patient with anti-Fya, as the M Negative units that were also Fya Negative had been sent out to cover a cross-match in a patient who had an anti-M, who didn't actually need M Negative blood.
Having said all of that (and I KNOW I said it at length), anti-M can, rarely, cause severe haemolytic disease of the foetus and new-born (particularly in people from the Far East, even when the anti-M does NOT react overtly at 37oC), and so I have a certain amount of sympathy with giving M Negative units, even in the situation in which you find yourself with your patient, as M Positive units, albeit found to be compatible by IAT, could well stimulate the anti-M to become stronger during the pregnancy, "turn it" to an IgG production and increase its (at present, non-existent) IAT titre.
I hope that helps and that you haven't fallen asleep reading it!!!!!!!!

Couldn't agree more, particularly, certainly in my own experience, many inspectors have a minimal amount of experience in the field (particularly Reference Laboratories), but feel they have to comment to justify their employment, even though they don't actually understand or know what they are talking about; not all, but far too many.

The site was giving @Malcolm Needs a spot of bother, so I have taken the liberty of uploading some spectacular images for him.

Congratulations! 

Unfortunately, NHSBT RCI reports now use "coded comments", rather than free text.  The "coded comments" are, almost universally, ungrammatical, reflect poor scientific (in particular, blood group) nomenclature, are frequently clinically inaccurate and are totally confusing, so I am not surprised you are not familiar with the term, because, in reality, it shouldn't exist, especially in a report from a Reference Laboratory.
The reason "canned comments" are used are two-fold.  Firstly, they can be put in quickly (striking one key can put in a complete sentence - although, as I said above, most of them are far from grammatically correct sentences - and, of course, hit the wrong key, and you have a comment that is even less relevant than hitting the correct key), so this is "LEAN".  Secondly, and much more insulting, is that one of the senior managers thinks that, if a CORRECT free text report is provided, the poor souls who work in a hospital laboratory will not be able to understand it.  How would you feel about that applejw?
Of course, in this case, there is probably an auto-antibody, directed against an antigen within the Rh Blood Group System, such as anti-Rh17 or anti-Rh18, that mimics more "common" Rh antibody specificities, such as anti-c and anti-E.  In this case, the antibody reacts with all antibody panel cells, but reacts more strongly with those cells expressing the c and the E antigen, hence the inaccurate, and scientifically poor (appalling) comment about "non-specific anti-E and anti-c".
I hope you are sufficiently intelligent to understand this.
THAT LAST SENTENCE IS MEANT AS A JOKE (although, not necessarily, if the person reading this happens to be the senior NHSBT manager who thinks hospital staff are thick)!

Personally, I think people are getting a bit "hung up" about this - not least the people who "write the rules", and I think that a lot of these problems are caused by the sloppy use of nomenclature (see my first ever post on BloodBankTalk back in March 2009 - before it became PathLabTalk).
When you are using antibody screening red cells, you are using, I presume, R1R1, R2R2 and possibly rr red cells, but are you actually?  These are "most likely genotypes", that are derived from phenotypes, but I very much doubt if the donors, from which these red cells have been derived, have been genotyped.  Even if they have been genotyped, it is extremely unlikely that full gene sequencing has taken place on the RHD and RHCE genes to determine, whether either the RHD gene is present in a homozygous state, a hemizygous state, or a heterozygous state, where one RHD gene is of the wild type and the other is mutated, and would produce a variant D antigen. or the RHCE gene is homozygous for the production of, in order, the C and e antigens, the c and E antigens and the c and e antigens, or whether they may be hemizygous with a silent gene (either with a normal RHD gene to encode a D-- or D.. haplotype, or with a silent RHD gene to encode an Rhnull haplotype), or whether they may be heterozygous with, for example, a normal C and e antigen and a CeS antigen in, for want of a better way of putting it (although this, strictly speaking, only applies to genes, rather than antigens) in trans.
The same principle applies to all of the other antigens and their genetic backgrounds.
So what am I saying?
I am saying that, day after day, we are excluding the presence of an anti-D, an anti-C and an anti-E (and, possibly, an anti-f) with screening cells that we actually do not know what antigens they are actually expressing, and yet we do not worry about this.  It is only when we detect a reaction with the screening red cells that we bother to perform an antibody investigation to determine the specificity of the antibody causing the reaction.  What, I ask, does this say about our logic?  I would contend it says nothing flattering!  So, if you are detecting an anti-D, and you (that is the collective "you", JustaKIDD, not a personal "you" - I am certainly NOT attacking you as an individual) are worried about the presence of an anti-C or an anti-E, because you only have one example of r'r or r"r red cells to exclude the specificities, I, unlike the people who "write the rules" would say "so what", but, if you are worried, why not just assume the antibody/antibodies is/are present, and cross-match rr units (if, indeed, the red cells in the bag actually ARE rr ).
Lastly, in all the years since anti-C and anti-E have been described (1941 and 1943 respectively), how many patients, with anti-D in their plasma, have had a fatal transfusion reaction due to the presence of an undetected anti-C and/or anti-E?  Not many (if any) I would suggest, and yet we, as a whole, get ""hung up" about such things, for no apparent reasons.

Well, that's me finished.  I am officially retired from work - but not from this wonderful site!

I am interested in the comment that really small remote labs in the UK do 20-30 Type and Screens a day.  The really small remote hospitals here do less than 10 per month!  The smallest one nearby is 130 miles from a bigger hospital (us).  We are the "big regional center" and we do maybe 20 per day.  It always amazes me that distances and population density are just so different in Europe than in the western US. And Alaska is even more remote!  UK 64 million people in 94,000 sq miles; Oregon 4 million people in 98,000 sq miles.
 
Another reason for the delay in taking up automation was the fact that Ortho lost their monopoly on gel in the US in 2012, immediately promised a new instrument to replace the Provue, yet did not get it approved by FDA until last August (2015) and Bio-Rad waited to come into the US market for a good 2 years after they could have and still isn't through FDA yet.  Through all of it we were told "just another 6 months", "early next year" ad nauseam. Throw the recession in there from 2008-12 and we are just now getting funding to finally get automated.
 
There are many ways to do your manual testing that can be safe with the correct safeguards built in and the best process in the world will fail if the people don't understand and therefore bypass the critical crosschecks and safety steps.

I agree 100% with you there Kellar, but, as things stand, even a full RHD gene sequence will not definitively tell you whether or not an individual with a particular Weak D genotype (and, by inference, the phenotype) will, or will not be capable of producing an alloanti-D.
 
Obviously, if the amino acid residue substitution is predicted to be in one of the extracellular loops, we are looking at a probable Partial D, and, therefore, there is a very good chance that an alloanti-D can be produced, but even if the amino acid residue substitution is predicted to be in either the intramembranous area of the protein molecule or the cytosol area of the protein molecule, there is no guarantee that the individual will not produce an alloanti-D - witness such individuals as Weak D Type 53 who have produced an alloanti-D.
 
It's a proverbial "can of worms".

I would agree that for patients this is overkill.  If they are SO weak that they don't come up in gel (and I can only talk for the Biorad cards but they can usually detect down to about 600 D-sites per cell - and the anti-D that you are using, Yorkshire exile, will go down even further) then I would not want to transfuse D+ anyway. What would you actually do with the result?? For cord bloods, well - is a cord blood with so few D sites likely to immunise a Dneg mum?  Donors is another question altogether.  I can well see that soon donors will be fully genotyped and then D will just be another antigen amongst many.  Currently though, there are papers that showed that a number of Del donors was being missed each year.  I also believe that Switzerland, who has been routinely typing their donors for about 2 years, have also found a couple.  Very interesting, academically, but it has pushed up the price of a unit of blood quite a bit and there's no actual evidence that they have actually immunised anyone, as far as I know.  I just get a bit upset sometimes when we in the developed world go to extraordinary lengths to maybe reduce the already negligible risk down further when many countries in the developing world don't have the resources to do more than an ABD slide - if they have the blood in the first place.

In my experience, reactions with anti-A,B tend to be stronger than with anti-A or anti-A1, even in this era of monoclonal grouping reagents.

Auntie-D, one of my absolte PET hates is receiving inadequate samples on patient's with an auto-antibody, especially as the User Guide and the back of the Request Form both have printed on them the MINIMUM sample volume required.
I sometimes think that people believe we can do the impossible (or, maybe, guess our results!!!!!!).

I found it to be a good site and Malcolm disagreeing with only one of the answers confirms it

I don't know what is going on at the moment, but, in the last two weeks we have had an anti-Ch, an anti-Rg, an anti-Ge2 in a patient with alcoholic liver disease, a pregnant Oh, an anti-Jk3 for surgery, an anti-Yta in pregnancy and an anti-K+Jkb+Csa in a bleeding patient.
Keeps life interesting!