Monique

I agree David.  I have read every book I can get my hands on (plus Journals) and I am still learning regularly having been in the game for over 40 years.

I studied Mollison, The Technical Manual, Garrity and Petz, and the Pittiglia Blood Bank Book plus made flash cards for the blood group systems.  If you are just looking for a book to study to pass the test . . . well I think that is the wrong attitude.  I had a tech who wanted to know if she should take the test.  I told her that if she could afford to lose the $$$ go ahead 'cuz look at all the knowledge you'd gain studying for the thing.

Remember that not all red cell antigens are expressed at adult levels.  By that, I don't mean just the well known weakness of the I antigen on cord red cells, but also the Lutheran antigens, the Lewis antigens and the antigens of the Chido/Rodgers Blood Group System.  Fortunately, antibodies directed against such antigens are rarely clinically significant, but it is worth being aware of the situation.

Tests on the adsorbed serum (with ZZAP-treated cells) give confidence that the are no underlying alloantibodies to common antigens. However, the use of allogeneic cells risks removal of a cold-reactive alloantibody to a high incidence antigen, e.g. anti-Vel, -PP1pK. A low risk, but still concerning.
Does you facility also test the ZZAP-treated patient cells (now presumably DAT-negative) back against the patient's own serum ? This is ultimate proof that the cold-reactive antibody is an AUTOantibody and adds more confidence in the results of the adsorption with allogenic cells.
I may be opening a can of worms here, but.....I question the use of ZZAP in this scenario. In this case, the adsorption used (presumably DAT-negative) allogenic cells. ZZAP was not required to "reduce the DAT and enhance antibody uptake" - which is a true statement about performing AUTOadsorptions with DAT-positive cells. I appreciate that the enzyme in ZZAP enhances the efficiency of the adsorption, but the DTT component is not necessary for most alloadsorptions, and can actually confuse the users. I suspect the answer/policy is related to ZZAP being commercially available, rather than in a well-founded technical reason.

I will quote (one of my favourite quotes) from Issitt Peter D and Anstee David J.  Applied Blood Group Serology.  4th edition, 1998, Montgomery Scientific Publications, pages 63-64 (only because I cannot get to my copies of earlier editions at the moment - as while looking for them, a large number of my text books almost knocked me sideways, as they fell off the top of my wardrobe, and my wife nearly "brained" me too for making our bedroom look a mess!).
"Reading Methods for In Vitro Tests.
Now that most routine tests are carried through to an antiglobulin reading the question of how to read them does not often arise.  They are usually read macroscopically in order that the cells and serum are left in the tube for progression of the test.  A few cells may, of course, be removed and examined microscopically at any stage if this type of reading is required.  However, one of us (PDI) has believed for years that routine use of the microscope in the blood bank creates far more problems than it solves.  Almost any cell suspension, including those in which washed cells have never been exposed to antibody, if examined carefully enough under the microscope will be found to contain a few small clumps of red cells.  Thus, while reading aids such as mirrors or hand lenses are acceptable, routine use of the microscope is not condoned.  This reasoning also applies to the reading of antiglobulin tests.  Again if agglutination cannot be seen with the naked eye, a hand lens, a convex mirror, or the type of microscope in which the contents of the tube are viewed while still inside the tube by placing the tube itself on the microscope slide, IT IS NOT THERE.  Were it not for special tests, such as those in which mixed-field reactions may have occurred or when a small percentage of fetal cells might be present in a maternal sample, the microscope should be banned from the blood bank.
Enzyme tests for agglutination or following conversion to antiglobulin reading, should NEVER be read microscopically."
Several things should be noted about this quote.
Firstly, there is NO distinction here between the indirect and direct antiglobulin test.  Peter Issitt (see PDI, although I happen to know that Dave Anstee agrees with him) talks about reading antiglobulin tests.
Secondly, this quote was originally written well before 1998.  Since that time, there have been huge steps made in improving the sensitivity of tests within blood transfusion and blood group serology (often at the expense of specificity, and certainly at the expense of making diagnosis from the results of these tests straightforward - see the introduction of the term "delayed serological transfusion reaction", when there is laboratory evidence of a transfusion reaction, but no clinical evidence of a "delayed haemolytic transfusion reaction" (Petz LD and Garratty G.  Immune Hemolytic Anemias, 2nd edition, Churchill-Livingstone, 2004).
Thirdly, both Peter Issitt (1986) and Dave Anstee (1997) have been awarded the AABB Emily Cooley Memorial Award and Lectureship (amongst numerous other international awards - Dave was the President of the British Blood Transfusion Society, the Kenneth Goldsmith Award in 1985 and the James Blundell Award in 2003; these two are far from idiots!
Lastly though, looking down a microscope is no panacea to detecting a transfusion reaction.  I would draw your attention to Sachs UJH, Röder L, Santoso S, Bein G. Does a negative direct antiglobulin test exclude warm autoimmune haemolytic anaemia? A prospective study of 504 cases.  British Journal of Haematology 2006; 132: 651-661.  This paper talks about the production of de novo antibodies and anamnestic antibody production post-transfusion, as well as WAIHA.  It comprehensively debunks the fallacy that a mixed-field reaction can, in all cases, be detected by the use of a microscope.
So, perhaps the question should be, if the DAT is negative to the naked eye, should we perform an elution in each case?  I REALLY, REALLY hope that nobody (seriously) answers YES to that suggestion (believe me, it was made with my tongue very firmly in my cheek)!
Sorry about the rant!

We assume that every patient is a COVID patient. We place each unit in a zip lock bag with the unit tag placed along the back of the bag, seal the zip lock and place a label across the top of the seal warning that if the seal is broken the unit will be discarded. We do this for every unit.

If you feel that you are not being heard or appropriate action is not being taken you have the option of reporting to your accrediting agency AABB, CAP, TJC. This can also be done anonymously. The agency will contact the lab for information/investigation.
If patient safety is being put at risk then you need to do everything you can to get these situations addressed which it sounds like you are doing.
The other thing I would highly recommend is that you keep written/hard copy documentation of everything. You may need it sometime in the future to have proof of your diligence in trying to force compliance. Always remember the old adage "If it's not in writing, it never happened"
Good luck

Are you asking about which labels can be placed on the bag and which have to be on the base label??  Some irradiation indicator tags - both Rad-Sure and Rad-Control - have a type of adhesive that can touch the actual bag.  Both can go above or below the base label (or at least that is what I have always been told).  Most little labels/stickers, like the original Irradiation label in this thread, do not have this type of approved adhesive and are not allowed to be placed directly on the bag.  You have to find somewhere to stick it on the base label without covering anything else up.  

When building psoralen-treated platelets into your computer product code database, what special feature will you be creating to capture the fact that these "illuminated" platelets are equivalent to "irradiated" platelets?

I am a little confused by your question, in as much as, in one place you say that the patient has the Partial D Type DAR, but in another you say that the patient has the Dw antigen, sometimes known by its trivial name Weil, or more properly as Rh23, which is a low prevalence antigen associated with Partial DV Type 4.  I think you mean that your patient has the DAR D Type, and that the D antigen is typing weakly.  Am I correct in thinking this?  I hope so, otherwise it doesn't make sense (at least, to me).
Turning to the CdeS type, there are several (at least 8) of these in terms of genetic background.  All have one thing in common, and that is a Leucine to Valine substitution at position 245 of the mature position, due to a point mutation in exon 5 of the RHCcEe gene.  Five of these also have the Tryptophan to Cysteine substitution at position 16, resulting in the expression of (normally) the C antigen, due to a point mutation in exon 1.  However, 74% of C-, c+ Black Americans with normal expression of c have Cysteine at position 16.
The thing is though, that any C antigen that is expressed is weakened, and some anti-C reagents do not react with it.  On the other hand, because there are at least 4 amino acid residues that are involved in the expression of the C and/or c antigen (at positions 16, 60, 68 and 120), it is more than possible (in fact, probable) where mutations are present, that the c antigen is expressed at a normal strength, whilst the C antigen is also expressed in the weakened form.  Indeed, the C antigen itself is a Partial C antigen, and such an individual can produce a form of anti-C, rather in the same way that an individual with a Partial D can produce a form of anti-D.
So, to cut a long story short, this is why the individual will express the c and e antigens in the cis position, even though they also express the C and e antigens (in a manner of speaking) in the cis position, and why the ce (compound) antigen can also be expressed.

I agree with this.  YOu may see rouleaux again at 37.  You can do saline replacement after this phase and then go directly to wash and ahg phases.

The point about warm auto-antibodies, even the ones that look exactly like an auto-anti-M, an auto-anti-Jka or a specific Rh antibody, such as auto-anti-e, is that they all tend to be mimicking specificities, and so, in reality, you might be fooling yourself by giving antigen negative units to the patient, but you will not be fooling the patient's immune system, and so the chances are that, in most cases, the antigen negative transfused red cells will last no longer than the patient's own red cells.
"Cold" auto-antibodies tend to have true specificities, but, even if you can find antigen negative units, the red cells will usually not last as long as the patient's own red cells, because the patient's own red cells are coated with C3dg, which gives them some protection from removal from the circulation, whereas the transfusion red cells have no such protection.
I agree with your Reference Laboratory - which, considering that is my own background, may not come as a surprise to a lot of people!

Thank you for making my day

Thank you for making my day

AABB has a guideline for pneumatic tube systems. Not too expensive.  $25 non-member/ $20 member
 
053045 Guidelines for Pneumatic Tube Delivery Systems: Validation and Use to Transport Blood ComponentsISBN #1563951924

We receive cord samples on every baby and only test the ones (ABO/Rh DAT) from Rh negative moms or those with a clinically significant antibody. Our LIS allows us to see both mom and baby demographics  at sample log-in. We never perform an eluate from the cord.

Well David, I see your problem, but I may be able to suggest an answer.
Firstly, the anti-D seems to be quite weak (which is what made me think of my proposed answer).
Secondly, of the "common" Rh types, the R2R2 type has the highest number of D antigens per red cell (15 800 to 33 300), and so will tend to give stronger agglutination than will an R1R1 (which may explain why you are getting agglutination with all your R2R2 cells).
Thirdly, and turning to the R1R1 red cells, some of these may, of course, be R1r', rather than R1R1, and, therefore, have fewer D antigen sites per red cell (about 9 900 to 14 600, compared with 14 500 to 22 800) and, unless the donor is genotyped, or you can do an informative family study, you may never know (but remember the Cepellini effect).  In addition, the number of D antigen sites expressed on a "normal" R1R1 can vary quite a lot from one individual to another (and, indeed, from one cell to another, in the same individual).  In other words, those R1R1 red cells that react with your patient's anti-D could be near the "22 800" end of the spectrum, whilst those that do not react with this anti-D may be nearer to the "14 500" end of the spectrum.
All figures are taken from Geoff Daniels' book, Human Blood Groups.  3rd edition, 2013, Wiley-Blackwell, page 205.
I am not saying for one moment that this is the only, or the most logical explanation, but it is, at least, one explanation!

I am going to be REALLY unpopular here, but I'm going to say it anyway (because I am a pedant)!!!!!!!!!!!
 
Antigens CANNOT be either heterozygous or homozygous; only genes can be heterozygous or homozygous.
 
An antigen can be described as either showing homozygous expression, or heterozygous expression.
 
That having been said, is a red cell sample that types as K+k- phenotypically, genotypically K/K or K/Ko, or even K/k, with a mutation within the Kell gene that prevents the k antigen being expressed and detected with all anti-k grouping reagents (just in case anyone doesn't believe me - we had one!).
 
That's got that off my chest.
 
Now then, there is NO doubt that there are some anti-K's around that only react with K+k- red cells (dosage), but they are fairly rare, however, how many people use antibody screening red cells that are K+k-?  I doubt if there are any.  Therefore, we are all ruling out anti-K using red cells with apparent K antigen heterozygous expression on every single sample that (apparently) has no atypical alloantibodies present.  Am I wrong about this?
 
It follows, therefore, that, over the years, there MUST have been occasions when a patient with a very weak anti-K (one that is only detected using red cells that are apparently showing homozygous expression) and who has been transfused with K+ blood (do the maths).  As far as I know, there are no papers within the literature that report a case of either a delayed or an acute transfusion reaction as a result of this.  Yes, this may cause the anti-K to become stronger (and, hence, be detectable using an apparent heterozygous red cell sample showing K+k+ expression), but then, if this happens, you give K- blood.
 
So, my considered answer is that you can exclude using K+k+ red cells.
 
I shall now go and lie down!!!!!!!!!!!!!

Do you know whether this is a real IgG anti-Cw, or is it an IgM?  the differences might all be due to temperature.

Also, I believe if you search this site you will find a few threads covering this topic.  I know I've responded to a few of them.  In 2002 we moved to a new facility that had a pneumatic system capable of transporting blood products.  It was the best thing that ever happened to us.  AABB has since come out with a validation program for pneumatic tube systems.  It's a little more thorough than we went through but then we were making up things as we went along.  One of the things it did for us was stop the need to send blood to OR and ICU in coolers.  The transport times were measured in seconds so the need for coolers went away.  The nurses really enjoyed not having to come all the way to the transfusion service to pick up blood for their patients.  I'm not sure why the thought of transporting blood in pneumatic tubes horrified you but rest assured many have been doing it for a number of years and there have been few if any problems.
Good luck, you won't regret it.

Thanks so much for posting the picture of Marion! She told me was getting the award and I so wished I could "hop the pond" to go. I'm glad she is enjoying her retirement but she is seriously missed over here! 

If the antigen testing is actually performed by the blood center, we do NOT repeat the testing.  They mostly send us "historically" typed units which we then reconfirm at our institution.

In an earlier part of my life, when I was working in Hospital Blood Banks, I was involved in dealing with the results of three IRA bombs (the Chelsea Barracks bomb, the Hyde Park Corner bomb and the Harrod's bomb) and two train crashes (the Selsdon train crash and the Paddington train crash).
In four of these five major incidents, the communication between the Blood Bank and the rest of the hospital, in particular the Accident and Emergency Department, was pretty appalling. They were far too busy to answer the telephone, and we were working blind as to how many victims to expect. On the other occasion, we had a very senior Haematology doctor who was quite wonderful. He kept out of our way whilst we were working, but acted as a runner between us and A&E. This kept us well in the loop. We were able to get messages to them, and they were able to talk to him and, because he was a doctor, he was able to tell us how many and which victims would require blood quickly, and gave us some idea about how many units they would need.
So, the first thing that I would say is that you need a dedicated runner between the Blood Bank and A&E, and that, if this person is a doctor, who understands the situation of both the victims and those other doctors who are actually dealing with the victims, so much the better.
You do not need too many people in the Blood Bank. In fact, it is best to call more people in than you need, but tell all but the minimum number of people to go to another room, where they can remain on immediate stand-by for when required, but who do not mill around in the Blood Bank, getting in the way of those actually performing the work. That having been said, it is useful to have one person "extra", who can work as the runner for things other than those covered by the person mentioned above, can field telephone calls and can immediately communicate with your blood supplier, so that those performing the cross-matching are not disturbed.
Try to estimate, as early as possible, how much blood and blood components you will need. This is terribly difficult to do, but, in most major incidents, the amount of blood and blood components actually required is far less than might be expected. The most blood used in a single incident within the UK within the last few years was not from a "normal" disaster, but from a single incident, when someone went made with a samuri sword in a church and badly injured 12 people.
For the Paddington train crash, we actually only cross-matched 6 units of blood, of which only two were used, and yet someone (I won't say who, but it wasn't me this time) panicked, and order 40 units of group O, D negative by blues and twos, and we then had a glut for about a month, whilst other hospitals struggled.
Have a practice at regular intervals. Prior to the Selsdon train crash, there had been no practice for years. This resulted in two very strange things that, fortunately, did not result in any real problems - but could have done.
Firstly, the only access to the crash site was down a cul-de-sac. Two different ambulance services attended the crash site. The first service had one person go to the crash site and the other remained with the ambulance. The second service sent both people to the crash site. This meant that when the first service had "swooped and scooped", they could not get their ambulances out of the road, because the other ambulances, with no crew members in the cabs, were blocking the way.
The second was that the Blood Bank were too far down the list of Departments to be told of the incident. In fact, within Pathology, the first person to be telephoned was the Microbiologist. Whilst British Rail sandwiches can be pretty toxic, it is unlikely that there would have been to many cases of acute poisoning coming in from the crash site!
Hope that helps a little bit. If I think of more, I'll get back to you.
:blahblah::blahblah: