Malcolm Needs

I, too, know little or nothing (probably nothing) about microbiology, BUT, I would not, therefore, put my views forward on matters microbiological. Sadly, it is often the case that someone who knows nothing about blood transfusion think that it is their prerogative to give their views, as "blood transfusion is easy", with only 4 ABO blood groups and D+ or D-. These are also usually the exact same people who are unwilling to work in Blood Bank, because they fear killing someone!!!!!!!!!!!!

Jsut returned from a break (watching Oz beat Engl in cricket 5 - zip {Sorry Malcolm}) to see a most interesting discussion. I remember something similar many moons ago in a cancer patient, but can't add specifics. That aside I would be most interested to hear if there is a resolution to this case Laurie.
Despite being bad for the patient, this is very interesting to all BBers as who knows when it could crop up in our hospital/s.
 
Cheers
Eoin (Wayne E)

Hi Amy,
My first thought was, why did the overnight person give group A blood, rather than group AB? But, perhaps you do not carry group AB in your stock.
Between 1 and 2% of the random White and Black population are A2B, and of those, only 25% produce an anti-A1. An anti-A1 that is clinically significant (reacts at 37oC) is disappearingly rare, so I wouldn't worry about it, but why switch to group O?
The ABO antigens are not direct gene products, but are the result of the action of transferase enzymes that ARE direct gene products (give or take a bit of post-translational jiggery pokery!) and the A transferase and the B transferase compete with one another to put their own terminal sugar residues on to the Type 1 and Type 2 backbones, and it is not unusual for the A antigen to be weaker than the B (so that an A1 reacts more strongly with anti-A than does an A1B, and an A2 reacts more strongly with anti-A than does an A2B).
This patient is also an elderly oncology patient, and both age and his condition can affect the expression of ABO antigens.
I would switch back to group A for transfusion if I were you (or, better still, AB).

Good luck with the staff capacity plan Rashmi! My own experience is that the plan is NEVER good enough to get more staff, but those that are far less efficient than you get a staffing increase. NOT BITTER, OF COURSE!

Good luck with the staff capacity plan Rashmi! My own experience is that the plan is NEVER good enough to get more staff, but those that are far less efficient than you get a staffing increase. NOT BITTER, OF COURSE!

To look at this differently- could it be that we all have so many other tasks to do now that we don't have time to do anything properly?
 
I can't remember having to clean fridges when I was training - I don't think we even considered these things before regulation! though I have probably cleaned more in my BBM role than ever before... I don't remember having to accurately trace blood units,let alone read SOPs (they didn't exist!), auditing, and what was Incident reporting?? .Though I do see the need for all of these  activities and they do make sense.
 
I am in the process of writing a staff capacity plan to obtain more staffing (!!!) and this really shows where the gaps are in our lab activities;  if we weren't all trying to juggle so many tasks, performance would improve, but, I do agree there is a need for a lot more professionalism to be shown by some staff.

Love it Anna, but what I meant was, if I (as the boss, as it were) am prepared to do such things, I expect my staff to be prepared to do them as well, despite the fact that they may think that they are too senior to perform such tasks. If REALLY NECESSARY, I will do the task in front of them (to shame them) and I have never had them say it is below them a second time. I don't often have to do that for three reasons.
1. The most important one, by far, I have wonderful staff.
2. IF I have to do it, then they are in BIG trouble.
3. I have honestly forgotten what on Earth I was going to put down as my third reason (I was also going to say that I must be getting old, but it would appear that I have already got old)!!!!!!!!!!!!!!!!

I tell anyone who refuses to do a job they think is beneath them to look at their job description, or look for another position.
 
I am a Band 8b, and I regard this to mean I am prepared to do any job from a Band 1 up to a Band 8b; in other words, I may not be qualified to do something a Band 8c or above, but I can sure as Hell clean down a bench.

I tell anyone who refuses to do a job they think is beneath them to look at their job description, or look for another position.
 
I am a Band 8b, and I regard this to mean I am prepared to do any job from a Band 1 up to a Band 8b; in other words, I may not be qualified to do something a Band 8c or above, but I can sure as Hell clean down a bench.

Here is my twopenny worth.  We have evolved into a culture where everything has to be done 'by the book'.  There's an SOP for everything and if the instrument says a reaction is + because it's interpreted a dust fibre as a positive reaction you can't change the result.  Well, it's not a bad thing to be standardised, but the problem is that when this becomes extreme, people stop using common sense.  In fact, they stop thinking altogether - sometimes thinking is just too dangerous.  Look back at some of the posts we've had where technicians have gone on to do further tests (because they were obviously needed) but were reprimanded because the doctor hadn't requested it and who's going to pay for it.  Also, we ask our 'qualified' people to have excessively high qualifications and get 'unqualified people' to do the majority of the work because it's cheaper that way.  But they're only allowed to do so much, and even if you've got someone who shows really a lot of aptitide they can't go any further unless they're prepared to opt into a long course of studies, for which they may well have good reasons for not being able to do.  Result - frustration and a lot of 'it's not my job' attitude.  I personally don't think that this is very good practise, and I can see why most of the problems listed above can be the result of these two factors

Hi Mabel,
 
IgA can activate complement via the properdin or alternative complement pathway.  JoAnn Moulds reminded us of this at the "Who DAT" session at the 2013 AABB meeting in Denver last October. 
 
At this session Patricia Arndt spoke about negative DATs in patients with clinical hemolysis.  Patricia Arndt mentioned more sensitive methods that can demonstrate antibody on RBCs in these patients.  These methods include cold LISS wash DAT method, flow cytometry, direct Polybrene test, also testing with anti-IgA and anti-IgM reagents.  Anti-IgA and anti-IgM reagents are not commercially available in the US, but Pat's lab has these reagents for research and special cases. 
 
But Pat also mentioned that anti-IgG reagents that are not heavy-chain specific can pick up IgA and IgM because these reagents may have antibodies to kappa and lambda light chains and can react with IgA and IgM light chains.
 
Pat presented a case of a 5 year old with clinical hemolysis (Hgb = 6.4, bilirubin high, LDH high, etc) and a negative DAT.  It turned out this 5 year old had IgA on his RBCs which was detected using anti-IgA reagent, but an anti-IgG reagent that was not heavy chain specific also detected the IgA on the cells (weakly).  The cold LISS wash DAT and the Polybrene agglutination did not demonstrate the antibody in this particular case.
 
The 5 year old was treated with steroids.
 
Catherine

Right then Rashmi, at long last I've got time to answer.
The answer to your first point is "NO". Part of the diagnosis of hyperhaemolysis (which is largely a diagnosis of exclusion, rather than inclusion) is that the post-transfusion Hb is ALWAYS lower than the pre-transfusion Hb.
The answer to your second question is also "NO". There is an increasing body of documentation that suggests that hyperhaemolysis is caused by hyperactive macrophages.
The patient to which you refer, as far as I know, has fulminating AIHA (remember, a negative DAT does NOT rule out AIHA). He did indeed have an anti-S-like specificity that was detected with papain-treated red cells only, and the reason we tried U- units was because, according to some work published by Jill Storrey a few years ago, this particular specificity is often an auto-anti-U that reacts preferentially with either S+ red cells or s+ red cells.
In this case it wasn't, because U- red cells, together with all the panel cells, reacted with the elution (unless, of course, the auto-antibody detected in the eluate had an Rh specificity that was also on the U- red cells.
I must admit that I am a bit surprised that he wasn't already on IVIG.

Anti-A1, natural or allogeneic, is not considered clinically significant unless it's reacting at 37C. The vast majority of patients with anti-A1 only react at IS.
 
In my opinion, this is just like any other patient. We don't worry about their phenotype and what antibodies they could form until they form one. If this were my blood bank, I would tell the techs to continue to transfuse AB or A blood to the patient.

Hi Amy,
My first thought was, why did the overnight person give group A blood, rather than group AB? But, perhaps you do not carry group AB in your stock.
Between 1 and 2% of the random White and Black population are A2B, and of those, only 25% produce an anti-A1. An anti-A1 that is clinically significant (reacts at 37oC) is disappearingly rare, so I wouldn't worry about it, but why switch to group O?
The ABO antigens are not direct gene products, but are the result of the action of transferase enzymes that ARE direct gene products (give or take a bit of post-translational jiggery pokery!) and the A transferase and the B transferase compete with one another to put their own terminal sugar residues on to the Type 1 and Type 2 backbones, and it is not unusual for the A antigen to be weaker than the B (so that an A1 reacts more strongly with anti-A than does an A1B, and an A2 reacts more strongly with anti-A than does an A2B).
This patient is also an elderly oncology patient, and both age and his condition can affect the expression of ABO antigens.
I would switch back to group A for transfusion if I were you (or, better still, AB).

I have found in the laboratory there are, essentially, two kinds of people, those who like blood bank and work in blood bank and everyone else.  Most of those who stay away from blood bank do so out of fear of hurting someone.  Granted, you can cause as much harm with a mistake in chemistry and hematology and even cytology for that matter but they don't seem to recognize that and they can usually blame it on the "machine". 

What SMW said . . .

Hi Amy,
My first thought was, why did the overnight person give group A blood, rather than group AB? But, perhaps you do not carry group AB in your stock.
Between 1 and 2% of the random White and Black population are A2B, and of those, only 25% produce an anti-A1. An anti-A1 that is clinically significant (reacts at 37oC) is disappearingly rare, so I wouldn't worry about it, but why switch to group O?
The ABO antigens are not direct gene products, but are the result of the action of transferase enzymes that ARE direct gene products (give or take a bit of post-translational jiggery pokery!) and the A transferase and the B transferase compete with one another to put their own terminal sugar residues on to the Type 1 and Type 2 backbones, and it is not unusual for the A antigen to be weaker than the B (so that an A1 reacts more strongly with anti-A than does an A1B, and an A2 reacts more strongly with anti-A than does an A2B).
This patient is also an elderly oncology patient, and both age and his condition can affect the expression of ABO antigens.
I would switch back to group A for transfusion if I were you (or, better still, AB).

Hi Amy,
My first thought was, why did the overnight person give group A blood, rather than group AB? But, perhaps you do not carry group AB in your stock.
Between 1 and 2% of the random White and Black population are A2B, and of those, only 25% produce an anti-A1. An anti-A1 that is clinically significant (reacts at 37oC) is disappearingly rare, so I wouldn't worry about it, but why switch to group O?
The ABO antigens are not direct gene products, but are the result of the action of transferase enzymes that ARE direct gene products (give or take a bit of post-translational jiggery pokery!) and the A transferase and the B transferase compete with one another to put their own terminal sugar residues on to the Type 1 and Type 2 backbones, and it is not unusual for the A antigen to be weaker than the B (so that an A1 reacts more strongly with anti-A than does an A1B, and an A2 reacts more strongly with anti-A than does an A2B).
This patient is also an elderly oncology patient, and both age and his condition can affect the expression of ABO antigens.
I would switch back to group A for transfusion if I were you (or, better still, AB).

Dear Desta
If this is a real case, then I am always amazed that clinics practising IVF don't look into the aspect of antibodies more closely.  I knew of a case recently where a woman with anti-U was advised not to have any more children, so went to a clininc for IVF (from sperm from a U+ donor) and was an absolute nightmare for the local transfusionservice who had to cope with the inevitable damage.
I think in this case, you might get away with it as anti-e does not usually cause severe HDN - but on the other hand, the baby will have to be homozygous for the e antigen, so this is not a normal situation.  Also, as the surrogate has already formed 2 antibodies she could easily form more to blood groups from other systems.  I hope at least that neither of the donors is K+!
I would say - keep an eye open for developing antibodies and boosting of the existing ones.

Dear Amy
There are two possibilities here. 
 1.  This patient is an A2B (or a weaker subgroup of A - maybe an A3) without an anti-A1.  Not all patients with weak A subgroups have an anti-A1.  About 20% of A2B individuals would be expected to have an anti-A1 - that still leaves the majority without.  The anti-A1 is naturally occurring.
2a.  If the patient has a 'haematological' cancer, it is well-known that the ABO antigens can be affected: They often return to full strength when the patient is in remission
2b.  If the patient has a stomach or bowel cancer, he may be producing excess soluble A substance which may be blocking the reaction between the A antigen and the anti-A.
As this patient is a group AB you should not really be giving group O.  If you don't like the idea of transfusing AB then group B would be the group of choice - but I don't see any problem with issuing AB for this patient.

Hi Amy--thanks for sharing your case.  The results you report suggest the patient may be an A2B.  The overwhelming majority of A2B (and A2) individuals do NOT produce an anti-A1, which if present is generally naturally occurring as you noted.  Although anti-A1 is somewhat more frequent in A2B than A2 individuals, in the absence of a 37C reactive anti-A1, it is completely safe to transfuse group AB, A or B blood and is actually preferable to using group O units.  The use of group O Red Blood Cell units would not be expected to be harmful to the patient, however since group O units are generally in limited supply, their out-of-group use is judicially reserved for those patients that must receive group O units.

I have only ever stocked the large dose of RhIg - why risk giving the smaller dose. The cost is the same (for me anyway) so I'm not harming the pt/mother in anyway with the larger dose (300ug)regardless of gestational age. As I stated above - the KB stain looks for fetal cells; the docs want to see if the placental circulation is compromised. Forget the rosette. (and I forget the samller dose; the docs have no choice in the mattter and I have never had a problem in a 700+ bed tertiary care hosp with busy ED and neonatal unit; a 350+ bed with busy maternity/ED; and a small 24 bed with busy Maternity/ED). Give the docs what they need 'cuz they are not always correct in what they want.

I, too, know little or nothing (probably nothing) about microbiology, BUT, I would not, therefore, put my views forward on matters microbiological. Sadly, it is often the case that someone who knows nothing about blood transfusion think that it is their prerogative to give their views, as "blood transfusion is easy", with only 4 ABO blood groups and D+ or D-. These are also usually the exact same people who are unwilling to work in Blood Bank, because they fear killing someone!!!!!!!!!!!!

True SMILLER, but, if the system forces you to scan the patient's arm/ankle band, so that there is bedside printing (or whatever) it more difficult to fool the system (although, I am absolutely certain, not impossible - human beings will find ANY way of getting around things). There is a lovely saying, "This system is fool proof, but it is not idiot proof"!

I agree 100% Marilyn.
Numerous studies have shown that multiple checking leads to more errors. This is because human nature, either as a matter of fact or maliciously, leads to checks being done badly (not at all) because there is a "feeling" that, well, if I miss something, the next person will pick it up, or, conversely, well, there can't be any errors, because they would have been picked up by the person who checked before me. On top of that, of course, there are checks that are done under great pressure of work, or when very tired, when a genuine error is made because of the circumstances.
The great thing is that, if computer programmes are written properly (and it is an "if"), computers do not feel either "pressure of work of circumstances" or cannot make mistakes because "they are tired".
Take the human out of it, and it is normally better; that's why electronic issue (under "normal" circumstances) is safer than a serological cross-match.