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Good tip!  We use temp indicators on the units, so that when they are returned, we can see if the unit was out of temp at any point.  We also asked them to provide a packing slip attesting to the proper storage of the units, similar to a transfer form used by our blood suppliers.  

Agreed, we also supply blood to a facility outside our system, and the FDA inspector did not visit their facility.

Good tip!  We use temp indicators on the units, so that when they are returned, we can see if the unit was out of temp at any point.  We also asked them to provide a packing slip attesting to the proper storage of the units, similar to a transfer form used by our blood suppliers.  

If you will be getting any of those units back then a FDA inspector may want to see their storage records.  Some will, some won't, depends on the inspector.  Better to be prepared for the one that wants to see them.  In this case a little paranoia may be a good thing.

I've had further thoughts upon this case (having told you not to worry about it - I live a sad life - NOT!).
It struck me that the patient has an Rh type of D+ C+ c+ E+ and e+, suggesting that the probability is that the patient has a genotype of DCe/DcE (R1R2), but this may not be the case.  She could have one of the rarer Rh genotypes, such as DCE/Dce (RzRo), DCE/dce (Rzr), Dce/dCE (Rory), etc, and this may be potentially important.
Some years ago, Joyce Poole explained to me that most grouping reagents labelled as anti-C are, in fact, a mixture of anti-c and anti-Ce, and this, she told me, included most monoclonal anti-C reagents (which surprised me, to be honest).  This is because the vast majority of the red cells transfused that stimulate an anti-C would have the haplotype of either DCe or dCe, or both, and will, therefore, also stimulate an anti-Ce.  As a result, these "hybrid" anti-C/anti-Ce reagents will react more strongly with red cells expressing the Ce compound Rh antigen (Rh7) and the C antigen (Rh2), than with red cells that only express the C (Rh2) antigen.
This would not, incidentally, explain the stronger than normal reaction with the e antigen.

However, if the patient does express one of the rarer Rh types mentioned above, say she is RzRo, she can actually produce an allo-anti-Ce, and most antibody panels only contain C+ red cells that are only Ce+ as well.  In other words, her antibody in the plasma MAY be identified as an anti-C, whereas it is actually a monospecific anti-Ce, which would neatly explain why she has an apparent anti-C.

Of course, she may also have an auto-anti-C, or a mimicking auto-anti-C (and, possibly, an allo-anti-Bg of some sort).  Sadly, for a nerd like me, I doubt if we will ever know!
I think it was John C Staley who once accused me of looking for zebras, when I hear horses hooves (I may be wrong, but I think it was John).  Anyway, this proves that he was absolutely correct about me!!!!!!!!!!!!!!!!!!!!!!!!

I could be wrong on this.....but I don't think the FDA would go to the other facility..........  We have several "sister facilities" that we send blood to for storage that are in our system and another facility that is not in our system.  When we get inspected, they don't go there.....  We are FDA registered because we irradiate and wash/deglycerolize units....ie - "create" products.  I think they just have to comply with CAP and or AABB standards for storage.

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So, this PROVES that CAP do not know the A from their elbow.
ALL Blood Transfusion Reference Laboratory Staff, not to mention MOST Blood Transfusion Hospital Laboratory Staff KNOW that not all antibodies can, by any means, be detected by ALL serological techniques (saline, albumin, enzyme, LISS, IAT, inhibition tests, recombinant blood group proteins, etc), let alone by ALL technologies (glass, tube, plastic tube, liquid phase microtitre plates, solid phase microtitre plates, column technologies, etc), BUT THOSE WHO RUN CAP KNOW BETTER THAN EVERYONE.

They should be thoroughly ashamed of themselves, and go back to kindergarten.

Not all of our moms get a type and screen when admitted.  I agree that the screen is redundant, but I am wondering if we did it for the sake of consistency, when a large portion of our staff was generalists.  At least we no longer repeat the antibody ID when they have D from RhIg. 

Well, the first thing to say is that red cells CANNOT be either homozygous or heterozygous (or, come to that, hemizygous).  These terms apply ONLY to genes, and red cells do not contain a nucleus.  The antigens can only be described as, at best, "homozygous", "heterozygous" or "hemizygous" expression, or, alternatively, "double" or "single dose" expression.

Then, it HAS to be accepted that, unless the maternal antibody is an autoantibody, it must be an alloantibody (or, possibly, an isoantibody), which means that to mimic the state of the foetal red cells, the red cells used to titrate the antibody MUST have a "single dose" expression.  However, that in itself presupposes that the foetal red cell antigens are all expressed at the same time, which we know is untrue (just look at the A, B and H antigens as an obvious example, but also the Kell antigens that are expressed much earlier than are the Rh antigens) or are ONLY expressed on foetal red cells, as opposed to other tissues (such as on the placental cells, which have, in some cases, been proved to adsorb the maternal antibodies).

Then, there is the fact that not all antibodies can be detected by all techniques.  This is why Reference Laboratories SHOULD have more than one technology available (and their workers should be provably competent in these techniques.  However, even then, not all techniques can predict the severity or otherwise of HDFN.  For example, antibodies within the Indian Blood Group System always show that they can cause severe HDFN by certain techniques, such as MMA, but they don't!  There is also the fact that the immunoglobulins may be IgM, IgA, IgG1, IgG2, IgG3 and IgG4 (to mention just a few), and I have yet to come across, or read about, an IgG4 immunoglobulin causing HDFN.

So, my answer is that there is a HUGE amount of knowledge known about the various antibody specificities, their titres, the expression of their cognate antigen, etc, etc, that there CANNOT be a single answer to your excellent question, but that the best thing that can be done is to read around the subject - and read around the subject from every source available - not just from a single country.

OKAY THEN, RIP ME APART!!!!!!!!!!!

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.

You did everything that was required in this situation. The patient was a trauma and needed emergency transfusion. The risk of death outweighed the risk of a hemolytic transfusion reaction in that scenario, according to the treating physician. I once had a trauma surgeon tell me "I can treat a transfusion reaction but I can't treat death!" That put things in perspective for me. That is why thy sign the consent.
Next step would be to report this to your risk management department so that follow-up can be made, including monitoring the patient for the s/s of DTR. 

We have seen this too quite a few times. We jokingly call them "gelibodies".

I attach a hybrid of my lectures on the differences between the A1 and the A2 ABO type, together with a very few slides from my lecture on lectins, and I hope that this will serve to be of some use to you.
It is hugely important to remember that many lectins, including Dolichos biflorus, are not specific unless they are diluted to ensure that they only react as desired.  For example, this particular lectin (Dol b) will react quite strongly with A2 red cells unless suitably diluted so that it only reacts with A1 red cells.  It is because of this that group B red cells are totally unsuitable to be used as the negative control for the Dol b lectin, and the same applies for group O and other group A subtypes.  Group B red cells will not tell you whether or not your grouping reagent is "specific" for the A1 antigen, or will still react with the A2 antigen.  In addition, the lectin will also react with red cells expressing the rare polyagglutination antigens Cad and Tn, and so, in the true meaning of the word, it is not "specific" anyway.
What is the difference between A1 and A2.pptx

Ah, hang on LisaMarie.  Was the patient D Positive?
If so, your eluate may not contain anti-D and anti-C, but actually may contain anti-G (which would also neatly explain why you are able to elate an apparent anti-C from a C Negative patient).

Where are you located?  Our Immucor rep supplied us with a coding guide for reimbursement, and you can also send specimens directly to Immucor for testing.  We send ours through our Red Cross IRL.  At this time, the last information I received is that reimbursement is for a complete HEA Genotype only, Rh genotype for weak/ partial D is NOT reimbursed because only the complete genotype is FDA approved.  I reached out to our Immucor rep for more information if you are interested.

As long as idiots exist in the world, they will thwart any solid plan we put in place to mitigate their recklessness.

In the UK, where this "rule" originated (I think!), our Guidelines do not "allow" the grouping of the same sample twice (what is the point of that, if the sample was taken from the wrong patient in the first place?  It would mean that, for example, the sample would be grouped twice as group A, and would be found to be serologically compatible with group A units, even if the patient was actually group O - and so, dead!).  We have to have two samples taken at different times (preferentially by a different person).
Of course, we would certainly NOT stop blood being given in a situation where the patient is bleeding to death - but we WOULD only give group O blood until the second sample is received and typed (and the Rh type would depend upon sex and age) wherever we can (obviously, in the case of a major incident, we may have to modify this, but the Guidelines allow for such a situation).
A VERY intelligent gentleman (Dr. Brian McClelland MB, ChB, ND Linden, FRCP(E), FRCPath), former Consultant Haematologist to the Scottish National Blood Transfusion Service, Edinburgh, UK) once wrote, "Transfusion has risks, but bleeding to death is fatal."

I've been told that the concentration of DTT in RESt is different that what is used for treatment of reagent cells.  But that sure would have been convenient.

It's Modern Blood Banking and Transfusion Practices.  It is what I used as a student, so it MUST be good
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Denise Harmening's book has been a good, basic reference since its first release.  I think it is called Blood Bank and Transfusion Medicine, but would not swear to it.  Many students use it.

Her books are excellent resources no matter  your experience.

If the tube testing showed 2+ or less reactivity with anti-D reagents (same as used on Echo) I would suspect that the reason for the negative results on the Echo is that the reaction was shaken away during the resuspension step of the testing.
Remember that Echo has an algorithm that it follows for resuspension. Shake so many times, swirl so many times etc. This can cause weak reactions (their limitations and warnings state 1+ or less) to be interpreted as negative by the instrument.
Techs who are resuspending a button in a tube are visually looking for an end point and immediately stop shaking the tube when the cell button is resuspended whether that takes 5 shakes/swirls or 15 shakes/swirls......Echo can't read for an endpoint in that same way, it must follow it's algorithm. Additionally techs consciously or unconsciously will adjust the intensity of their shaking in response to what they are visualizing. A good way to demonstrate this is to take that same specimen and have a tech who doesn't know what the reactions have been resuspend it with their eyes closed. Tell them to shake it for say 15 seconds and then see what the reaction looks like. It's a fun experiment.
Having said all of that.....if you see this often you can always have your FSE come in and adjust the resuspension step.

I doubt if this is the answer, but just to put it into the "public domain" as it were, you are saying that the sample was an EDTA, kept at around 4oC, were the anti-D reagents also kept at that temperature, or were they brought to whatever room temperature may be in your laboratory?  The reason I ask is as follows:
Thorpe et al have reported that monoclonal anti-D molecules possess a V4-34 moiety, that is also present in anti-I and  anti-i.   As a result, if papain-treated D- red cells are tested with such antisera, or untreated D- red cells are tested with such antisera that have not been brought to room temperature, they may agglutinate.  This could result in D- red cells being mistyped as D+ - a particular danger in females of child-bearing potential.  Thorpe SJ, Boult CE, Stevenson FK, Scott ML, Sutherland J, Spellerberg MB, Natvig JB, Thompson KM.  Cold agglutinin activity is common among human monoclonal IgM Rh system antibodies using the V4-34 heavy chain variable gene segment.  Transfusion 1997; 37: 1111-1116.  Thorpe SJ, Ball C, Fox B, Thompson KM, Thorpe R, Bristow A.  Anti-D and anti-i activities are inseparable in V4-34-encoded monoclonal  anti-D: the same framework 1 residues are required for both activities.  Transfusion 2008; 48: 930-940.
As I say, I doubt if this is the answer, but just to put it out there for colleagues who do not know about this phenomenon.  It is MUCH more likely to be something else that, at the moment has escaped me (as my mind is still on zebras, rather than horses John C. Staley!!!!!!!!!!).

That's nothing, Karen: My OR has a monitored refrigerator for platelets!
BC