Ensis01

Question to those wiser than I. Is the primary reason for these required validation comparisons to ensure we in the lab know how to follow the package inserts and so use the reagents correctly? I ask because I can't imagine any lab will be able to test the reagents to the level the manufacturer can with respect to numbers and variants (see package insert).

Question to those wiser than I. Is the primary reason for these required validation comparisons to ensure we in the lab know how to follow the package inserts and so use the reagents correctly? I ask because I can't imagine any lab will be able to test the reagents to the level the manufacturer can with respect to numbers and variants (see package insert).

My greatest apology for leaving you all hanging. We've been so incredibly busy and short-staffed that I could not even think about anything else but trying to finish up my daily duties. Anyway, seems that the patient also had an impella device that had to be "adjusted" and I believe that corrected the hemolysis. I'm only reading the responses today (2 weeks later)☹️so hats off to you all who thought mechanical causes. I would have not thought that the device would be that far-off to cause the gross hemolysis we saw. We do see slight hemolysis with impella devices but not like this one. I guess never say never. Thank you all for your responses.

Are you doing the immediate spin for a crossmatch or antibody screen? Well, we use the prewarm method for Cold agglutinins. We enter the results to the prewarm technique which is Negative, so the computer doesn't have a cow. Then we write in the test comments that the prewarm technique was used due to cold agglutinin, or history of cold agglutinin.

I leave that for the physicians to respond to, but I suspect that since there will be lingering lymphocytes, no, they would not be protected.
I, too, was part of a large level 1 trauma center.  Our inventory was typically 700 - 1,000 RBCs.  We were 100% irradiated.  Once they were received, they went right into the irradiator room (we had a double door fridge in there.  We usually had someone in irradiating most of the first and second shift, we had two old cesium irradiators.  It was very hard to keep up.  We looked into getting two x-ray irradiators, but it was cost-prohibitive, even with the government program where they would take the cesium ones away and pay for half the cost of the new ones.

I do not see how a genuine massive protocol can be supported with irradiated products. This is based on experience supporting patients during many massive transfusion protocol in a level 1 hospital, and also working in/with two facilities with three different types of irradiator. The irradiating process is just not that fast. I imagine the practical solution would be to give irradiated blood once the patient's bleeding is getting under control. I wonder if the patients stressed systems would prevent GVHD response? 

I am retired now and will never forget the sound they make when they are dropped on the floor.
 

Hi,
I realize you are not un the US; however, AABB has a lot of terrific resources available, for free.
https://www.aabb.org/news-resources/resources/donor-history-questionnaires/blood-donor-history-questionnaires
There is a questionnaire that you can administer, which will uncover the conditions you are looking at, and they also have guidelines on how to proceed should you receive an unexpected answer.
These should be reviewed with your medical director to ensure the suggestions are what they would like implemented.
In the last blood center where I worked, we pretty much followed them exactly.  Why reinvent the wheel 

This may be a little outdated, it's from a prior facility.  We did a tremendous amount of transplant infusion, and this evolved over the decades I was there.
Management of Hematopoietic Progenitor Cell Transplant Recipients.docx

In our lab, we do 30 patients ABO typing daily in average. In those tests we will find out forward and reverse typing mismatch at least once daily. Maybe because we tested patients' sample, the incidence is higher than donors', but just as Malcolm said it is definitely necessary to do forward and reverse typing and make sure they are matching.

In the UK a unit of blood would NEVER be sent out to a hospital without a full (and matching) ABO type - both forward and reverse.

We would also do everything possible to ensure that, if the forward and reverse ABO types of any patient do not match, we find out why before transfusion.

An ABO mismatch is probably the most common cause of fatal haemolytic transfusion reactions (although, thank goodness, they are NOT common), and this is why we will always go "the extra mile" to try to prevent any such situation.

If you issue blood via a pneumatic tube system, this introduces some additional processes.

Perhaps this is one rare physician who actually reads the medical literature on the subject or has thought things through.
The history of this is very simple.  Based upon the experience of severe or fatal hemolytic transfusion reactions to whole blood, it was discovered that when a patient's ABO type was unknown, and urgent transfusion was life saving, group O was the least likely to result in disaster.  When group O red cells became available during the middle of the last century, with modest amounts of plasma left, it was decided by the then experts that this could be used for non-urgent, routine transfusions of all patients. So-called universal donor O red cells.  The problem, with the 100% accuracy of hindsight, was that we had no evidence this is was good, much less optimal practice. But it was convenient. It meant blood banks didn't have to stock all 8 Rh and ABO types, so it was good for us in the transfusion service. It wasn't good for patients.
Why is that?  Well, there is residual incompatible plasma with anti-A and anti-B in all group O red cells that haven't been washed or thoroughly volume depleted. Well, you might ask, and all of us have assumed for decades, that a few dozen milliliters of incompatible plasma is not a big deal.   The answer, now known to some extent, is that it is a big deal for some patients who are groups A, AB and probably B.  This small residual plasma can on rare occasions cause severe hemolysis.  It's 100% severe if it happens to you as a patient.  This has been known for decades. What is new is the data that recipients of ABO mismatched red cells (Group O in general) have a higher rate of red cell alloimmunization to other red cell antigens, (Transfusion 2012 Mar;52(3):635-40. doi: 10.1111/j.1537-2995.2011.03329.x; 2025 Mar;65(3):588-603. doi: 10.1111/trf.18135. higher rates of febrile and allergic reactions, (Transfusion 2012 Mar;52(3):635-40.doi: 10.1111/j.1537-2995.2011.03329.x.) higher rates of HLA alloimmunization, and perhaps overall higher rates of mortality (Transfusion. 2016 Mar;56(3):550-7.doi: 10.1111/trf.13376).
So, if you are a recipient, you want ABO identical transfusions, or compatible red cells that have had all or almost all of the plasma removed, as by washing, for example.
 
 
 

The +s stands for strongly expressed.

The expression of the P1 antigen varies considerably from person to person, but the reaction strength with anti-P1 is an inherited trait (i.e. the strength of the expression on the red cell surface).

"I apologize for this dumb question."  BBnoob69, NO QUESTION IS A DUMB QUESTION, IF YOU DO NOT KNOW THE ANSWER.  If you don't know the answer, the dumb thing is to not ask the question in the first place.  NEVER be afraid to ask a question on here,

We have educated our multiple myeloma specialists to send a type and screen before administering the first dose of a daratumumab (Darzalex).  Our standard operating procedure is to have a panel of three cord blood cells (we have a large OB service) that is a laboratory developed test of sorts.  Cord cells do not express CD38 at interfering levels.
As it turns out we have made more of an issue of this than it warrants.  Patients who have negative antibody screens essentially never develop new antibodies to red cells after being started on daratumumab probably because it potential inhibits B cells function.  Minimal B cell function apparently yields little ability to make antibodies to red cell antigens, which are relatively weak alloantigens, especially when there is no adjuvant or inflammation in the recipient.  That said, a manufacturer is making a soluble CD38  analog that will inhibit the anti-CD38 activity and make testing easier from what I've read.  DTT treatment is also reasonable.  But the good news is that patients on this drug do not make new antibodies. There are literature references to this, and we have probably tested about 500 patients with no new alloantibodies. Mostly non-transfused patients, obviously.

My experience with DARA patients is panagglutination with tube testing, both in LISS and PEG. This may be manufacturer dependent. For a first time patient we need to serologically explain the gel reactivity even if the tube was negative. For subsequent visits negative reactivity in tube would be sufficient. I suggest you discuss with your pathologist to see what they are willing to accept. Other BB have different policies with regards to DARA patients, which I hope will be described.    

In this context two people means that one person is from the floor or OR (an RN for example) who brings a transfuse order, a physical piece of paper, for a specific patient to the lab. One person in the lab issues the relevant product to the RN. This issuing process therefore involves two people representing the two involved departments comparing the name, MR#, product type and product # and any other requirements (Irr, antigens etc.) prior to formal issue.  This theoretically ensures no errors. That being said I have had an RN bring a valid transfuse order for a different patient to the one she wished to transfuse. 

reactivity "all over the place" describes my experience of anti-P1.  I have seen negative reactions from cells labelled as strong and cells labelled as weak have been positive. P1 substance (if you have it) to neutralize the anti-P1 provides an elegant resolution.   

In this context two people means that one person is from the floor or OR (an RN for example) who brings a transfuse order, a physical piece of paper, for a specific patient to the lab. One person in the lab issues the relevant product to the RN. This issuing process therefore involves two people representing the two involved departments comparing the name, MR#, product type and product # and any other requirements (Irr, antigens etc.) prior to formal issue.  This theoretically ensures no errors. That being said I have had an RN bring a valid transfuse order for a different patient to the one she wished to transfuse. 

reactivity "all over the place" describes my experience of anti-P1.  I have seen negative reactions from cells labelled as strong and cells labelled as weak have been positive. P1 substance (if you have it) to neutralize the anti-P1 provides an elegant resolution.   

Column agglutination technology is an excellent technique, but does have a tendency to detect antibodies that react at temperatures well below 37oC, even after fairly prolonged incubation at 37oC.  However, the fact that the blood group, including the "reverse grouping" is clear of atypical agglutination suggests that this may not necessarily be the case for this patient.

Just to be on the safe side though, and if you can, I would either treat the plasma from the sample with rabbit erythrocyte stroma (which will adsorb out most "cold" agglutinins), treat the plasma with 0.01M dithiothreitol (which will denature the J-chains of IgM molecules, meaning that, although they can still sensitise the red cells, they are no longer able to agglutinate the red cells) or, and my personal favourite, is to pre-warm the plasma and red cells to 37oC before mixing, perform the IAT at strictly 37oC in glass tubes, wash with saline warmed to 37oC and use monospecific AHG.  If any, or all, of these techniques lead to negative results, the chances are that the antibody is a clinically insignificant "cold" IgM antibody, such as an auto-anti-HI (given that the patient is group A, and the test cells are all group O)..

Failing the above, send a sample to a red cell reference laboratory.

I hope that helps a little bit.

Can you convert the tube panel cells from 3% to 0.8% and test in gel?  We primarily do that to run selected cells that are not already diluted to 0/8%

Just a suggestion; see if your pathologist can find something that would/could be part of a physician's continuing education. The doctor's equivalent of our ASCP credits. 

Over the years have I discovered that information like this is best provided to physicians by physicians.  There were a few that recognized my knowledge and expertise on the subject but the vast majority did not and some were even reluctant to get it from my blood bank medical directors.  I would recommend having your medical director provide the book recommended by Malcolm.  I wish I had a copy in my library when I was still working.  Good luck.  Let us know what you end up doing and how it goes.  I'm sure that this kind of problem will be with us for ever!
Malcolm, you are correct, the info is relatively simple.  It's getting them to step down, swallow their pride and listen that makes it difficult! 

 
 

Agreed, we also send blood all over the USA with no thought of time zones, however not when product is close to or day of expiry