Emelie

Found this old gem while cleaning out our retired doctor´s office. It´s Claes Högman, a real giant in Swedish blood banking, who (among other things) was a delegate in AABB during the 60's and recieved the Karl Landsteiner award, James Blundell award and the ISBT award. He sang in the Uppsala band "Blodsbandet" (transl Blood relations)  under the name "Captain Blood". The song on the tape is "Give blood! Mr Sagman", which I suspect is a cover of "Mr Sandman"... 
Enough written, now I've gotta go find a cassette player!

Found this old gem while cleaning out our retired doctor´s office. It´s Claes Högman, a real giant in Swedish blood banking, who (among other things) was a delegate in AABB during the 60's and recieved the Karl Landsteiner award, James Blundell award and the ISBT award. He sang in the Uppsala band "Blodsbandet" (transl Blood relations)  under the name "Captain Blood". The song on the tape is "Give blood! Mr Sagman", which I suspect is a cover of "Mr Sandman"... 
Enough written, now I've gotta go find a cassette player!

The mechanisms of what have been termed TRALI (actually a subset of acute lung injury/acute respiratory distress syndrome) and TACO (actually something very common, congestive heart failure) have been widely misunderstood due to unjustified assumptions/dogma. There are many biologic mediators other than antibodies that can cause lung injury after venous infusion which directly subjects the lung vascular endothelium to these mediators (antibodies, activated cells, lipids, mediators such as sCD40L, DNA/histones).  Likewise there are many mediators that can cause or exacerbate cardiac failure after venous infusion (inflammatory mediators, excess volume).  Cardiac failure is not just volume overload, but can be caused by fever, inflammatory cytokines and vascular/myocardial muscle dysfunction.  The notion that these are distinct entities is also at variance with clinical experience.  Many patients have signs of both cardiac failure and pulmonary failure simultaneously.  So the definitions and pathophysiology used in reviews and texts are lacking in validity and just plain oversimplified and wrong, in my view.  There are compelling data to support these iconoclastic contentions for TRALI, and some for TACO.
Most germane (see attachment), when we introduced universal leukoreduction, we saw a sustained 83% drop in reports of TRALI and 50% in TACO over the following years.  This suggests that white cells/DNA/histones play a role in causing lung and heart inflammation and dysfunction.  This clinical observation was confirmed in animal studies from Denisa Wagner's lab at Harvard demonstrating that neutrophil extracellular traps (NETS) infused intravenously can cause acute lung injury (see attachment).  To me these observations are convincing evidence that leukoreduction alters cardiorespiratory injury and failure post-transfusion and represents one of the strongest arguments for universal leukoreduction.  Needless to say, this challenge to dogma has been ignored by the transfusion medicine community which continues, at least in the USA, to infuse deadly white cells and their degradation products (free DNA/histones) to patients, one of the great tragedies of the last 20 years in the USA blood bank field.  We got this entirely wrong and tens of thousands of patients have probably died unnecessarily due to complications of non-leukoreduced transfusions.
ULR TRALI TACO PMC version.pdf NETS and TRALI Wagner 2012.pdf

When using Immucor Solid Phase I have Rapid ID, Extend I (all Rh+ cells w 5-6 c neg and e neg cells), Extend II (all Rh neg cells w 1 Rh+)
3% panels:  Immucor Panocell (10 cells + 1 rare cell).
Used to use Ortho 0.8% panel A and Panel B
BioRad has 3% and 0.6% panels

Found this old gem while cleaning out our retired doctor´s office. It´s Claes Högman, a real giant in Swedish blood banking, who (among other things) was a delegate in AABB during the 60's and recieved the Karl Landsteiner award, James Blundell award and the ISBT award. He sang in the Uppsala band "Blodsbandet" (transl Blood relations)  under the name "Captain Blood". The song on the tape is "Give blood! Mr Sagman", which I suspect is a cover of "Mr Sandman"... 
Enough written, now I've gotta go find a cassette player!

Found this old gem while cleaning out our retired doctor´s office. It´s Claes Högman, a real giant in Swedish blood banking, who (among other things) was a delegate in AABB during the 60's and recieved the Karl Landsteiner award, James Blundell award and the ISBT award. He sang in the Uppsala band "Blodsbandet" (transl Blood relations)  under the name "Captain Blood". The song on the tape is "Give blood! Mr Sagman", which I suspect is a cover of "Mr Sandman"... 
Enough written, now I've gotta go find a cassette player!

You bet!  There is NOBODY better!  ANYWHERE!

It's Martin who's analyzed it (we've sent new samples so they can confirm their findings) We'd better do as they say, then 😄

Thank you! I found it difficult to find general recommendations regarding Bel. I discussed it with our reference lab just now, they weren't convinced about the transferase's ability to produce a complete antigen, since the expression was extremely low. I thought, as you say, that the absence of anti-B would implicate a normal B antigen but they were unwilling to recommend anything but A or 0 blood. This particular patient has a mutation not earlier documented, so it might be their cause for taking extra caution. Thank you for some great insight! It's an amazing forum for gaining new knowledge!

Putting aside the A antigen for the moment, which is probably "normal" in the case of your patient, it is not the B antigen that is abnormal in the case of a Bel person, but the 3-alpha-galactosyltransferase enzyme (the direct gene product of the ABO gene) is less active than normal, due to a mutation in the gene.  The actual carbohydrate residue that is on the red cell is "normal" - just less of it.  In addition, there is competition between the "A-transferase" and the "B-transferase" for the H-backbone.  In the case of your patient, the "A-transferase" will "win" this competition and this will accentuate the weakening of the B antigen even further - but the actual structure of the B antigen will be the same as the normal B antigen - just fewer in number.  This explains why there is no anti-B present in your patient's circulation.
This (rather long-winded) explanation should serve to prevent you worrying about giving your patient group AB blood should they require a transfusion.

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Sorry, I mssed that part when the system was first introduced.

Tricore; yes, in Sweden many larger hospitals use PI instead of irradiation when preparing platelets, the methods are equivalent. In moderately sized hospitals it's more convenient and cost efficient to irradiate the (rather few) components needed at the irradiation center instead.

Where I work we're alone during nights and weekends, so situations that would have been perfectly fine daytime with a couple colleagues around can easily get quite overwhelming with only a doctor on call-duty to discuss with. Like when there's a traffic accident or some other trauma with several badly injured victims and one of them turn out to have a pos ab screen - it can be quite stressful to set up an ab panel while simultaneously handing out lots of blood and keeping up with the thawing of FFP, and if our stocks are getting low, managing the transfer of blood and platelets from other hospitals to our own. I rarely encounter those extreme situations, but I had a slightly annoying weekend a couple months ago, working alone, when an ER patient needed a lot of blood acutely and of course she had a pos ab screen with several ab's. There wasn't a chance for me to identify them properly so I phenotyped her thoroughly and cross-matched units. I tested her against more than 20 units that fit her phenotype as far as I knew (Rh, K, Fy, Jk, MNS) and still only found 2 that were compatible. She received a lot more units of rbc's that weekend and we do all xm manually, but the most frustrating thing was when our primary "help-lab" sent back the results from her blood work marked as "Un-identified antibodies"... and it's not a one-time only patient, this one was at the hospital for quite some time getting several more transfusions and will most likely be back. We've sent new samples to a ref lab and hope for more exciting answers this time
In my opinion, it's important to always double-check with the medically responsible doctor before doing anything when you're uncertain, rather ask for expert advice one time extra than one too little, and document everything they say in order to keep your back free. As a blood lab tech I am not qualified to make decisions regarding patients, no matter what opinions I harbour (though it's obviously important to always give sufficient info about ab's and other findings to the patient's doctor to help them make proper decisions).
And, of course, always do a background check on a patient when something seems really odd, bm transplants and recent transfusions at other hospitals can mess things up, and there might be important information to be had