BBNC17

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Our collection facility is going to start sending out patient samples and donor units for RBC genotyping on the Immucor Bioarray HEA system and I'm curious as to what this could mean.  Will they be able to label units based on the HEA results since it's FDA licensed?  will they still need to confirm serologically?  Will they need to run more than one donation from the donor to confirm the genotype ("predicted phenotype") before labeling it or confirming serologically?  How would this differ if they were using a non-licensed platform like the Grifols ID Core from Progenika?
Thanks for any guidance!

Is the supplier of the affected panels the same as your source for Red Cell Storage Solution (Alsevers)?

remember you have to validate your spin times.  There is an algorhythm for that.  An inspection should ask to see those calculations.

Short answer - No, you can't

I was wondering the same about the platelets in WB.  There article addresses it briefly stating "In Pittsburgh, the decision was made to keep WB for up to 14 days in the refrigerator as it was clear from the literature that cold-stored PLT function was well maintained for at least that length of time. Continuous agitation of WB is not recommended as it does not enhance PLT quality and contributes to increased hemolysis during storage. On Day 15 the unused units of WB are returned to the CTS laboratory where the WB is concentrated into an RBC unit by removing the PLT-rich plasma, and the resulting RBC unit can be stored for an additional 6 days."
 
Not sure what is meant by "the literature", but there are a few cited articles that seem like they may shed some light on this, but I have yet to look at them..
Reddoch KM, Pidcoke HF, Montgomery RK, et al. Hemostatic
function of apheresis platelets stored at 48C and 228C. Shock
2014;41 Suppl 1:54-61.
Nair PM, Pidcoke HF, Cap AP, et al. Effect of cold storage on
shear-induced platelet aggregation and clot strength.
J Trauma Acute Care Surg 2014;77:S88-93.
Becker GA, Tuccelli M, Kunicki T, et al. Studies of platelet concentrates
stored at 22 C and 4 C. Transfusion 1973;13:61-8.
Yazer MH, Glackin EM, Triulzi DJ, et al. The effect of stationary
versus rocked storage of whole blood on red blood cell
damage and platelet function. Transfusion 2016;56:596-
604.

From the transfusion article
"WB offers several benefits over component therapy including providing simultaneous treatment for both oxygen debt and the coagulopathy of trauma; it is a more concentrated product compared to reconstituting WB using component therapy; and cold-stored WB contains PLTs that appear to have equivalent or better hemostatic effect in both in vitro tests and in clinical trials, compared to PLTs that have been stored under conventional room temperature conditions. Another benefit of WB that is perhaps harder to quantify is the simplification of the resuscitation effort with its use, especially in the prehospital environment. In such settings, where the clinical staff are task saturated, patient intravenous access is limited, and storage space in helicopters and ambulances is very limited, having the ability to provide a balanced resuscitation fluid in one bag instead of up to four bags is valuable. This is important because any delay in the provision of blood products in hemorrhagic shock can be lethal; mortality is increased by 5% for each minute there is a delay in the delivery of blood products."

From the transfusion article
"WB offers several benefits over component therapy including providing simultaneous treatment for both oxygen debt and the coagulopathy of trauma; it is a more concentrated product compared to reconstituting WB using component therapy; and cold-stored WB contains PLTs that appear to have equivalent or better hemostatic effect in both in vitro tests and in clinical trials, compared to PLTs that have been stored under conventional room temperature conditions. Another benefit of WB that is perhaps harder to quantify is the simplification of the resuscitation effort with its use, especially in the prehospital environment. In such settings, where the clinical staff are task saturated, patient intravenous access is limited, and storage space in helicopters and ambulances is very limited, having the ability to provide a balanced resuscitation fluid in one bag instead of up to four bags is valuable. This is important because any delay in the provision of blood products in hemorrhagic shock can be lethal; mortality is increased by 5% for each minute there is a delay in the delivery of blood products."

Our ARC is starting to offer these products. They are using a titer cut-off of 200.  The whole blood units will cost 3 times the price of a RBC. It's good for 21 days.  Oregon Health Sciences University will be stocking them for traumas. They are the 4th hospital in the country supplied by ARC to use WB in their trauma program. Our ARC is the Pacific Northwest region in Portland.

Please discuss the importance of donation with this donor, and register the donor with the American Rare Donor Program. I remember having a pregnant patient with anti-Rh17. I believe there were only a couple of units available nationally. If I remember correctly, we had to resort to autologous donation, iron, and EPO.

The D--/D-- or D../D.. phenotypes (the two are almost synonymous, but the D--/D-- type is negative for the Evans antigen, whereas the D../D.. type is positive for the Evans antigen) are both EXTREMELY RARE.
Unfortunately, these individuals have a nasty habit of producing anti-Rh17 (essentially, an antibody directed against the C, c, E and e antigens), and can only safely be transfused with units that are themselves D--/D--, D--/D.. or D../D.., and if these are not available, units of Rhnull blood.
An exciting find, but I wish you luck!

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Our facility hasn't started CD47 yet, but anticipate that may happen in 2018.  I've been dredging through the internet to find anything, which is how I found the NY blood center pdf.  Besides the use of Immucors Gamma-clone IgG antisera (for antibody screens), I haven't seen anything mentioned on how to avoid it. 
I was thinking along the line of using Platelets (which have cd47 on them) to remove the antibody, but have seen nothing regarding if anyone has tried this.  The search continues....

I don't know if/how silica might affect testing, but I think that might only apply to the stopper, not the tube proper.
You could certainly use regular 16 x 100mm (borosilicate) tubes, rather than the "vacuum" versions. We get generic tubes from VWR, cat # 47729-576.

Absolutely the advice given to you was correct.
For a start off, as you say yourself, 80% of A2B individuals do NOT make an anti-A1, but of those 20% who DO make an anti-A1, how many will make that anti-A1 as a result of immunisation as a result of transfusion or pregnancy?  The answer to that, if you read any book concerning blood group serology (and that is NOT a criticism of you - we all started somewhere, including the very best, such as Herr Dr Willy Flegel, and others - and I have HUGE respect for Willy), you will see that a clinically significant anti-A1 is amazingly rare.
For an anti-A1 to be clinically significant, it has to react strictly at 37oC, and that is a VERY rare "animal", and no example of anti-A1 has EVER been implicated in a case of HDFN, so, PLEASE, do not worry about giving A1B (or even A1) blood to an A2B individual, even if they have an anti-A1 in their circulation, UNLESS they have an anti-A1 that is actually active at strictly 37oC.

This is our policy as well.

Our policy as well.  

There are two types of "antigen negative" units we can get from our supplier here in Michigan.  One is "historically negative" -- those have to be retested when they arrive.  The other type is "confirmed" -- those units have been confirmed negative for a particular antigen at the supplier and do not need to be retested here.
Scott

Thanks much for all the information. This Blood Bank community is of immense help & I really value your opinion. I am fairly new at my job as a Lead and counting on you for advice. 

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It sounds like if at that point (after throwing everything at it including DTT and papain) you don't have the rare antisera/cells and reagents to identify the antibody then you are going to have to send it out anyways and the reference lab will probably end up repeating most of that testing in order to ID the reactivity on their end.  You are right, you have to consider that implementing trypsin is a big project with SOP revisions, may involve added costs, is known to have stability issues, and how often do you expect you will really need it and keep your staff competent?  Will it really have any added benefit to your testing?  
From personal experience in a smaller reference lab with limited rare reagents as well as in a larger IRL, I would say it sounds like you may want to wait on the trypsin until you have a better inventory of rare reagents to aid in completing antibody ID?   

Curious as to the benefits vs. the time it takes to prepare, validate and store these enzyme stock solutions (alpha-chy, pronase and trypsin)? 
Currently at a reference lab that would likely send antibody to high-incidence antigen workups out as we don't have much access to rare antisera and cells at the moment.  However, before we send it out (or while it's being worked up), we would like to at least try a narrow down the classification of the antibody and also perform enzyme and/or DTT treatment on pheno-similar cells, or adsorb out the antibody, to investigate any underlying allo to common antigens.  This way we can at least provide the hospital with a preliminary report of the patient phenotype and a potential aby to high-incidence antigen and any ID'd underlying aby.  
Eventually, when we build up our rare antisera inventory, we'd like to perform these IDs in-house.  For now, do you think DTT and papain are sufficient enough since we are sending these workups out anyways?  Looking at a few enzyme/chemical reactions on high-prevalence antigen charts and, other than -Yta, trypsin doesn't seem to determine any of these abys.