BBNC17

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."

Thanks for the info! Any idea how they are testing the titrations? I've heard I.S. from some sources and others are taking it through an IAT in gel.

We (blood collection center) are looking into providing Group O Whole Blood, with low anti-A and anti-B titers for treatment of trauma patients. Is anyone else doing this? If so, what is your testing protocol on how to identify a donation as "low titer"? What are your titer cutoffs for anti-A and anti-B? Thanks for any assistance!

We had an Rh positive donor tested at another facility as D+ C- E- c- e- . Typings were confirmed at our facility. Don't have any demographics on the donor yet, but how common (or uncommon) is this?

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We currently have a ficin-treated panel from Immucor and the papain-treated panel from Quotient. We have a tech that claims they used PEG with enzyme-treated panel cells at their previous job. Is this necessary? Their rationale was, since the panel has 10 untreated cells and then 10 enzyme-treated of those same cells, so they would run both the untreated and treated in PEG and perform a rule-out based on comparing the reactions. The package insert from Immucor says to not use potentiating reagents and the Quotient package insert says you may use potentiating reagents. I've always thought of enzyme treatment as a potentiating reagent for certain antigen groups, so why would you need to need to add PEG and risk diluting out a possible antibody? Thanks for any assistance!

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Amazing and fun campaign out of Community Blood Center of the Carolinas in Charlotte, NC to bring "..awareness about the tremendous and constant demand for blood donors as we work to better support the needs of hospitals and patients in our own communities around the world." Join thousands of others and sign the petition and share the movement with others in our wonderful blood banking/transfusion medicine community and beyond! Write up: http://www.cbcc.us/blog/2028-join-the-blooddonoremoji-campaign Campaign website: http://www.blooddonoremoji.com/

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!

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Just out of curiosity.. in your experience, how successful have you been able to remove the CD47 interference? I've read numerous adsorptions using enzyme treated cells have shown to do the trick. Also, the Immucor anti-IgG clone that doesn't detect IgG4, but we haven't seen these type patients yet and are anticipating seeing them soon.

Hello all, We are looking for larger tubes than our normal 12x75 tubes to use when performing adsorptions. I'm finding that a lot of serum glass vacutainer tubes, that would be the perfect size (16x100), are silica-coated. Would this silica coating interfere with any of our adsorptions or post-adsorption testing? Thanks!