rravkin@aol.com

Malcolm, Given the fact that this patient has been transfused within the last three months how can we call this new antibody an Autoantibody?:)

BB enthusiast, Can you give a full and specific history including diagnosis, transfused products, age, gender, and previous type and antibody history if any?

Hey Malcolm, I hope that you are feeling alot better; I'm guessing that you are . With respect to platelets I fully agree. I guess it is always best to keep our options open. But I can tell you that I have encountered patients like this and I have given the Rh-Neg PC product because there is no question, no possibility, of developing an antibody (not withstanding the inventory issue); and I have practiced under management that promoted this practice. :)

BB enthusiast, Has the patient been transfused within the last three months??

Hey Steve, Thank you for your response. I agree with you and Malcolm that the chances of this patient developing an allo D are highly remote. However, this patient's condition is also somewhat remote and unless untilizing O Neg PC's for therapeutic transfusion was going to deplete the O Neg PC inventory and/or there would be a significant difference in cost why take the chance of producing yet another complication. You and Malcolm would have to agree that the very best PC product for this patient is O Neg, IRR, and CMV-Neg (dispite the potential redundancy).:)

Hey Malcolm, I'm reading the posts here and seeing all of this bold lettering and letters in red and I'm not sure why. I have to say that given this patients situation I would disagree with giving Rh-Pos blood for therapy because why potentiate an additional problem with an already complicated situation. If the patient were exanguinating Rh-Pos for sure. I understand where you are coming from; it is just as easy to change to Rh-Neg PC's when issuing therapeutic PC's for transfusion and I also understand the associated inventory issues; but we are not speaking of large volumes here, so I think that it is best for the patient to give PC's that would not potentially incur any additional complications. :)

I don't have a difinitive answer to your question but I do have experience working in two different Blood Banks one of which recommended no auto control and frounded upon it's very mention, and the other that seemed to not be able to live without the auto-control. The BB that didn't want to run the auto control regularly states that they do not want to open up a can of clinically insignificant warms where as the other BB said that they want to know everything. Both are viable opperating BB's each with a different outlook on auto controls. I hope this helps a little! :)

If I may say with respect to this situation it seems that poor management is begetting poor staff. One hinges off the other and it will always be this way. This problem tech was retrained by a manager that knows little of blood bank. How much more proficient was the problem tech suposed to be. Now this tech avoids more complex work probably because they do not have a good understanding of the work. Cuple that with an apparent lack of integrity and we have the making of a poor reputaion for all of us in the field. This tech needs to lose the part that promotes a lack of integrity and be properly educated about the work that they are responsible for and the effect on patient outcome. But with an apparent lack of proper education and the persons to deliver it this tech seems destined for failure and unfortunately her failure has the potential to be everyones in the eyes of persons outside the feild.

Well I have to say that I am a fan of the "see-food" diet with a side of self control.:):)

Thank you L106.:):):):):):) or can I call you Donna?

Sonya, I wanted to thank you for submitting this thread and all the posts that follow. It is very interesting to consider the variables affecting post transfusion Hgb and outcomes in general. I particularly appreciate this thread because it points us to consider variables of the donor unit itself which can sometimes be overlooked especially when dealing with a problematic recipient.

PammyDQ, After your process do you still enter the unit volume printed on the unit lable in your LIS or your calculation?:)

Trisram, I think that what Malcolm and others were trying to explain is that after the first panel is complete and you can not rule out two antibodies you must then continue with selected panel cells of panels in your blood bank other then the panel just used. These selected panel cells are cells that you select that are negative for the corresponding antigen of one of your two suspected antibodies and positive for the other; and vise versa. Here's an example, your ABSC is positive, your subsequent panel concludes with two antibodies that you cannot rule out; lets say Anti-E and Anti-Fya. Your next step would be to review the histograms of other panels that are in your blood bank (even outdated panels) and look for cells that are positive for Ag-E and negative for Ag-Fya; and look for other cells that are positive for Ag-Fya and negative for Ag-E. Now, here's a question for you; how many positve cells do we need in order to rule in an antibody? It is this number of positive cells you want to accumulate for each of your suspected antibodies individually; ie a cell that is positive for Ag-E and negative for AG-Fya, and vise versa. Please let me know your answer.

Malcolm, Forgive my post. I thought that you were speaking of actually titering the units of PC's for their corresponding ABO antibodies. My bad! I am aware of the info you gave here; not the actual dates or sites of the testing you wild and crazy serologist. If you don't mind me saying since you have mentioned an apparent illness in a previous post; I hope that you are feeling much better. I'm sorry but there is no allowence for ill Malcolms on this web site; please read your contract; Ha..ha..:)

Deny, Nice process. I'm wondering when you pull the segments from the units. I'm imagining the refrigorator door opened whiled segments are pulled and lable a few at a time; and if so how do you keep track of the units that still need segments pull. Also, feel free to express any ideas related to the post I left for adeiscast.:)

adiescast, Thank you for the info. Do you have a seperate receiving area in your BB. I used to work at a BB that had a seperate area for receiving products and I'm thinking that you may have the same situation. There seems to be two temp criteria for PC,s based on storage and transfusion. The storage criteria is somewhat stringent but based on what? Where the transfusion critia is based on the potential of bacterial comtamination when the bag is spiked and it's growth potential to clinically significant levels during the course of transfusion, as Deny has mentioned. Do you know what the storage temp criteria is based on? I had mentioned time/temp abuse; and of course I realize that bacterial growth is the consideration here as well but the bag is not spiked and not at room temp for extended periods of time, so why the stringent temp requirements, especially when we consider the collection process as well. And can I further say that if there was some bacterial contamination of the unit at the point of collection wouldn't it be better for the recipient if we knew the unit was indeed contaminated prior to transfusion?:)

Malcolm, Really great practice here; but can I ask how are these titers detemined and when during the process of component preparation would this testing be performed? I am assuming we are speaking of transfusing packed RBC units here.

Deny, Can I ask you when do you enter the units into your computer system during your process? When we receive PC's we enter the units into the computer, pull segments (one for testing and one for reserve), place the units in the refrig, then compare what we have on screen to the invoice, then test the segments, entering the results on another screen. We can peice-meal the process five units at a time while leaving the remainder on ice in the transport box. This process can expose the PC's to RT for longer then 7min if not done a few at a time. But hears a fact that I was just realizing; when the PC is tranfused it can take up to 4hours; extremely long exposure and yet practiced regularly. There seems to be some contradiction between recommendations of storage and RT exposer temp and actual practice. I am wondering if these temp recommendations are takiing into account the potential for "time/ temp abuse" over the course of the unit's shelf-life. Time/temp abuse being that the unit will be out at RT for given periods of time and then placed back in the refrig repeatedly. Sorry for the lengthy post but what do you all think?:)

KKidd, I'm still laughing! Thank you.:):)

SveiksRita, I am having trouble visuallizing a gel card well being resulted as negative and then upon use of another well in the same card the previously resulted negative now being 2+ positive. The cells at the bottom of the well (Negative result) would have had to migrated back up into the gel and agglutinate (2+ Positve result). This seems impossible. Is it possible that a layer of cells was present at the top of the gel in the well when it was resulted as negative that perhaps was not noticed. I have seen this happen but I've not seen this layer migrate down into the gel upon standing at RT and then incubated at 37C and spun when another well was being used.

We practice that a unit of PC's can be returned within, and up to, 30 min of the time of issue. Apparently not a good practice especially given the info provided by John C Staley and adiescast. If you don't mind me asking; How does everyone practice receiving PC's from your providers? It would seem that each unit would have to be processed very quickly in order to maintain temp. Lets say specifically 50 units of PC's.

At my facility the ER typically draws extra specimens and then adds testing as needed. Pretty difficult and interesting task Tony R.

Deny, Realy good post. Does this info come from the current issue of AABB Standards?

Hey Fiza, I think that you answered your own question here. I have not responded to this thread because I could not remember the exact reason why we add non-cellular reagents first. I'm remembering! It has to do with the way we detect agglutination using the tube method. The only way we detect agglutination is through the dispercement of the cell button. If one takes a test tube, holds it horizontally, places a drop of cellular reagent in it, and spins the tube immediately at the most minimal time in the serofuge one would see a partial cell button at the bottom and a streak of cells running along the side of the tube. We would not be able to detect agglutination in the streak of cells therefore they would be excluded from any reaction interpretation. The procedure I state here is an extreme case but brings home a valid point. We add our non-cellular reagents first, not only to know that they were added, but also to coat the side of the tube so that, as you said, the cells will not stick to the side of the tube. Also remember that when we make our cell suspentions there can be some varience in concentration. Idealy you would want to try to place the cellular reagent drop similarly as the noncellular reagent in the tube. This will assure that all the cells make it to the cell button so that they can be a part of the reaction, if any. Given the fact that we can see weak reactions macroscopically; in these cases every cell counts. Most importantly, however, is that in the Blood Bank the very worst interpretation that can occur is the false negative and in practice we do everything we can to avoid this, even something as simple as adding noncellular reagents first. I hope this helps. rravkin :)

Fluffy Agglutinates, Thank you for your response. I do have an immunology book, Kurby Immunology, and I have some backround in it's study. I am aware that there is a broad spectrum of maternal IgG that crosses the placenta conveying immunity to the newborn. I unfortunately read what appear to be some general statements in the AABB Technical Manual 15th Ed. that prompted my thread. I was focused on the effect, if any, of materal IgG of the A B concentration because of what I read. Appearently, according to the article the Malcolm has suggested, the iniation of Anti A or B in the neonate is initiated do to the immune system's recognition of foreign proteins on the normal intestinal flora. These protiens are similar in structure to the A and B antigens. Thank you again.