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Everything posted by jojo808

  1. I understand now, had to read the thread over again and the reasoning with my simple mind. Well if the patient's antibody screen was negative prior to Darzalex treatment, then given K neg units once the antibody screen was affected by the DTT technique, then I can understand how giving 'regular' units once the antibody screen is negative would be acceptable because none of the units given would have caused that immune response (Aha moment). duh. Thanks everyone.
  2. I don't see the difference. Just because you give Kell neg units due to DTT denaturing Kell antigens, doesn't mean a Kell antibody was never there in that very sample. Is there any way you can prove that? Yeah I know I'm playing the devil's advocate, I really don't want to but if we are saying we can't rule it out, then you have to consider it may have been there right?
  3. I need clarification. I once asked on this site that if you could not rule out an antibody could you 'ignore' it once your screen is negative and I believe the answer was no. If in these cases with Patient's going off Daratumumab, if you could not rule out Kell (due to DTT treatment of cells), even once, don't you have to consider that a permanent problem even though we know that the probability that an allo anti-K developed is probably null?
  4. I think we need to add an OMG emoji to our selections!
  5. Some physicians are requesting that our IT build an Emergency release XM test to avoid having to sign 'the paper' for it. It will be a normal crossmatch test with the understanding that it is uncrossmatched and 'emergency released' via the verbiage that will be attached to it. Does anyone know if that is not acceptable to any agency? I will definitely require that the phone call to blood bank still be in the process, this is not my choice but I feel being forced upon us. I feel I'm the only one who objects to these things. Thanks in advance for the comments.
  6. When you say that the antigens are soluble and will inhibit the patient's anti-Lea in vivo, does that mean there will eventually be no Lea antigen on the donor rbc's? And let's just say it is certain that this patient has anti-Lea. Would there (theoretically) be no further problems with the first unit? or subsequent units?
  7. Fast forward: We think the cause of the incompatibility was (maybe) an Anti-Lea. We came to this conclusion because the 2 units that were clean were LeA negative and the other 2 that were reactive with the patient's plasma were LeA positive. This would be the only antigen that did not match the patient's phenotype. Anyway we are hoping our blood supplier can continue to get these (few) donors in. I think I've read in the past where anti-LeA is not clinically significant, but if this is an anti-LeA, it is not being detected by our ref lab who uses solid phase and tube. We use Ortho Gel (we do not have automation yet), soon to get the Biorad IH 500. Can't wait with all our antibodies!
  8. So we did perform the tried and true tube method with Peg enhancement (actually our secondary method) and both units came out a clean negative. The MD wanted to transfuse only one unit and see how the patient does. I'm so ok with doing that. I will try and keep you all posted thank you all again.
  9. I apologize for the delivery of my plea. The patient only has anti-Jk3, anti-E, and anti-c period. The others listed is what he tests negative for regarding his antigen typing. Thank for for the quick responses, we will have a discussion with our pathologist and the patient's MD and decide from there. Malcolm I know you are retired but your expertise is welcome each and every time. I'm just wondering how to result our crossmatches. I guess we can result the units as "least incompatible" (because they are) and enter a comment on this sample such as " Phenotype matched (or identical) rbc's given for transfusion" ?? With phenotype identical blood that is incompatible, would the results of the bioassays, (MMA, ADCC ,CLT, IgG subtypes) possibly show that maybe he has an antibody to a low frequency antigen? Gee how 'unlucky' can this person be? I guess anything is possible.
  10. Patient has the following antibodies: (Pt is B+) Jk3, E,c, He phenotypes K, Fya, S, N negative. Our ref lab found us 2 units that are phenotyped matched, one B+ and one O+ rbc. They are both incompatible, the O+ is 1+ in Gel, the B+ +/-. Auto control Neg, DAT neg (reference lab results). What's our next step??? BTW hope you all are doing well during this time.
  11. Forgive my ignorance but what is the positive reaction you get when testing reagent Anti-A with A2 cells due to??
  12. There is an article from George Garretty called Problems Associated With Passively Transfused Blood Group Alloantibodies that kind of mentions this. Although I feel it is perfectly safe to give out of group platelets, (we have done so for years) my concern was at what point would it interfere, if ever, with ABO/Rh type testing with tube method? According to the article worst case would be positive DAT but again I wonder if it would be detected in the plasma
  13. Hope someone can clear things up for me: 1. Can a type B recipient have 'testable' anti-B, acquired passively via transfusion of a few type A and type O platelets?? Let's say one out of type per day for a week. 2. Does Type B and Type O persons have naturally occurring Anti-A2?? Inquiring minds want to know, thanks in advance.
  14. Previous Quote from Malcom Needs while searching older content on this subject: "In most cases, TRALI is caused by donor leucocyte antibodies reacting with alloantigens present on the patient's leucocytes, although patient alloantibodies have been involved in some rare cases. The antibodies concerned are usually HLA class I and II specific, but HNA antibodies have also caused this". The thread was actually discussing solvent detergent plasma. When investigating possible TRALI, exactly what tests are usually ordered on the implicated donor? (Antibodies against HLA class I and II? And what are HNA antibodies and what's the difference between HLA and HNA antibodies? Aren't they both testing for antibodies against white cells?? Also if donor is found to have HLA antibodies, does it matter to identify them and then test the recipient for the antigen??? I'm a little confused.
  15. Just wondering why most use a 2nd sample only within 24 hours of collection. Does anyone see anything wrong with testing an older sample, say 3-4 days old??
  16. Does anyone audit the units transfused in the OR? How does the individual units transfused in the OR go into the patients record? Does the units go on a flow-sheet and someone transcribes this into the chart? Does the whole flow-sheet get scanned somewhere in the chart? I'm just trying to get as much information prior to a meeting about this. It seems like most are using coolers in the OR which seems 'more safe' than one refrigerator to 'share'. I'm willing to trust the process once it leaves the blood bank as long as that is compliant with AABB and CAP.
  17. I do almost exactly like AmcCord except I do not discard thermometers every year (but it's sounding really nice right now). I also have a spreadsheet with the serial numbers listed and the location (refrigerator/ freezer/ room temp .....) there is a column on the spreadsheet to answer if the calibration was acceptable or not. If the answer is no (>1C from the NIST) then a comment of "discarded" is added to that row. Our old SOP had instructions for correction factors that meant if the thermometer is 0.5 C higher (warmer) than the certified, a label must be affixed to the thermometer that lists the correction factor (- 0.5 C correction factor) which means you minus 0.5 C from that thermometer reading. I wouldn't waste my time with correction factors, all techs will not remember to use it, just discard it and purchase new ones, less headache for you.
  18. Thank you everyone for your responses. As wrong as it sounds, it gives me some peace knowing that there are others going through or have gone through the same battles. And like John stated there are others 'stepping in' and just complicating the situation for blood bank with solutions that make matters worse, not better. I really appreciate the pep talk and I will pick my battles carefully and continue to do the best that we possibly can for the sake of our patients that we serve. I feel better now
  19. I have read several threads, some maybe 10 years ago regarding this matter but I didn't see anyone really addressing the following. My question is does anyone work at a hospital where anesthesia scans in the blood unit prior to transfusion?? According to AABB 5.28.4 "The transfusionist and one other individual (or an electronic identification system) shall, in the presence of the recipient, positively identify the recipient and match the blood component to the recipient through the use of 2 independent identifiers". There is also a similar statement from CAP TRM.41300. We had a near miss several years ago, same situation, different place. One refrigerator being shared in the OR, 2 big cases going on, you get the scenario. To me, it doesn't matter how great the cooler, refrigerator, blood tracking .... there is no fool proof system but can we get close to one? one of the threads addressed the Joint Commissions Sentinel Event Alert regarding blood for multiple OR patients in the same refrigerator among other things (1999). This was 20 years ago!!!! Have we not improved this in 20 years???? Is it that hard to scan in a blood unit? Does it not take more than 5 seconds to do this??? The people making these computer decisions at our facility just can't see how important this is. Geez and in this day and age of computers all I get is "Our computer system cannot currently check this and that and blah blah blah is all I hear. Calgon take me away! Sorry for the rant but I needed to get that off my chest.
  20. I totally agree with David. I would say most of our Anti-M's react only with the cells that have the homozygous expression and not with the heterozygous expression. I would say you have to call it an Anti-M especially if Gel is your primary method of testing with tube as your backup. I don't think you can call it negative just because the tube has no reactivity. We sometimes (very rarely) would have a Warm autoantibody that showed pan-agglutination in Gel but was negative with tube method at one hour incubation, no enhancement excluding the auto control which is usually still reactive. We would just add a comment about the negative results in tube method just for proper documentation but still result as a Warm autoantibody.
  21. Let's try this again. Anyone using negative controls for their backtype reagents (A1 cell and B cells)?? If so, what are you using?
  22. Hi all, I am trying to overhaul our policy for transfusion reactions as recommended by our last CAP inspector. We were basically culturing all reactions except urticaria and the inspector said we were wasting time and energy and I agree but I need more assurance for the definite criteria so I want to know what are your criteria for culture and gram stain for blood products that are in question. I've looked online and found some use only temperature increase while others use temp increase with or without other symptoms What my research has found is the following: Most call febrile reactions bet 38-40C, or an increase in temp bet 1-2C from the baseline (pre-transfusion). The ones that use other symptoms use tachycardia and/or hypotension. Just want a poll for several things: 1. At what temp do you call it a Febrile reaction? 2. Do you also use temp increase from the baseline? If so what is? 3. Do you use other criteria with Temp increase for culture? If so what are they? 4. If you do have one, what is your definition for tachycardia (eg =>100 bpm?) 5. Same with Hypotension, any numerical definition? I know there are threads on this but I don't want to sort through it all. Please, I would love as much input as possible. Add any advice or other pertinent information is greatly appreciated. Thank you all in advance.
  23. We have had a couple cases like tkakin where the 'cold' shows in the tube but because the Gel is incubated at 37 it is spun to a negative screen. Not sure what a settle test is but what usually works for us is warming the patient's plasma well at 37C prior to testing with a1 cell and b cell. Sounds like a pesky cold agglutinin if warming corrects your MCHC.
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