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Showing content with the highest reputation on 05/24/2019 in all areas

  1. The size of the patient can be a factor in how much incompatible plasma you can safely give, but in an MTP you are poring the blood products in, and often it is poring right back out. The comment on giving platelets is well founded.
    2 points
  2. consult with pathologist and keep in mind If you absolutely have to give incompatible plasma the ideal is to give it while patient is actively bleeding. If possible give RBCs that will be compatible with patient and the plasma so in your case O and as the bleeding is beginning to come under control start giving ABO compatible plasma to "top them off". The idea is that as long as patient is actively bleeding give them the incompatible product which is then being bled out onto the floor or wherever. Once bleeding is under control give the good stuff to help dilute the incompatible out and leave them with the most compatible antigen/antibody combinations possible.
    2 points
  3. Malcolm Needs

    Gold Medal.

    Well jnadeau, be it on your head! You might receive insulting posts from others on the site now! Unfortunately, the photographs of me actually receiving the gold medal and glass plaque were not of great quality, but this is one taken at the Institute of Biomedical Science soon afterwards. Even here, my hair and beard look a bit like I have just poked my fingers into an electrical socket, my tie has gone awry and, these days, a wide angle lens is required on all occasions, but here it is in all its glory!
    2 points
  4. Ok Lets try the first one here. Background - A 31 year old African American male, Bpos, C-E+c+e+K-S-s+Fya+Fyb-Jka+Jkb+. This patient was not previously transfused or pregnant. Plasma reactions tested with 18 cells antibody panel and the reactions are....... 3+ reactions with C+e+ cells, 1+ reaction with C-e+ cells, negative with e- cells AutoControl was negative. Reactivity in DTT-treated cells were similar to that of untreated cells. The reactivity with ficin-treated cells were enhanced, C+e+cells 4+, C-e+cells 3+, negative with e- cells Eluate reacted 1+ with D- cells, 3+ with D+ cells. non-reactive with DTT-treated cells cord cells yielded similar reactivity as that of the adult. Panagglutination 4+ was observed with ficin-treated cells. What are the possible antibodies that the patient can have? If genomic testing is warranted, I will be back next week to tell you what genomic testing the results are. Lets give a chance for the transfusion service folks to work on it before reference lab folks share their wisdom regarding this case.
    1 point
  5. If I understand the question, I think that you could say that any negative reverse reaction on the patient's ABO typing would serve as a negative control--however, this would not be good enough for O patients. For a positive control, you would likewise be stuck on AB patients. But I do not think that patient specimens are regulated as "QC-able" materials in the case of a IS XM. Regardless, I would think that the "pos/neg" QC regulations are concerned with validating reagent reactivity and system integrity, and not so much with one patient's specimen reacting with another's RBCS. Scott
    1 point
  6. I just answered this question. My Score PASS
    1 point
  7. One possibility is state regulations on who can do what testing and the decision to train someone has been taken out of their hands. Now I'm going to get on my soap box and please don't take this too personally. There is a very big difference between training and teaching. Over the many years I have trained more people in blood bank than I care to remember. Every one of them had the basic knowledge and understanding of what was going on in the testing and knew at least one way of doing the testing. I was training them to do it our way, not teaching them the principles and background of the testing. It is simple enough to train some one to add A and B to tube C, spin for 15 seconds, shake the tube and see if it clumps but that is not teaching them anything about the testing or what to do if it doesn't work as expected. With out the basic knowledge behind the testing and processes you would find it nearly impossible to pass the BB test. I am curious, just exactly what have you been doing in the Blood Bank for the past few years? I know organizations that will allow only MT/CLS registered staff work in the Blood Bank and exclude even MLTs. My suggestion to you would be to find a program that fits your needs and complete at least the MLT level education. Another option would be to find a facility that still offers internships if there are any. They are set up to provide the training and education you are requesting from your current employer. I'm afraid this is probably not the response you were hoping for.
    1 point
  8. A few things as far as human reagents. Firstly, you never know what else may be in them in terms of antibodies directed against low prevalence antigens, because there is absolutely no way that the producer has the ability to test for all such specificities (I can remember once a human-derived anti-D reagent produced at one of the places I worked, also had a Gm antibody in it that we didn't know about. It is highly unlikely that this would have caused too many problems, but there is, nevertheless, a small chance that this could have caused a false positive). Secondly, you never know what else may be in them in terms of viruses, some of which may, as yet, be unknown to us (remember, HIV, used not to be known). This is a danger to the producer and the person using the reagent, rather than the patient. Thirdly, the avidity of human reagents is, in general, pretty poor (particularly anti-D). A few things concerning monoclonal reagents. Some of them cross-react with other specificities (although not many), but, famously, monoclonal anti-D reagents will react with the I and i antigens if used straight from the fridge. They have to be blended by experts to ensure that the desired epitopes are detected, but certain Partial D types (e.g. Partial D Type VI) are not detected (unless required). They are very specific and very avid (both of which are greatly to be desired). Virally, they are almost certainly sterile. Hope that helps.
    1 point
  9. Considering the push to using Low Titre O Whole Blood for MTP and trauma's, i'd say the benefit outweighs the risk. I have personally seen two incidents where a panicked Blood Banker accidentally issued O FFP in emergency release situations. In both cases, the patients turned out to be incompatible blood types (one A one B). Guess what, there was no adverse effect whatsoever in either case. No sign of hemolysis or transfusion reaction weeks later.
    1 point
  10. There is some truth in that, and especially from his perspective. However I have found that surgeons are not the best when it comes to understanding Transfusion Medicine.
    1 point
  11. Malcolm Needs

    Anti-Inb

    Sadly Neil, it is not the case that anti-Inb is wholly or largely IgM; indeed, it is almost always IgG. It is thought that Indian Blood Group System antibodies do not cause HDFN because they bind to CD44 on foetal monocytes and macrophages and, therefore, have a blocking effect on FcγR1. This being so, or likely to be so, plasma exchange is likely to be less effective that might be thought, because of rebound from the extra vascular spaces.
    1 point
  12. We use it during a computer downtime when the transfusion is needed before the computers come back up. Then once the computers come back up the units are retroactivity computer xm/dispensed
    1 point
  13. Mabel was kind enough to share this sample with our lab as we had not had the pleasure of seeing one of these. The sample was limited and it technically was not a referral, so my work was centered on getting to know anti-CD47. The patient forward typed as an A with no issues (I've heard the forward type can at times be affected), but reverse typed as an O, with 2+ reactivity in the A1 and A2 reverse cells. The patient typed Rh positive; no reactivity noted in the Rh control. The DAT was micro positive with poly specific AHG, heavy-chain IgG (HC) and C3, but was not interpret-able due to a micro positive saline control. Warm washing x4 with 37C saline resolved the positive saline control and still demonstrated micro reactions in the previously mentioned AHG sources. Interestingly, the reactivity was actually slightly stronger than the initial testing. Initial antibody testing was 2+ reactive in saline at initial spin, 3+ in saline at 37C spin (post 30 minute incubation) and 3-4+ reactive in saline at IAT with HC IgG, 3-4+ reactive in PEG at IAT (4+ reactions with the Rh negative cells tested as compared to 3+ reactivity with Rh positive cells; consistent with reports in literature), and 4+ reactive with papain treated cells (carryover reactivity was noted as a "no spin read" was 3+ and agglutination was noted prior to the addition of HC AHG). Testing with Immucor's murine monoclonal IgG Gamma Clone in PEG at IAT was macro negative, micro positive. Alloadsorption x2 (using 2 volumes of cells to one volume of plasma) onto papain-treated R1R1 and rr cells of known phenotypes (we usually do R1, R2 and r cells, but with the limited sample I dropped the R2 adsorption) removed the initial spin reactivity and confirmed the patient was group A. Alloadsorptions x3 were 1+ reactive in saline at 37C, and 3+ reactive at IAT using the HC IgG. x4 adsorptions yielded the same results. Out of curiosity, I did run a D-- cell with the x4 and it was nonreactive at 37C, but 2+ reactive at IAT. For fun, I performed titration studies on both the R1 and rr x4 adsorptions (saline, 60 minutes 37C incubation). Macro reactivity at 37C was noted at 1:32 in both samples, but technically they had a titer of 4 (1st observed 1+ reaction). At IAT, both samples had a titer of 16,384.... AFTER 4 adsorptions! A recent report in IMMUNOHEMATOLOGY stated that using equal volume (cells:plasma) adsorptions onto papain-treated cells x3 and x4 resulted in "the majority" of the samples being nonreactive in saline at initial spin and in PEG at IAT. Lastly, I did perform EGA treatment of the patient's red cells to see its affect on the positive DAT. The micro reactivity was removed following a 1min. 30sec treatment of the patient's cells, but since the sample was way beyond the manufacturer's specimen recommendation, I'm not totally confident in the observed results. Net result: It looks like alloadsorptions will be needed to resolve any observed ABO discrepancies due to reverse cell issues and PEG testing with Immucor's murine monoclonal Gamma Clone, with a macro only read, would resolve any the issue of detecting underlying alloantibodies. Thanks much Mabel for sharing this sample with us!
    1 point
  14. Cliff

    Gold Medal.

    The site was giving @Malcolm Needs a spot of bother, so I have taken the liberty of uploading some spectacular images for him.
    1 point
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