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Mabel Adams

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Everything posted by Mabel Adams

  1. Is it required to perform temperature mapping in a 5.3 cu ft refrigerator? This is for blood and iStat cartridge storage at an airplane hangar. It will be on our temperature monitoring system. It seems too small for needing mapping, but I have never done it myself so don't know how small an area requires it. Any advice appreciated.
  2. We have a patient with hereditary spherocytosis who is pregnant with twins who are due in a few weeks. We have been notified that the babies could require exchange transfusions due to hyperbilirubinemia from the spherocytosis if they inherit it. Does anyone have any experience with such a case? Besides small volume or exchange transfusions of one or more babies, mom is starting with a chronic anemia so will be in more trouble if she bleeds much. It will be a busy time if everyone needs transfusion, but I wanted to see if there are any concerns I haven't thought of. Fortunately, no antibodies and mom is A pos.
  3. Are there Proficiency Testing samples available for TEG 6s? I didn't find them on the CAP website but maybe I am not using the right search term.
  4. Consensus I am getting from other sources is that we should either defer to our medical director (who doesn't feel comfortable making the call not to titrate on her own) or we confer with the obstetric providers and decide as a team what makes the most sense for this patient. As long as the titer remains quite low, we could probably trust it. If it approaches 16 (not a cut off determined with Lutheran antibodies in mind) then we couldn't be sure of its precision (to the extent any titer series is precise) but it would not be harmful to move to monitoring with Doppler US--just more expensive.
  5. My detailed ABID SOP prevents a certain number of midnight phone calls. It also reminds me what the heck I decided last time this came up.
  6. Resurrecting this topic to ask what CPT code is best to use for flow cytometry for FMH. Thanks.
  7. Thanks for your input. I was hoping you might respond. The Daniels book says that "No case of HDFN caused by anti-Lua or -Lub and requiring any treatment other than phototherapy is reported, although raised bilirubin or a positive DAT may be detected." Does this description equal "clinical significant HDFN" by your definition or is there newer information on more severe HDFN from these since Daniels published the 3rd edition? My thought is that, if there is no evidence of any case needing any early intervention, then there is no point in running titers to determine when to begin early intervention.
  8. If you have any references that you wouldn't mind sharing, I would appreciate it.
  9. If it isn't too much trouble, do you have any references on this? Or should I refer to the recent papers on cold stored platelets?
  10. We have a pregnant patient with anti-Lu b. Because of the variability of the antigen strength and the likely mild impact on the baby, is it recommended that we try to provide titers of this antibody?
  11. I always figured that, if it was benign enough in the donor that they met donor requirements, it was likely to be relatively benign in the recipient. Not perfect, of course.
  12. Now that we know that activated platelets are good for plugging holes in bleeding patients, if we get a platelet unit back out of temp because someone stuck in the cooler on the ice with the RBC units, would it be safe to use in an emergency in a bleeding patient? I'm sure we would need to get pathologist approval to use it outside of regulations. We are ~4 hours from our supplier and stock 3-6 platelet units. All input appreciated.
  13. I recently learned that there is a study underway on using them in heart surgeries at the University hospital in our state. Maybe there will be useful evidence at some point in the future. It's probably non-inferiority to room temp platelets so won't address Dr. Blumberg's concern.
  14. They give them if they note excessive oozing when the patient comes off the pump due to the pump "beating up the platelets". We will be getting a TEG analyzer (finally) so maybe they will have evidence from that testing that they don't need to give platelets in this scenario? Of course, they have to order the test and wait for the results.
  15. Can heart surgery patients coming off the pump be given cold stored platelets? They aren't hemorrhaging, which is the usual indication for these platelets, but I would think they could make use of activated platelets. If any references are available, I'd love to have them.
  16. This is from our ABID SOP (sorry the format is weird): a. Warm Autoantibody Guidelines –(Expert judgment is required on a case-by-case basis to supplement these guidelines. Contact supervisor or Reference Lab for advice) [return to top] i. Clues it’s a Warm Auto 1. Reacts with most or all cells tested—usually at a fairly consistent strength. 2. Positive DAT. 3. If it is severe enough that there is hemolytic anemia, the patient would be anemic with a high LDH or bilirubin and high reticulocyte count. The patient’s plasma sample may appear hemolyzed or icteric. Haptoglobin would be low. 4. Contact Blood Bank Supervisor for further consult if uncertain. 5. Patient has not taken anti-CD38 (daratumumab/Darzalex/DARA) or anti-CD47 drugs in prior 6 months. ii. Clues it’s NOT a Warm Auto 1. Reactivity with most or all cells in gel, usually 2+ or less, varying strength could be HTLA-like antibody or antibody to gel diluent. It’s not uncommon for patients to have a positive DAT without having a detectable warm auto antibody so the positive DAT could be present coincidentally. a. To confirm antibody to gel diluent, convert 3% screen cells to 0.8% to run in gel. If negative, turn out the 3-cell gel screen and document situation in the patient record. b. An HLTA-like antibody will usually remain detectable (although sometimes weaker) in PEG and even saline techniques. 2. Alloantibodies: a. If patient transfused in the prior 3 months, confer with the most expert person available before calling it a warm-auto. b. Elution may produce both a panagglutinin and another specificity or may show only a new alloantibody. The panagglutinin may be so strong a weak allo is undetectable. c. If the DAT looks mixed field (repeat IgG DAT in gel for clear-cut mixed field), it may be an allo. 3. Drug-induced antibody: a. Research patient’s diagnoses for multiple myeloma, amyloidosis, or other autoimmune diseases. Look for recent surgeries or infections as a clue for cephalosporin treatment. Research their drug history for cephalosporins and anti-CD38 or anti-CD47 drugs. There is variability whether these present with only a positive DAT (more common with cephalosporins) or with a negative DAT and positive screen or with both positive. b. Rarely, other drugs cause what looks like a warm autoantibody. iii. When the Auto control (AC) or DAT is positive, first check transfusion history. The AC could be positive due to a delayed serologic/hemolytic transfusion reaction and NOT a warm auto. See Positive autocontrol. iv. If not already done, perform a DAT (Direct Antiglobulin Test Procedure). Warm autoantibody patients can have RBCs coated with IgG only or IgG and complement both. Occasionally, only complement may be present. v. If not already done, perform an antibody panel in gel (or other primary testing method). vi. People who make warm autoantibodies are more likely to make allo-antibodies as well. We need to identify any allo-antibodies in the sample so we want to avoid detecting the autoantibody if possible but still be able to detect allo-antibodies (at least strong ones). vii. If reactivity in gel is < 1+ or there are some negative reactions, start a 3% tube PEG antibody screen. If reactivity in gel is ≥ 1+, start a 3% Saline (no enhancement) 30-minute tube antibody screen. If amount of specimen is minimal, skip PEG screen and only do saline or, if some negatives, rule out with negative reactions found in gel and run selected cells needed to complete ruling out the usual antibody specificities. viii. If patient has not been recently transfused and usual specificities can’t be ruled out in tube testing, a PEG Autoadsorption should be considered. PEG adsorptions should not be attempted with patients who have a strong complement coating. ix. If can’t rule out usual specificities in tube testing and the patient has been transfused in the past 3 months, send the specimen to the Reference Lab for allo-adsorptions to determine the presence/absence of underlying alloantibodies. See Red Cross (ARC) BloodHub/Connect--Standard Work. If the patient is too critical to wait for the workup, contact the on-call Pathologist and Blood Bank supervisor. Phenotypically matched units may be indicated. See Increased Risk Transfusion Release Form. x. Turn out ABID results as Warm Autoantibody plus any other specificities detected. xi. Approach to crossmatching in the presence of warm auto-antibodies: Situation Pt Hemolyzing* XM Methods XM Results Enough negs in gel to rule out all usual Ab specificities Yes Gel Incompatible Enough negs in gel to rule out all usual Ab specificities No Gel Compatible Can rule out all usual Ab specificities in PEG Yes Gel Incompatible Can rule out all usual Ab specificities in PEG No PEG Compatible Can rule out all usual Ab specificities in Saline Yes Gel Incompatible Can rule out all usual Ab specificities in Saline No Saline Compatible Alloantibodies identified or can’t rule out some Ab specificities in Saline Yes Saline** to assess compatibility with allos, then gel to turn out results Incompatible Alloantibodies identified or can’t rule out some Ab specificities in Saline No Saline Compatible Autoadsorption required and able to rule out usual Ab specificities Yes or No Gel with neat plasma Incompatible Autoadsorption required and alloantibodies identified or can’t rule out usual Ab specificities Yes or No With adsorbed sample** to assess compatibility with allos, then gel with neat sample to turn out results Incompatible *If patient is hemolyzing, no transfused unit will be truly compatible. Use “incompatible” XM result code in STTx, not “least incompatible” for these cases. **If second XM method (that’s not to be turned out) is required, record on log sheet. 1. Warm Auto Notes: a. The purpose of the PEG or Saline Antibody screen or PEG adsorption is not to be able to call the primary antibody screen negative, but to rule out underlying alloantibodies. Generally, these tube ABSC’s will NOT be reported in STTx. b. Incubation in the presence of enhancement (gel/PEG) reagents may cause reactivity in the AC that is only an in vitro phenomenon. If the DAT is negative and the AC is positive, antibodies to enhancement constituent or autoantibodies reactive only in enhancement medium should be considered. An Antibody Elution (Eluate) may help determine the presence/absence of warm autoantibody reactivity. c. If the patient is demonstrating active hemolysis, use gel or PEG to crossmatch units. The units still may suffer shortened red cell survival in vivo so calling them incompatible is justifiable. d. Consult with Blood Bank Supervisor about performing a full phenotype with the available monoclonal (non-AHG) antisera. Consider giving phenotypically similar RBCs for transfusion. If alloantibodies are ruled out in a current specimen, units that are only historically antigen-negative are acceptable. If we must transfuse before alloantibodies can be ruled out, confirmed antigen-matched units are advised if time permits. e. Warm autoantibodies can be confirmed in one of two ways: demonstrate that EGA-treated (antibody removed) pre-transfusion autologous cells react with neat plasma or prove that the antibody reactivity is adsorbed out with pre-transfusion, autologous cells. f. Patients on daratumumab (Darzalex or DARA or other anti-cd38 drugs) may appear to have a warm auto antibody but it is actually the drug reacting with the cd38 antigens on the red cells. They may have either a negative or positive DAT and AC. The only effective way to test these patients is to test against DTT treated cells, recognizing that this will miss antibodies to antigens destroyed by DTT like the Kell system. These patients benefit from having a pre-treatment antibody screen run and possibly antigen typing for K (and if K positive, for k). In most cases molecular genotyping may be indicated. See Dithiothreitol (DTT) Treatment and Anti-CD38 Drugs (daratumumab/Darzalex)--Blood Bank Testing. g. Additional anti-CD38 drug therapeutics are in clinical trials in addition to Daratumumab (Janssen Biotech) include MOR202 (MorphoSys), Sarclisa -Isatuximab (Sanofi-Aventis), and TAK-079 (Takeda) for treatment of systemic lupus erythematosus, Amyloidosis, or other autoimmune diseases. Daratumumab and Sarclisa are approved for treating multiple myeloma. h. CD47 is a glycoprotein expressed on all cells including RBCs and platelets, which usually signals to prevent phagocytosis. Anti-CD47 blocks this signal targeting cells for destruction. Samples from patients taking anti-CD47 drugs (Hu5F9-G4 or avelumab) will react with everything like a warm auto and the reverse type may be affected like a cold auto. Anti-CD47 interferes with all RBC and platelet serological tests performed including ABO reverse typing. False positive reactions can be seen in all phases of testing (immediate spin, 37°C, and IAT) and with all forms of IAT testing (i.e., tube, gel, solid phase). Reactions with D negative cells may be stronger than with other Rh phenotypes. False negative phenotyping test results can occur due to RBCs heavily coated by anti-CD47. DATs may be falsely negative due to a “blocking effect” caused by high levels of antibody present, but eluates are strongly positive. Plasma interference and strong panreactive eluates are observed as soon as 1 hour after drug infusion. CD47 antigens cannot be denatured with DDT or other common denaturing agents. It is highly recommended to perform pretransfusion testing, including blood type, antibody screen and extended phenotype (either serological or predictive genotype) before initiating treatment. Using monoclonal Gamma-clone Anti-IgG in indirect antiglobulin testing (which does not detect IgG4 immune classes like anti-CD47) may avoid most of the interference in AHG testing. Giving antigen-matched units may be an option if full phenotyping is available. [return to top] i. Additional CD47 drug therapies are also in clinical trials and include the CD47 targeting antibodies CC9002 (Celgene), which, like Hu5F9, is also an IgG4 antibody, and the human monoclonal SRF231 (Surface Oncology). CD47 agonists are also in clinical trials. These include TT1-621 (Trillium)31 and ALX148 (ALX Oncology), which are fusion proteins with the Fc region of IgG1 antibody fused to the CD47-binding domain of SIRPα with the goal of interrupting the CD47-SIRPα survival signal. Unlike CD47-targeting antibodies, TT1-621 appears to bind only minimally to human RBCs and interference in pretransfusion testing has not been observed or reported to date.
  17. Titer cut offs are usually between 50 and 256. We would need to use whatever cut off our supplier chose which I think is 200 for ARC.
  18. Resurrecting this thread with a related question. Is the potassium level in stored blood considered the same regardless of whether the units are leukoreduced? I have an old table for non-leukoreduced units but can't find data on leukoreduced units. This is in the context of large transfusions to neonates who hemorrhage at birth or come into the ED as traumas etc. We don't have time (nor ability at our small hospitals) to replace plasma in units nor to aliquot but I want to understand the potassium and mannitol (AS-1) risks if we are transfusing more than 20 mL/kg emergently to a baby. We usually use our stored, irradiated pedi units for neonatal emergency massive transfusions, but I am wondering if we should use non-irradiated RBCs for lower potassium. We don't have an irradiator so use stored, irradiated units for our NICU for small volume transfusions with no problems. It is when they give larger volumes quickly that I have concerns. Any advice appreciated.
  19. Oh, John, you are missing all the fun! Everyone wants to give blood pre-hospital now--on air and even ground ambulances. They prefer WB because it is easier to transfuse, has some platelet activity (yes, cold platelets work for trauma) for the first couple of weeks. and doesn't dilute the coag factors. It started with the military and then got going in Texas. With the O blood shortage, we can't give it to ground ambulances who would seldom use it, but we might be talked into providing liquid plasma (group A, never frozen, good for 26 days). The link below may be educational for you. Not everyone agrees with the research, but it is increasing everywhere. STRAC Blood
  20. I think some have created a new product class in STTx for low titer O Whole Blood so they can use different compatibility rules than are built for WB that may have all ABO antibodies in high titer.
  21. Do you take care of final disposition documentation or do they? Will they manage market withdrawals and the rare lookback notification, or will you? If you take units back from them before expiration, they must provide documentation of proper storage and tracking, right?
  22. Is there or will there be a new edition of The Blood Group Antigen FactsBook, 3rd edition, 2012? Does anyone know?
  23. Does anyone know of a program for training EMTs and Paramedics how to store and transport blood products as well as transfuse safely (which will probably be a rare task for any one individual)? And then how about a process to assess that they are remaining competent? I don't want to administer such a program as I already have a full-time job but would like to point them in the right direction or make clear what it would take to accomplish this. We might consider providing liquid plasma if they can check all of the required boxes. Our Air Ambulances already carry blood products, but they get a lot of opportunity to transfuse and are accustomed to following strict FAA regulations. I think a lot of them are RNs also. This would be ground ambulances.
  24. We use some tie tag things. Think zip ties but really fine and the line and connector are round not flat. No gun required although I have used that process in the past and we never punctured a platelet in any way that affected quality, purity or potency. We put our bag tag labels on manila cards and tie tag those to the units, (through the hanging hole on platelets).
  25. Mabel Adams

    TEG 6S

    I'm resurrecting this old thread to see if anyone has updates on how you charge for TEG or ROTEM testing.
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