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  1. Today
  2. Thanks for your answer. In the cases of alloimmunized women who lack/forgo prenatal care for their 2nd or future pregnancies, how is it that a O-Pos fetus could survive to near term or term even with critical titers? I understand they're severely jaundiced by this point, but why do some survive and have moderate/severe jaundice and others don't (miscarriage, hydrops, stillbirth)?
  3. Yesterday
  4. Just curious but does your billing indicate that these charges are specifically for testing in regards to a potential transfusion reaction? I had an insurance auditor deny a claim for crossmatching when the patient was not transfused on the grounds that, obviously the crossmatch was unnecessary because the patient used no blood. The procedure was for a TURP and at the time the usual order was for 6 units. Very rarely did a patient not use at least a couple of the units.
  5. Does anyone use the transfusion service software - eTrace Line from MAK? If so, what do you think and how large is your facility?
  6. Absolutely. We charge for every test performed working up a transfusion reaction. i.e Post transfusion DATP, repeat ABORh, ABSC and if positive, post DATG, DATC, ABID, pre DATG, DATC, and repeat crossmatching, etc.
  7. Place a Blood Temp Indicator on the bag when it leaves the BB and inspect the indicator and take the temp when it is returned.
  8. Last week
  9. The unit was just sitting on the counter.
  10. Does CMS allow billing for the component tests in a transfusion reaction workup in the U.S.?
  11. I document as a % of units w final disposition that month.
  12. It should be noted that IgG crossing the placenta is, over all, a good thing in that this is the mechanism by which the mother is able to confer active immunity to many diseases to the fetus which lasts for some time after birth.
  13. As the baby's DAT is negative, it could be that the anaemia is being caused by another underlying pathology, such as Parvovirus B19.
  14. The actual place where there is a feto-maternal haemorrhage probably will heal (although some of these are chronic), but by then the damage has been done. If the mother is going to make an allo-anti-D, she will have been stimulated so to do. However, it is not through the "fistula" between the foetus's and the mother's circulation that the anti-D gets to the foetal circulation, but by passing through the placenta. Indeed, not only does the maternal IgG pass through the placenta, but it is actively transported across the placenta, so that the concentration of the anti-D is often higher in the circulation of the foetus, than it is in the circulation of the mother. The reason so many foetuses survive HDFN even if there is Rh incompatibility is mostly down to the skill and dedication of the staff who work in Foetal Medicine Units, all of whom deserve utter admiration.
  15. I have met two cases of babies. Their plasma had anti-A or anti-B, as their correspond type. And the doctors had not seen HDFN signs clinically. We found it through crossmatch.( we issue same type blood to infant have no ABO HDFN).
  16. The baby's DAT is negative. Yes, the baby has anaemic and very bad sicked on the machine to help him breath. He has very servere infection, maybe this cover the symptoms which shows HDFN. And ABO HDFN is always mild. The jaundice is normal.
  17. Thanks! Let's say there is a slight FMH. Does that FMH eventually heal, preventing the mom's Anti-D from further contact with fetal RBCs? Is that why so many fetuses survive HDFN even if there is Rh incompatibility?
  18. I have always used total number of outgoing RBC's for that month, used + wasted. The issue with using the number received is that some months you may receive a large quantity for that month but due to expiry they wont expire till the following month where your received stock may be less than the month before hence this will skew the figures giving a higher % waste for this month. Using total outgoing RBC's gives a better indication of the waste against use for each particular month. My previous lab had a stats program built in that was based on MHRA and UK BSMS requirements and this always reported waste as a % of total outgoing RBC's. Steve
  19. One might add that use of transfusion in acute chest syndrome has almost no evidence base and may indeed do more harm than good. In transfusion, less is usually better than more.
  20. " I know we will be getting another order for an Erythrocytapheresis" That's not to say that is good clinical judgment. There is not a shred of evidence that 30% is better than 35%, and to expose the patient to the risk of another 6-8 units of red cells and an invasive procedure is, in my opinion a serious misreading of the benefits and risks of transfusion in this setting. Not to mention that the same goal (30%) could be achieved by simple transfusion of AA red cells. But neither apheresis exchange nor transfusion is indicated for clinical benefit.
  21. If you are seeing a lot of weak results in your anti-D well that subsequently turn out to be negative, I suspect the reason to be one of manipulation rather than anything serological. I would guess that NONE of these babies are group O. I am guessing that you are seeing carryover from your anti-AB. It can happen that if cards are stored somewhere where condensation can take place then drops of antiserum can condense into the reaction chamber and 'jump' into the next well or even next 2 wells when you remove the aluminium. This can cause false positive results. I suggest you check the cards before pipetting in them and see if there are any signs of these drops. Don't use the cards if there are and look for another place to store them
  22. what is the baby's DAT? Is it anaemic? Jaundiced?
  23. My experience and knowledge in bloodbank is so little. This is the first time I met an warm reactive anti-A1 and which can pass the placenta barria. It is new to me.
  24. Sorry , I cannot sure about that. Is there IgG anti-A1 exist in subgroup people?
  25. Hi, Epic recently published support for the ISBT Compound Barcode in their Blood Administration Module. Is anyone hearing of any plans of blood suppliers moving to this anytime soon? I found the attachment on the ICCBBA website, published in 2015. Outside of that, I've not been able to find much info on it. Thanks! P-004_Standardized-2D-Label-Design-for-Blood-Products-handout.pdf
  26. I’m certainly not a doctor, but from a technologist perspective, when we give the clinician a Hgb S level of 35% and their goal was 30% or less for their patient suffering from Acute Chest Syndrome, I know we will be getting another order for an Erythrocytapheresis meaning we have to find 6-8 more units that are negative for C, E, and K antigens and all the other antibodies they may have developed to get their Hgb S level below 30%.
  27. One unit of hemoglobin AS blood will contribute perhaps 5% to the S level in a patient with hemoglobin SS whose overall post-apheresis hemoglobin level is 10 g/dl. Not enough to make a real difference. A lot of work for pretty much nothing in my view. But we do it anyway. Probably would be less work to test donor units if the %S doesn't drop quite as far as expected. Hemoglobin S in AS red cells does not behave the way it does in SS red cells, so this has absolutely no clinical implications. The hemoglobin S goal for most treatment is 30% or less. 5% is not going to make any difference in treatment plans. Just an alternative view from the usual :).
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