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Whatever the administration set manufacturer says should be okay. I know you can hang blood without any saline but many nurses like it diluted a bit for easier flow. That was more of an issue with CPDA-1 units than with Adsol.

We keep 2 thawed (5-day) A plasma ready for trauma. My pathologist would only let us issue 2 to an unknown type. I tried to push for 4 but couldn't convince him. If we still don't have a blood type we have to go to AB. Thus far we have been able to get a specimen and recheck before we have had to thaw AB. Once we find out the patient's type, we go to type specific FFP. We also have one ER doc that loves to say MTP but they also send back most of the blood we send down. Good for the patient, aggravating to us

AMcCord said it better than I did, but that is how we do it too.

We are using Echos and prior to that we had a Galileo. There's an interesting phenomenon that can occur with automated solid phase that can cause a positive screen and then a negative panel. I have personally seen it happen at least twice. If there are bubbles/foam on the top of the specimen the instrument will pipet the bubbles/foam and this underpipetting of specimen can actually cause the absc to be look positive. When the panel is performed, the bubbles have already been removed and the instrument pipets the plasma correctly, the panel is negative. All of our techs are taught during training to inspect the specimen for bubbles/foam prior to placing on the instrument but sometimes it is a step that is overlooked when it's busy. Another cause of false positive can be using cold undermixed indicator cells. If a new bottle of indicator cells is placed on the instrument without allowing them to warm the cells may not resuspend completely prior to being pipetted. Since the instrument pipets from just below the surface of the reagent it's possible to not have the proper amount of cells. This also occurs when bottles are loaded without a stirball having been added to the bottle. Just a couple of other ideas for troubleshooting.

I will say that the only reason we have such compliance on antibody moms is due to the blood banker calling L&D and telling the nurse that a cord needs to be collected. If they fail to, we ask for a heel stick.

Recent scenario we had, I thought was relevant: Patient with newly positive antibody screen, ordered for transfusion of two RBCs. Had been admitted for about a month; now diagnosed with numerous medical problems that were previously unknown to the patient. Patient was transfused a total of six RBCs with the last transfusion five days prior. The bench technologist wasn't able to determine a specificity with plasma testing but the autocontrol was positive. (Recent grad, a more seasoned technologist might have suspected the specificity based on pattern of positivity.) DAT was positive with polyspecific AHG and anti-C3. Our procedure indicates to proceed with elution in this case if the patient was transfused in the last 45 days. Eluate testing clearly identified anti-Jka.

That makes sense to me as well, although we would rather save the patient (or hospital) money that would be spent on a reference workup and just do a gel crossmatch. So I may make an M37 that's significant. After skimming through the entire The Blood Group Antigen FactsBook for transfusion reactions and HDFN, it is my decision that according to that book A1, DRHIG, Lea, Leb, Lua, M, N, Wrb, XGA and Yka are clinically insignificant, as well as cold auto, and warm auto without specificity once underlying allo-antibodies are ruled out and a negative screen. Does that sound right? We have a current warm auto patient in house with no underlying allo-antibodies and they recommend transfusion with E-, c-, K-,Fyb- and Jka- red cells. Yikes! I should just order antigen negative units from the blood center, because otherwise I would have to screen 159 units to find 1 negative! Maybe she will move out of state when she has recovered!

I simply could NOT agree more with you. How on Earth can anyone say that an undetermined antibody specificity can be considered to be clinically insignificant?

It's interesting that you posted this because the supervisor and I reviewed our Meditech Antibody and Antigen dictionaries just recently. It hadn't been done in many years and whoever set it up previously configured antigen warnings and IAT XM for every antibody, so review/revision was a long time coming! One difference from the discussion here that we decided upon was to retain the requirement of IAT XM for antibody of undetermined specificity (INC).

So, the easy questions first eh Mari?????!!!!!!!!!!!!! Personally, I think the IT guy gave you a poisoned chalice. The reason I say this is because we can all list antibodies that are not generally considered to be clinically significant, and then, all of a sudden, one comes along amongst these specificities that has not read the appropriate text books and goes ahead and causes a clinically significant reaction. Then what happens is that the person who said "anti-X" is not clinically significant, and this single example of anti-X turns out to be clinically significant, and you have to defend this in court. The real problem these days is that the technologies available to us are now much more sensitive than when I started (when cross-matches were recorded on a stone slab with a hammer and chisel) and many antibodies that were not clinically significant (because we just didn't detect them with the technologies available at the time) are now readily detectable - BUT, they are not necessarily detectable at strictly 37oC, as , for example, many examples of anti-M are now detected by "IAT", even though they do not really react (in real terms) at 37oC. The real problem comes when, for example, an anti-M genuinely DOES react at 37oC, and it is treated as clinically insignificant, electronic issue is used, and one or more of the units is M+ and the patient has a severe reaction - who answers in court? The worrying thing is that there have been papers published over the last few years quoting an anti-Leb as causing a transfusion reaction, and an anti-P1 causing a transfusion reaction (a certain Garratty G being a co-author on this one). I would say, therefore, that the best thing to do is to read through the relevant parts of The Blood Group Antigen FactsBook, Human Blood Groups and Mollison's Blood Transfusion in Clinical Medicine (latest editions in each case), and use their experience, rather than your own (no insult intended) as the courts would probably take the authors as "experts" should you come across any of these clinically significant "outliers". I wish you the very best of luck!