janet

We have a Provue interfaced with Meditech 5.5. It is not bi-directional (though in training they had a set up that was). We send the batch of completed test results over to Meditech once completed then verify the group and screens there when attached to the patient file. Provue is great for batch testing!

A weak DAT could be due to the Rh immune globulin but if it was any more than weak I might suspect the mother made an allo anti-D. We had 2 women in 2006 that were given the usual prenatal care (ab screen at the beginning of pregnancy, ab screen and Rh immune globulin at 28 weeks, both ab screens were negative and patient did not report any bleeds) At delivery both presented with what we thought may be a passive anti-D; until the baby was born with a 3+ DAT. Both women received Rh Immune Globulin again since we couldn't prove passive or allo D at that time. 6 months later they still have an Anti-D. That rare chance Rh immune globulin doesn't work!?!

We also see 'junky' reactions in gel but we don't use PEG. If we can't get compatible units by gel we go to saline IAT testing. If there is no reaction that way we go with saline IAT crossmatched compatible units. If the saline IAT is reacting and we still can't figure it out off it goes to our reference lab.

First time we would send out to our reference lab for autoabsorbtion and phenotype. They would cross with autabsorbed plasma if allo-antibody present or computer crossmatch if no antibodies in the autoabsorbed plasma. Both have a comment added "normal survival cannot be expected". After that initial testing we would give phenotypically matched "least incompatible". Our computer system lets us give out these "least incompatibe".

Mixed fields are often due to cold agglutinins.....my 'theory' is that some cells get sensitized before plasma/cells warm up OR some antibody dis-associates during incubation leaving you with some positive cells and some negative. Try prewarming (may have to resort to tube method since 10 minute spin at room temperature won't help with the strong colds). Rouleaux could also cause this 'look' - would have to go to the tube method for this one.

We've had 2 Clay Adams (used for sample centrifugation though they were bought for serologicaly testing). We've owned them 4-5 years and had to replace the part you speak of on one of them about a year ago. The first replacement didn't even last a few days. I haven't noticed breakage again on the replacement or the original one, but to be honest I haven't really looked.....I'll check tommorrow

You would only want to auto absorb if the patient was not transfused....if you absorb after transfusion you could be absorbing allo-antibody onto those transfused cells......or am I wrong. We will send our autoantibodies to our reference lab for autoabsorbtion only if they have not been transfused. We also request a full phenotype. Once you know there are no allo antibodies present you could give 'least incompatible' but after that if first transfusion you wouldn't know if allo antibodies were stimulated because the auto would mask it (unless it was a higher titre than the auto). An auto absorbtion can't be trusted (for my thinking above) so we try to give as close to the patient's phenotype as possible (you'll prevent the patient making an allo antibody or if you've given units not the patient's phenotype and it stimulated an allo antibody you won't be introducing those cells again). But....when the auto shows specificity (ie; anti-e) some literature thinks antigen negative cells may last longer. Then there's the Rh:negative patient who shows that auto anti-e....you would probably not want to give them Rh:positive blood even though it would be your only chance of giving e negative. There is a good write up on California Blood Bank Society site (www.cbbsweb.org then search for "auto immune hemolytic anemia", it was the first 'hit' for me). I also have a good write up I found from Dr. L. Petz "Emergency transfusions guidline for AIHA" ....not sure where I found it but I could e-mail it to you:)

In Canada Ortho Diagnostics supplies some Diamed products. We use the gel DAT card containing IgG/C3d/Ctl......we love it.

I looked at what the Provue does.....it seems to consistantly leave a space between the plasma/cells and gel !!

How could you hope to control where the plasma and cells mingle.....as long as they are together, I would think sensitization should happen. I'll have to check what happens in the Provue!

We follow what ISSITT said and give crossmatch compatible. I have seen more than a few strange looking M's that go along the side of the gel (almost like the card wasn't pushed down in the spinner all the way)

Does anyone have a policy for how often to test for antibodies to IgA in an IgA deficient patient? Standard practice is that patients with no detectable anti-IgA can be transfused with standard blood products with no requirement for future anti-IgA testing. OUR PROTOCOL If a patient claims to be IgA deficient, we have our chemistry lab do an IgA level. If they are IgA deficient, we err on the side of caution and obtain washed red cells from CBS. We will also send a sample for anti-IgA testing, but I'm questioning our protocol. The only place that tests for anti-IgA seems to be the American Red Cross, indicating a low demand. What do we do with antibody results? Will a low level increase? When do we test again if a patient with no antibodies before transfusion develops anti-IgA? Or should we even be testing for anti-IgA before a reaction occurs? Should the IgA level be below a certain value?

Our T.S. does cold agglutinins....not a kit method, our control is a negative only: Saline instead of the patient plasma titrations against the 2% pooled O cells, all incubated at 4C overnight.

We stopped using A,B routinly over 10 years ago....still used for cord and infant types though since you don't have a reverse to aid you. Occassionaly we will troubleshoot mixed fields or weak forwards + one time our supplier sent us a group A we grouped as an O until they told us it was a subgroup and the A,B helped us then.

Would this "super" DAT be clinically relevant???

Our policy is: Patient considere Rh:positive if result is 2+ at immediate spin with one of our Anti-D's (we use 2 monoclonals, one will pick up VI but the other won't). We did have a male patient form an Anti-D and Anti-C. We said he was Rh:positive based on the 2+ reaction, gave him Rh:positive units....low and behold at next admission there was the Anti-D One never know what's going to happen!

We use gel also....I will also run a tube panel at room temperature (or need be 4C) to prove an M, P or Lewis. Makes me feel better to put a name to it and know it's insignificant!

When you have a cold agglutinin present that will not go away until the crossmatch is performed by IAT prewarm method do you inform the nursing unit to use a warming coil? What about those crossmatches that interfere at immediate spin but will go away if put in the warmer for 5 minutes?

We used to do the IgG portion by gel and the C3d by tube....now we use the DIAMED DAT card purchased through ORTHO, manufactured in ?Europe. It has 3 wells-IgG/C3d/buffer control. The cards are wonderful and not much more expensive than if we used the polyclonal card before going to the expanded DAT.

We will do an eluate if the cause of the positive DAT cannot be explained by either IAT testing on the cord plasma or phenotyping the cord cells. I have witnessed two cases where all the antibody was all on the cord cells and the cause of the positive DAT could only be solved when the antibody was eluted off.

I've come across this a couple times now. Gel showing weak reactions and some missing positives, my "gut" telling me it's an anti-e....confirmed by our reference lab (not sure if only by PEG IAT or they actually did enzymes). I've even had this happen when I make up antibody samples for students...add anti-e for them to work up but not all cells react the same (1+ to weak, some missing)....could be the monoclonal reagent I'm using in these cases I guess. ?????

Question....by "micro" do you mean 120uG or 50uG?? "full dose" 300uG?? We give 120ug in most "end of pregnancy" situations and 300uG if during pregnancy. I've had requests for the 50uG in early terminations/miscarriages and they have ended up giving a partial 120uG dose. I tried in the past to convince our medical director to only carry the 300uG but didn't succeed....I felt it would save having to ask questions on whether the pregnancy was finished or threatened, etc. Better to overdose than underdose!

Some "massive transfusion" protocols I have seen give timelines for testing(INR, PTT, Fib, CBC) and product support (PC,FFP, Plt and Cryo). Personnaly I feel a physician should have the where-with-all to order his/her own testing and order product based on those results!

I recall reading there are two different options for the flow test....one looking for Rh:postive cells in your Rh:negative mother and one actually looking for HgF. If you go to the California Blood Bank site and search Fetal screen there are some discussions avaliable!

Hemolysis in a plasma sample would not be a reason to reject (seeing as in the plasma sample you would not see hemolysis as a reaction since the complement cascade has been stopped in anti-coagulating the sample!). On the other hand if you use serum samples; pre-existing hemolysis could prevent interpreting a hemolysis reaction.