Mabel Adams

Sometimes by adding requirements, be they bands or identifiers, we just create more things to check and more ways to make mistakes. Case in point: we recently ceased providing a transfusion slip with our units. Now we don't have to check that against the unit when we "dress" it or issue it. Nursing makes up their own forms for the chart with the info that used to be documented on the slip. We no longer get back a copy of anything and the computer puts the units in as "presumed transfused." The nurses were kind of confused by not having more paper to check at the bedside with another nurse, but I think it puts the focus in the right place--does this unit match this patient? Sorry, bit of a tangent. Hope someone besides me can see how it relates.

We also had physician's saying to continue transfusions without reaction workups. We finally changed the protocol so we have to do ID checks and DAT and retype on post specimen before they continue (except for hives, which they merely document, treat and continue). The hospital and lab felt that there was too much liability if a transfusion was continued without any workup. Pretty indefensible to continue an incompatible transfusion until the symptoms are overwhelming. My favorite line from doctors was for an autologous transfusion--"How could it be a reaction? It's his own blood!" They have such faith that no one ever hangs the wrong blood and bacteria don't grow in auto blood!

The latter.

Check your contract. I understand that Mediware changed it a few years back so you don't own the software and can't continue to use it without their support. We are off it now, but got some nasty letters insisting that we return the software to them or send a letter verifying that we had destroyed it. They threatened to send in a software verification team to see if we were inappropriately using any vendor's software. They didn't make many friends with our administration with this attitude. They were a great company to deal with when we started in 94.

Why can't the nurses weigh them and do the math?

CAP says Medical Director or designee (except if you have a new director, they have to review them once) and I believe CAP has deemed status for CLIA.

We generally require one double-dose cell for rule-outs (from a homozygous donor--sorry, I know John Judd still lurks). For K, we accept 2 single-dose cells. For C and E in the presence of anti-D, we accept one single dose cell for rule out. The 3 pos and 3 neg rule applies to the statistical likelihood that a particular set of reactions could occur by chance rather than due to the presence of a specific antibody. By requiring 3 pos and 3 neg (or 2 pos and 5 neg) TO IDENTIFY AN ANTIBODY (not to rule one out) you are statistically pretty likely that the ID is accurate and not due to chance. These are the basic rules taught to our bench techs. More complicated cases, like multiples and antibodies to low-incidence antigens are handled by experienced staff on a case-by-case basis and occasionally some of the rules are not applied to the same degree. Of course, Lewis can't actually have double dose cells, but they all look like they are double-dose on the panel, so it makes the rules appear consistent to the average generalist.

My husband seems to remember Spock's blood being copper based rather than iron based. Don't some insects have copper based blood? I don't think sterile hybrids necessary lack the urge--just the offspring. Also, occasionally mules are fertile--as have been Pizzly bears (polar-grizz cross) I think I read recently. Shall we see how far this can range? I think we have the right kind of minds here to go far.

What kind of timing are you all seeing for CAP inspections now that they are surprise? Are they coming the first month you are eligible for inspection, 2-3 months later or is it widely variable? Please share your experiences. Thanks.

Since Bob already has a hobby I'm thinking it might be time for him to up his ADHD meds--or maybe sign into rehab for his speed addiction. I am still trying to figure out how he fit 30 years of train driving in with everything else. The only logical thing is he kept driving trains while he went to college, MT school and law school. Aren't there rules about running a train with no sleep?

I only read the abstract and it seems to refer to refrigerated storage, not room temp. Should I quit being lazy and read the whole article? Also, did they correlate the results with regular (not SD plasma)?

I'd like to see some research on some of our old assumptions that were probably never tested. How long is a serum or plasma sample really stable for antibody testing? At room temp? At 4 degrees? What variables affect this? Is freezing really better for them? I just had a titer specimen get left at room temp for 2 days accidentally. I needed to repeat it just to make sure the new tech did it right. I got exactly the same results on both the old and new samples as she got on them both when they had been refrigerated for a couple of days. Another of my pet ideas is to determine what the risks are of transfusing a unit of thawed FFP that has been out of the fridge for over half an hour. There seems to be some data about the effects of letting red cells hang around too long at room temp or be returned to refrigeration, but I wonder if anyone ever tested plasma. Do the factors deteriorate sufficiently for us to care? What is the increased risk of bacterial contamination? As long as it is a closed system, why is it that different from platelets in this regard? The bacterial contamination one would be hard to test since contamination is so rare. I don't think you could mimick real life by spiking units with bacteria. The only way I can see to increase your data points is to split plasma units into many small ones and monitor each for bacteria. When we wash a cell suspension or cell button, why do we actually care if there are cells down the side of the tube? Was that just something that made the original workers feel neater? Do the cells actually get "cleaner" if all the cells make it to the bottom of the tube. ( I am after a shorter wash time than 60 seconds here.) Did anyone ever test that it has no effect on any antibody specificity if we stick a wooden applicator stick in and fish out some fibrin? Thanks for listening.

I also find Helmer has great customer service.

But how do you know if an antibody that reacts with only 1 cell is clinically significant if you can't identify it?

Mom is not genetic mother of baby? Donor egg? One of mom's gene's is for a C deletion and baby inherited that one??? Or am I looking for zebras when hoofbeats only mean horses? (Sideline: I assume the A1 and B cells used were reagent reverse cells so they are both Rh neg--thus both c pos. So we don't know if the reactions to them are ABO or the anti-c, right? Don't know how much you would care either.)

http://www.psbc.org/bcrm/index.htm Try this website for the Puget Sound Blood Center's online Blood Component Reference Manual. Maybe it will also give you ideas for your "Orange book". It looks like their site might have other useful info too.

There is such a thing as DAT negative immune hemolytic anemia, isn't there? Occasionally an IgA or something??? Probably Issitt mentions it--maybe even Tech Manual.

We use Gammaclone control. (Our typing reagents are all Gammaclone.) You can use 6% albumin and I think some use saline.

Is this a bone marrow transplant using 2 units of cord blood as the source of bone marrow stem cells? If so, the patient's original immune system will not make any ABO antibodies and his new immune system, as it gets established, could eventually make both anti-A and Anti-B. He has tissue cells that will still express the AB antigens. I believe this sometimes absorbs out the antibodies made by the graft so he may not make much in the way of ABO antibodies. Still, I can't see where you could go wrong by transfusing O red cells and AB plasma. Platelets would be harder. It is customary to make sure the product is plasma compatible with the patient red cells before worrying about the ABO of the plts themselves, but you may have a hard time getting AB plts and will have to give whatever you have. Someone else can feel free to clarify if I have not got this right. I just can't stand an unanswered post for too long.

We run a gel xm QC to test the diluent, testing a negative patient plasma sample and our reagent QC kit positive serum sample against a unit made up to 0.8% in the Diluent 2. We don't do gel DATs. They seemed to be almost too sensitive for general antibody ID workups. When working up transfusion reactions, that sensitivity might be more appreciated.

Since units aren't really compatible in vivo in the presence of a warm auto, how do you all handle crossmatches? Assuming you found no underlying allos and no cold antibodies, do you: crossmatch the units by AHG with the absorbed sample but still turn it out as incompatible, IS crossmatch the units with unabsorbed sample to confirm the ABO type but still turn it out as incompatible, AHG crossmatch with unabsorbed sample and turn them out as incompatible, not crossmatch at all but call them incompatible, do some combination of the above or something else. My computer will insist I call them Least Incompatible because it won't keep the unit associated with the patient if it is entered as "incompatible." Or I could call them "compatible" and add some caveat to the results.

I can't ever get the "Quote" button to work how I think it should--or at all for that matter. Maybe you could include that secret.

Since this case was originally posted last July--maybe it's time to test the kid again! Of course most moms aren't excited to have their babies' blood drawn so it might be a tough sell.

When was the platelet transfusion and was the donor type O? Do I understand correctly that the eluate did not react with any O reagent cells, but did react with A1 cells? if your sample was drawn soon after the transfusion of an O pheresis platelet, you may be finding passive anti-A in the eluate. It would be pretty much all stuck to the patient's A cells so it is not interfering with the back type. Was the crossmatch by an antiglobulin method or immediate spin? An antiglobulin method might be able to pick up a small amount of anti-A in the patient's plasma, but one would expect an IS xm to behave like the back type. Did you test the patient with anti-A1 lectin? ...Or is this what you meant by Anti-A1 positive? Then the question becomes, "Did you test the eluate against A cells?"