Frequently calling "cold autos"

[kjmt]

I work in a small-to-medium sized hospital with a Blood Bank supervisor that has only worked in the same hospital her entire career. Nearly everyone else agrees that she gets worked up about many things that other experienced techs would not think twice about. For instance, she claims that about 25% of our patient population has "cold autoantibodies" which require extra time to work up and patients ultimately "require" blood warmers because of this. We use the gel system as a primary method of performing antibody screen and crossmatch (yes, gel crossmatch even in patients without antibodies). With the smallest speck of an rbc not completely forming a button, she wants a DAT, antibody panel, and "mini-cold panel" performed. She claims that all of these are cold-autos after nothing else proves significant. Then you are forced to do a strict pre-warm tube every single time due to a "history of cold auto."

Many times it is rouleaux showing up in the gel... and it WILL go away with strict pre-warm tube testing, have a negative panel, negative DAT....but this is not the solution to the problem. A simle tube test, without the extras, would demonstrate compatability/negativity.

The funny thing is this: I had a nurse manager call from another hospital because they were trying to transfuse one of our regular patients. The patient refused to receive blood without a blood warmer. The patient told them that she required a blood warmer at our hospital, and was of course scared what would happen if she didn't use one there. They had no issues with her screen/xm. They did not have a blood warmer on site to use, therefore they called me to ask about her history and reason for blood warmer. This caused all sorts of confusion. The patient has no significant auto and did not need a warmer. It was somewhat difficult to explain to that hospital why we say that she must have a blood warmer, but indeed she does not.

This is only the beginning..... But it all seems like a waste of money, tech time, and leads to patient confusion. Any ideas on how to solve this problem? i.e., how to approach the issue?

[Rh-fan]

Solving this problem will not be easy. Your supervisor sound a little bit hard to convince, and in your words I hear that you are not the only one who thinks this way. Maybe some extra training (technical) and maybe a visit to a bigger hospital or transfusion center is a way to go. Don't suggest that she could learn things there but say that it is always smart to see how things also can be done.

On a technical way I would say that any "trick" you perform in this field only may be used when you now it is needed. Pre-warm (and warm admission) should only be used if you now there are cold antibodies. The fact that you find (very) weak reactions in gel (I assume you mean an anti IgG gel) can be caused by cold-auto but can also be something else (weak allo, HTLA, weak HFA). Before you say the patient has cold antibodies the panel should be reactive at 15-16oC (not at 4oC, then everybody has cold antibodies).

You say the conclusion of cold antibodies is made by “exclusion” of other explanations, that is not the way to practice transfusion science.

In our lab you hardly ever advice to transfuse warm units, and we a national reference laboratory so we see a lot of patients with (very strong) cold antibodies.

I hope I have been helping you a bit, and wish you the best in solving/dealing with the problem.

Peter

[Auntie-D]

Sounds like she isn't up to date in her CPD - found a lot with 'lifers' who are now in charge. IME all will come out in the wash as soon as the lab undergoes and inpection...

[Yanxia]

If an antibody react at 15-160C but not react at 37 0C, then how to deal with it?

[Auntie-D]

If an antibody react at 15-160C but not react at 37 0C, then how to deal with it?

I think Rh-Fan meant that an auto at 4oC isn't likely to be significant but one at 15-16oC could be. If we got an auto and it disappeared at 16oC then we wouldn't recommend a blood warmer, if it stayed we would.

[Rh-fan]

Reactivity at 16oC to RT is a labortory problem en not a clinical problem, so the problem should not leave the lab, so no blood warmer. The cut-off for clinical significant for cold antibodies is at 30oC (but testen after prewarm (at 30oC) and 30oC centrifugation (30 minutes and no aditives (like albumin or LISS))). reactivity at that temp can couse in vivo destruction of red cells. Non reactivity will cause no destruction.

[SMILLER]

We aslo went overboard on a number of things like this when we first started with gel, and then backed off a bit policy-wise.

But I think you have an administrative problem. I would think you would have to ultimately have to have your pathologist decide what Lab policy is, especially for a high-visability area like the blood bank.

Having said that, you probably do not want to go over your manager's head. I am guessing that neither your manager or pathologist will appreciate going outside the chain of authority on a policy issue. I would suggest that somehow you need to take time to get your manager to at least understand your point of view, and then casually suggest you talk it over with your pathologist. Good luck.

[xyzcaa]

GEL tech will not tell you anything about CAA and you cannot confirm this antibody is CAA without resorting to PEG/LISS. In case of PEG, for a typical CAA, your immediate spin will give you all positive reaction. At this stage, you may want to rule out roleaux just in case. Then you carry to AHG and you most likely get positive reactions. At this time, you switch gear to 1 hour prewarm or 2 hours strict warm (shaking tube, not centrifuging). You will get negative reaction at AHG. If still positive, you need cold adsorption. Also CAA will interfere your ABO typing and DAT. Prewarm red cells and reagents can fix. DAT IgG negative. use blood warmer if CAA showing.

[Barbarakym]

Currently we only call something a caa if the auto control is positive at IS ( room temp.).

Otherwise we call these irritating reactions cold agglutins (assuming tube abs is pos at is)

Our flowchart:

Gel abs pos=. Gel panel=. Now if gel auto is pos= tube auto. If tube auto is pos we evaluate.

If gel panel has neg auto control= interpret. If all clinically significant ab ruled out and no pattern on panel of lower incident ab we call this non specific ab and just do AHG Crossmatch.

Ortho gel system frequently has what I call garbage. High plus, plasma particulates as well as things mentioned will cause pos reaction. What does it matter in real life tech as too much to do and not enough time. In real life it is most important I think to make sure blood is compatible. And thus rule out CS abs.

Cold for us we do not try to Id in general. Tube is abs is called cold.

[Auntie-D]

Barbarakym - I'm glad I'm not the only one who thinks Ortho gives nonsense results. I'm a Diamed girl through and through

[Deny Morlino]

Biorad is due to enter that market in 2012 I believe. Ortho's lock on "gel" in the United States expires this year I believe. Will be interesting to see how this all plays out.

[Auntie-D]

Biorad is due to enter that market in 2012 I believe. Ortho's lock on "gel" in the United States expires this year I believe. Will be interesting to see how this all plays out.

Diamed in the UK now uses Biorad for their reagents. I've been suitable happy with them.

[Deny Morlino]

Good to hear that. Looking forward to more than one player in the column agglutination arena.

[Auntie-D]

Good to hear that. Looking forward to more than one player in the column agglutination arena.

What I should have said is tha Biorad have bought out Diamed...

[Barbarakym]

Reactivity at 16oC to RT is a labortory problem en not a clinical problem, so the problem should not leave the lab, so no blood warmer. The cut-off for clinical significant for cold antibodies is at 30oC (but testen after prewarm (at 30oC) and 30oC centrifugation (30 minutes and no aditives (like albumin or LISS))). reactivity at that temp can couse in vivo destruction of red cells. Non reactivity will cause no destruction.

Actually I thought 37 C was significatnt. Normal testing in most labs is RT and 37 (heat block). We don't worry about a cold unless it shows up at coombs. Have never had a problem. That is body temperature.

[Rh-fan]

Actually I thought 37 C was significatnt. Normal testing in most labs is RT and 37 (heat block). We don't worry about a cold unless it shows up at coombs. Have never had a problem. That is body temperature.

Not the hole of the body is 37C, only the core, in some parts it can be lower, down to 30C. Then some cold antibodies can bind and couse destrunction of red cells.

[Barbarakym]

I have worked 5 hospitals. 3 top tier. Not one tests at 30. Nor do I find it in AABB technical manual. Did I miss it somewhere? Plz reference?

[Malcolm Needs ☆]

It is in Petz LD, Garratty G. Immune hemolytic anemais, 2nd edn. 2004, Churchill Livingstone, in relation to "cold" auto-antibodies, and whether or not they are likely to be clinically significant to the patient, when the ey are writing about Cold Agglutinin Syndrome, Page 71 and onwards for a few pages. On page 71 they state,

"The clinical manifestations vary greatly from patient to patient, probably depending on the thermal range of the cold antibody. Clinical symptoms are more serious for patients whose cold agglutinin is active at higher temperatures. Temperatures of 30oC and lower are normally attained in the superficial skin vessels of those parts of the body exposed to cold air or water. The thermal range of the antibody is more important than the aggluination titer for clinical purposes." I've left out all the references they cite!

Certainly, in my Reference Laboratory, we always test for the thermal amplitude of the "cold" auto-antibody at 30oC, but I cannot remember the last time we performed a titer or a specificity.

[Rh-fan]

Thanks malcolm,

I was still looking in the books (Petz and Garratty) and just have found it, but you beat me by more than 2 hours.

Peter

[Malcolm Needs ☆]

Well, I did a review of the book for the BBTS, so I know it pretty well!

[Auntie-D]

Ha ha after all I said in my post earlier, we get one in the lab and I still err on the side of caution until it is confirmed lol

[Barbarakym]

It sounds like reference lab testing. At what point do hospital labs decide a cold is important enough to send to a reference lab (costly). My heat blocks don't even adjust to 30.

What we do presently is if mf in gel or back type doesn't match front type is we go to tube testing and include an AC. This gives us IS readings (and an o cell), 37, AHG , cc and pt control.

If reactions are only in IS Phase, AHG is negative then we call it a cold. We do XM to coombs while cold is showing but other than that we are done.

Only time we send colds to ref lab now is when cold interfers do much we can't get typing we are comfortable with or rule out all clinical significant antibodies or get compatible blood.

In 20 years in a 500 bed hospital we have never had a problem with any cold handled this way. Do people working in regular service hospital blood banks do any different? At what point do reference lab techs advise people who call in on a busy night with an interfering cold to send it in rather than try and work it up themselves? I know ARC always gives us tips to solve it myself and I have never been told to inc at 30 or send it in. Just wondering in real world work. Want to do what's right. Also have to worry about cost and delay to patient (ARC workup min 12 hr delay, often longer).

[Rh-fan]

I agree that a investigation of reactivity at 30oC is not nessecerry before transfusion but is needed to determine if the antibody is causing red cell destruction in the patient. Our work is not only getting the right units of blood but also give info to the MD on proper treatment of the patient. That is for reference labs and for hospital labs. Treating a patient (to lower the red cell destruction) is alwas better that give a transfusion.

[Barbarakym]

Do you work in a reference lab? If in a hospital lab what area do you work where you have budget for explorative testing? I wish it were like the old days. But now if dr orders Tc2 units we get reimbursed just straight $$ with 1 extra charge for antibody workup and that's if pt has ppo insurance. Medicare/*** only reimburse by diagnosis. Explorative (why) can be ordered by drs and we will do it but if they do it too much medical review steps in. I hate all this budget stuff but we are fighting to keep staff and stay open. So sad.

I can justify, for my dept, sending workup to reference lab in order to get blood for pt. That's it.

Even our bench workups are now severly restricted. No more enzyme panels bought or special reagent. Bo more elites here. Cost analysis has determined that it is cheeper in tech time and supply time to send the occasional pt out when blood can't safely be found here than stock, staff, and competency test on house. Yes. It used to be funner.

Actually I think even ARC ref lab is having much the same problems as they have cut back on lots of available tests (as determined by what they bill us by) quite a bit and when called try to get us to do stuff here to resolve (staffing on their end?). Sign of the times?

[Malcolm Needs ☆]

As Rh-fan says, if the cross-match is compatible at 37oC, for transfusion purposes, the transfusion is as safe as any transfusion is safe.

However, if the antibody is a "cold" auto of wide thermal amplitude (is detected at 30oC or above), it is clinically significant. The think is, on occasions, a "cold" auto of wide thermal amplitude can mimic a warm AIHA, but the preferred treatment for these are different, and so it is vital for the clinician to known with which they are dealing. Therefore, although I have every sympathy with your position, if I were you, I would try to pursuade the doctor looking after the patient that these tests are, actually, vital, in order to diagnose the type of auto-antibody (warm, cold or mixed), so that the correct treatment can be given. If the correct treatment is given, in the long-run, it may actually be cheaper for the insurance people.