Joanne P. Scannell
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Posts posted by Joanne P. Scannell
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I agree with Mabel ... you did 'the right thing'. What did he/she really expect a reference lab to do with this anyway?
And, as she reminded, we do 'rule out' clinically significant antibodies with one homozygous (with exceptions, such as Anti-K which doesn't show much dosage anyway) every time we have a negative Antibody Screen.
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True ... agreed.
My point was that we shouldn't 'jump' to the conclusion that a baby is an A3 just because mixed field reactivity is present without considering the testing platform/sample and the possibility of maternal-fetal bleed/contamination.
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Just a thought:
How are you testing these babies? If you are using cord samples or if there were some maternal-fetal bleeding (how was the birth?), the child you are tagging as an A3 because of the 'mixed field' reactions may actually be a normal Group A ... the mixed reaction due to maternal red cells in the cord sample/baby.
If you are using MTS, this is obvious and I know there is some literature out there illustrating this warning because it is a change from what we were taught 'way back when', i.e. that cord samples/babies may have weaker reactions with Anti-A and/or Anti-B ... but that was the days of tube testing. Today, we know better.
Which parent is Group A1? What is the mother's blood type?
I'm with the group suggesting to use Group O to circumvent this question ... but then, you have this directed donor to deal with ... a more psychological than a practical problem.
On this same line of thought, I assume that you would also give type A1 blood in the following scenario: Twins <1 month old at our hospital. One is type A (positive with A1 lectin), and the other is possible type A3 (mixed field reactions with anti-A, has not been transfused, negative with A1 lectin). Neither has anti-A1 in their serum at immediate spin or IgG. We have a directed donor type A1 unit from one of the parents. Unit is fully compatible with the A subgroup twin. Do we give the directed donor unit to the A subgroup twin? If so, should we get specimens every 3 days to ensure that the baby doesn't start making anti-A1? I know that babies don't normally make anti-A until 3-6 months, but I'm not sure I want to take any chances. -
We have a similar situation with our 'Cancer Center'. The patients keep the bands on ... no more than a month because the policy is for them to re-register monthly. I don't know why that is.
New band = new Pretransfusion specimen = new ABO/Rh typing.
What do you do about OP transfusions of platelets for patients that get them once or twice a week for years? Do you have special rules for OP transfusions? Do they keep the band on for a month at a time and then you redraw and retype them? Or??? -
This is EXACTLY why we require a BB Band ... attached at the time of draw and must be intact.
You never really who who's in the bed ... the BB Band links the patient to the specimen. Once the band is removed, no more link = no more transfusions until a new specimen is obtained.
It's a pretty sad world where we have to have people cheat the system in order to get healthcare.
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We BB Band all pretransfusion specimens/patients ... as long as they are wearing that BB Band, they can recieve plasma products (plasma, platelets, cryo). W
nb. We have patients who move between our facilities that we service so to say 'this admission' is not applicable.
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Am I 'hearing' this right? So when manufacturers state that testing has to be performed within x days (and they always say that donor units are ok until outdates), there is NO scientific evidence for these statements?
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CAP and FDA.
Out of curiousity, who accredits your transfusion service? -
We don't have a refrigerator in the OR.
Our promise is that blood will be ready in 5 minutes. We do what we need to do to fulfill that promise, e.g. crossmatch ahead if the patient has clinically significant antibodies.
(In those cases, we automatically set up 2 and call the surgeon ahead of time to see if more is necessary.)
Basically, they call for blood and then come get it ... they have no idea what we are doing in the BB.
Joanne, what do you do about surgery cases? We have a blood fridge in the OR and they routinely take units down there and bring back those not needed. Did you have to train them not to take blood unless they planned to transfuse it? How were you able to convince them that they would have blood available before the patient "bled to death"? -
Sunquest with Invision.
Ordering via various vehicles ... e.g. CPOM.
We are in the process of changing Invision to Epic.
Joanne, what LIS and HIS do you have at your facility? what order entry system?Thanks, Amelia
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Yes.
00:01 Jan 1 will expire on 23:59 Jan 4.
AABB 5.13.3.2
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AABB changed 72 hours to 3 days many years ago.
Date of draw being Day 0.
This way, the specimen expires at midnight ... just like everything else.
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I agree ... instinct/training/experience has it's effects. It comes down to 'When in doubt, don't rule it out'. We have a whole set of LIS codes for 'Possible Anti- ___' because of this. And yes, they function to restrict allocation of antigen-pos/antigen-untested RBCs.
Aside from that, the basic answer to the original question of this thread is 'Do not rule out using heterozygous cells.'
My conclusion from all of this is that you can have some rules of thumb as you start interpreting an antibody ID but it often moves into a realm of knowledge and judgment that you just can't write rules for. -
Lalamb ... who do you buy your panels from? I need larger panels.
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What happened to the 'good old days' when we used to call the floor in the middle of the night to tell them that unless this was a life-threatening situation, the transfusion will occur during the day?
Tired patient? Go to bed, go to sleep.
Poor Malcom! How did your patient pan out? More antibodies (a responder, for sure!).
More support for transfusing 'phenotype-identical' to these frequent flyers? (Was this patient phenotyped?)
I've worked all day, and am now on-call.The one on which I am working is a sickle cell patient who (literally) walked into hospital feeling a little tired, with an Hb of 29g/L. She is known to have an auto-antibody (she certainly has!!!!), with an anti-E+Fya underneath, and has had episodes of hyperhaemolysis. Just what I want at this time of night (now just gone 3 in the morning)!!!!!!!!!!!!!!
I'm just about to see if her B cells have been "encouraged" to pop out another specificity, prior to cross-matching. I do so hope not. I'm tired and hungry, but this promises to be at least a three mug of strong coffee case!!!!!!!!!!!
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We do not use heterozygous cells (with few exceptions, e.g. Anti-K, -Cw, -Lua) to rule out. I have several examples of clinicaly significant antibodies that react ONLY with homozygous cells in our files.
I got validation of this concept at an AABB session in Baltimore, MD (was that 2005?). A well known reference lab mid-USA was presenting case studies and a big 'take home' was 'Do NOT rule out with 'heterozygous' cells!' In fact, be wary of ruling out with 'all' 'homozygous' cells because what may appear 'homozyous' on the panel sheet may actually be 'heterozygous' with an allele that is not tested, e.g. Fya+/Fy3 is not 'homozygous' for Fya even though it may appear that way on the panel sheet being displayed as Fya+/Fyb-.
nb I'm using semi-quotes because we are not supposed to be using 'zygosity' for expression of an antigen ... but we all do.
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Helmer by a long shot!
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Lots of ideas presented here.
Basically there are these possibilities and they all need to be considered/investigated:
1. Specimen from prenatal/previous testing was mislabeled, e.g. someone else's blood.
2. Tech made an error somewhere along the testing path or recording during the previous testing.
3. Tech made an error somewhere along the testing path or recording during this testing.
4. Sample 'today' is the 'wrong' patient ... misdraw, misidentification or maybe another patient who is not who she says she is (e.g. using someone else's insurance card, it happens a lot in my area).
5. You are picking up a large fetal-maternal hemorrhage.
6. Patient is Rh Pos (weak D).
Possibility 1 + 2: Cannot be determined at this time.
Possibility 3 + 4: I'm assuming you've investigated these already.
Possibility 5: A KB Stain and/or Fetal Hemoglobin Assay could answer this question.
Possibility 6: The content of Anti-D reagents differ quite a bit, so we cannot expect the RBCs from some patients to elicit the same results if we change reagents. The 'Ortho vs Immucor' reagent difference has been expressed in here, but this goes for other manufacturers as well. Check out the information in the Quotient website about their various Anti-D reagents (beta, optimum, delta, etc.) as an illustration of the vast differences of detection capabilities. And this includes, as someone brought up in here, technique and timing. It all depends on what you want to see (DVI, for example) and how you want to see it. (Note that some Anti-D reagents do not require an AHG phase to detect 'weak D', some don't even require an incubation, some pick up DVI while others won't, etc.) So, in order for you to address this possibility, you need to find out what reagents were used and what is their capibility.
'nuff said?
Did I forget anything?
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I see.
We eliminated the 'crossmatch x units' orders ... they don't exist in our system. No purpose for them.
The only orders the MDs have to choose from are 'Transfuse RBCs', 'Transfuse Plasma', etc.
The MDs are oriented to this ... order only what you want to transfuse.
I must add that when we are performing pretransfusion testing for pre-ops, if the patient has atypical antibodies, we DO crossmatch 2 units and we call the surgeon to see if he/she thinks that more will be needed for the particular surgery so we can be ready with them ahead of time.
So, if you can change your order description to read 'Transfuse Red Blood Cells' and orient your staff, you can eliminate the double order system (crossmatch + transfuse) = less work for BB and the MD.
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Point taken.
But ...
... if the antigen on the donor cells deteriorated to the point where a demonstrated strong, freshly produced antibody cannot detect it, why would an old chemically rich reagent be expected to be better? Some of these reagent antisera actually deteriorate over time as our QC records show ... which is why we have to do QC using reagent RBCs on each day-of-use.Aside from storage issues, reagents from different manufacturers/cell lines/clones do not always correlate with each other.
The QC is the same:
Patient Plasma vs reagent RBC and vs donor.
Reagent Antisera vs reagent RBC and vs donor.
So, I put more value on a 2+ fresh antibody produced by the patient who is going to recieve this unit than a 1+ reaction from a stored reagent approaching it's outdate that is not really guaranteed to detect all antigen variations.
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Yes, well aware of the zygocity issue.
Ok, bear with me while I clarify our criteria:
n.b. We are using MTS, so testing is very sensitive and standardized.
During Antibody ID, we run heterozygous cell(s) to establish whether the patient's plasma will react at least 2+ (MTS).
We perform an extended crossmatch (MTS).
- If the antibody fulfils the above criteria, the extended crossmatch is sufficient (no further testing).
- If not, reagent antisera must be used to verify the absence of the antigen.
Our CT Ratio is 1.3 ... we have a lot of oncology/antibody producers.
- If the antibody fulfils the above criteria, the extended crossmatch is sufficient (no further testing).
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CT Ratios don't mean what they did many years ago. Back then, we crossmatched upon request ... mainly because in those days, we had to do a 'full' crossmatch every time creating a natural delay between order/need and crossmatch.
With the implementation of 'immediate spin only' crossmatches, the meaning of the CT Ratio changed.
Today, we (in 'my' hospitals) crossmatch only under the following conditions:
a) An order to actually transfuse (i.e. there is no such thing as 'hold')
Patients with atypical antibodies that would require a search that may take longer than, say, a half an hour OR for patients who are going to surgery (we have a 'we'll get you blood in 5 minutes' promise so we do what we must do to maintain that).If a patient has atypical antibodies, sometimes, if certain criteria are met, we use the patient's plasma to screen the units. Since we have to allocate those units in our LIS, they are counted as a 'crossmatch'. This will skew our CT Ratio.
In addition, we crossmatch all Autologous Units (why wait?) ... another skew (but very minor).
So, the CT Ratio is not a universal standard, it is more of an internal indicator of activity. For us, increases are usually simply because we've had more than usual patients with atypical antibodies that we are able to use patient plasma to crossmatch with (i.e. not use expensive reagents).
Example: The CT Ratios for Cardiac OR and the Main OR run higher than the floors ... that's a given based on what I just told you about our protocols.
The CT Ratio is no longer a punative measure for the ordering physicians.
If you want to bring your CT Ratios down, then you need to look at your BB protocols and stop crossmatching when you don't need to.
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Ditto ... i.e use the same protocol as you would for a 'routine' transfusion ... whatever that is for your facility. Here, we require 2 techs/2 blood types on only BB Banded specimens.
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Did you run the eluate with MTS? MTS is changing a lot of the 'old rules' we grew up with and I do remember something about 'A1 not being a pure antigen' ... hmmm, ok here it is in Peter Issitt's book: " ... the difference between A1 and A2 is primarily quantitative, meaning that A1 and A2 cells carry different amounts of the same antigen." So, yes, you can 'type' A2 cells as A1 positive if you use a very sensitive method, e.g. MTS.
I agree with the others:
You have a patient who is now making Anti-A1 and it has attached to the donor cells.
Ah, life was so much simpler when we had very simple tools to play with!
My thoughts: Given that all this discussion is 'merely academic' (Hey, this IS how we have fun, right?) ...
a) report the antibody as Anti-A1 (if it reacts at 37C, it is 'clinically signficant') for now
give him O cells for the next few months to eliminate the confusionc) if this patient continues to have a positive IgG-DAT due to Anti-A1 after all those A1 cells are out of his system, then I'd change it to an auto-antibody and transfuse accordingly.
Keep us posted about how this goes in the future, ok?
... if the antigen on the donor cells deteriorated to the point where a demonstrated strong, freshly produced antibody cannot detect it, why would an old chemically rich reagent be expected to be better? Some of these reagent antisera actually deteriorate over time as our QC records show ... which is why we have to do QC using reagent RBCs on each day-of-use.
Patients with atypical antibodies that would require a search that may take longer than, say, a half an hour OR for patients who are going to surgery (we have a 'we'll get you blood in 5 minutes' promise so we do what we must do to maintain that).
How would you have handled this?
in Transfusion Services
Posted
Ditto and ditto!