exlimey

Basically there is a bias with the selected samples. I would not be picking a patient with a SPD (Solid Phase Dependent) antibody to compare with manual tube methods. We pull samples that have already been run on the Echo and repeat them in tube testing. I also include a "disclaimer" of sorts in the SOP by stating that the methods may not compare 100% due to the sensitivity and specificity of each test method. The goal is not to achieve perfect correlation, but to document comparable results given the difference in sensitivities, specificities and general limitations between the methods. As we all know and love - no one method will always detect all clinically significant antibodies!

They're handling the transport bag though David.  We don't have staff wearing gloves in public / visitor spaces (e.g. elevator).  It would look like they were in a contaminated area and forgot to take them off when they left.

Perception is important, but education can help smooth over the concerns. I think it's important to remember that the outside of the bag "lost it's shine" as soon as it left the shipping box and was used to collect blood. There is nothing sterile about a church hall, a high school gymnasium or any other of the myriad of places blood is collected. I wonder how hospitals reconcile the fact that "dirty" blood bags are transported into and used in their super-clean surgical suites ?

You could always irradiate the blood bag (as well as the blood), while the stupid nurse is holding it!!!

This is directly from the AABB recommendations:
 
Consequences of current practice
Current practice for testing and interpreting Rh typing results appears to be highly successful in preventing alloimmunization to the D blood group antigen and Rh hemolytic disease of the fetus/newborn.4 However, there are unwarranted consequences associated with the practice of avoiding detection of weak D phenotypes, including unnecessary injections of Rh immune globulin and transfusion of Rh-negative red blood cells – always in short supply – when Rh-positive red blood cells could be transfused safely. If all pregnant women in the United States with a weak D phenotype were identified and their RHD genotype determined, an estimated 13,360 pregnant women who are currently managed as Rh-negative could be managed as Rh-positive, avoiding 24,700 injections of Rh immune globulin annually.1
Recommendation of the Work Group
RHD genotyping is recommended whenever a weak D phenotype is detected by routine Rh blood typing of pregnant women and other females of childbearing potential. The Work Group rates this as strong recommendation, based on high-quality evidence from observational studies (1A).5 The Work Group also considered a recommendation to standardize routine laboratory methods for Rh typing that would increase detection of all patients with D variant phenotypes, including partial D, as well as weak D phenotypes. While desirable, such a recommendation is technically complex, likely controversial, and would divert the focus from our advocacy for phasing-in RHD genotyping when a pregnant woman’s routine Rh typing detects a serologic weak D phenotype. The immediate benefit of determining the RHD genotype of pregnant women with a weak D phenotype will be fewer unnecessary injections of Rh immune globulin.
It's common for hospital blood banks to treat potential mothers who type Rh (D) positive at the weak D phase of testing as Rh negative. It's not uncommon to hear stories similar to yours where a patient has been told one time they are D- and then another time, D+.  
If you want to get a better handle on your D typing, request that your hospital sends it out for molecular testing.  It can be expensive...ballpark $300...but it is the only way to determine whether or not you truly need Rh immune globulin.

We had a nurse report that she was issued a unit of blood by a tech and they hadn't removed or changed their gloves before retrieving, tagging and handing her the unit.  Now I know that the fridge handle, computer keyboard, and the outside of the unit bag are not "sterile" and the techs obviously wear gloves in the lab.  Aside from changing gloves to issue a unit (which of course still become contaminated by touching the aforementioned) what can be done to hand a "clean unit" to a nurse or courier?  We place the unit in a plastic bag but we're touching that too!  The whole thing is perception - isn't it?

In addition to being a financial and quality issue, I've tried using the ethical approach (donors giving up their blood as well as time, etc.) I can't say it's been successful but I suppose it can't hurt to throw that in to the discussion at each facility.

Thanks for the responses. I read in one article, the incidence of DCT positive among donor is only around 1 in 1000 to 14,000 depend on the specificity of the methods used..i think its about time for my country to omit AHG crossmatch in the procedure..the other argument is that the reagent/screening panel cells is of caucasian origin, so we might missed out some low frequency antigen that are prevalence in our population but not in among caucasian..but again, form our experience, such case is extremely rare. Usually if antibody screening is negative, the AHG crossmatch will be mostly compatible, except in very small percentages will give AHG crossmatch incompatible (and almost all of it are due to DCT positive donor).. 

Oh, I see what you mean, and you are, of course, correct!

A valid point. It is not uncommon to find a spurious positive DAT in a sample collected in EDTA tube, especially in "older" tubes.
My point is that crossmatches use segments (pigtails) and the presence of the sugary-goodness in the collection systems can also cause positive DATs.

I see from where you are coming, but, when we used to test donors for DAT in the UK, it was done on the satellite tubes, where the blood from the arm was allowed to flow straight into EDTA tubes, and only a small percentage gave a positive DAT.

Have not been transfused, and DAT is pos. If this anti-c can be absorbed out by his own cells, then it is  auto antibody.

Personally, I would not worry too much about a donor who has a positive DAT.
We know that a certain percentage of fit, healthy individuals have a positive DAT for no apparent reason, but the fact that they are fit and healthy, and have a high enough haemoglobin and haematocrit to be able to donate blood, and not keel over themselves, means that their red blood cells are almost certainly surviving normally in their own circulation (or, at the very least, the red blood cells are surviving long enough not to compromise the donors health), and they will almost certainly survive long enough in the recipient's circulation to be efficacious, even if they do not survive quite as long as would be expected.  Such red blood cells are most unlikely to be the cause of some form of haemolytic crisis, just because they are DAT positive.
In fact, the NHSBT no longer routinely test their donors for a positive or negative DAT, and we have seen no incidents as a result.

If you are using a commercial anti-D reagent as your starting material, you might be creating your own problems. Most reagents are now monoclonal and as such they often have very peculiar formulations (additives, diluents, etc.) that ensure their stability. When end users dilute or otherwise modify the reagents, they may lose the key element required for reactivity and/or stability (even when frozen).
I suggest you try a polyclonal (human) source (which is probably what Malcolm's group is using). If you need to dilute it to get to the desired reactivity, I recommend using either inert normal human serum or 6% BSA. Both diluents should maximize your chances of stability, either in the liquid state or frozen.

I do not believe giving phenotype matched units allows you to ignore the reactivity that you are observing that may or may not be due to DARA.  I'm not aware of any standard that allows a blood bank to do that.
In addition, giving phenotype matched units can be a waste of a valuable resource.  If a patient needed E-, K-, Fy(a-), that's approximately 1 in 5...no problem. If they needed c-, E-, K- S- Jk(a-) now you are looking at approximately 1 in 50.  That can take time, raise the cost and remove from inventory a valuable resource for patients who actually have antibodies.
Again, I'm not aware of any standard that allows a blood bank to ignore reactivity that is observed at 37C.  Specifically, AABB standard 5.14.3.1 states: "When clinically significant antibodies are detected, additional testing shall be performed."
Section 5.14.3.3 goes on to state: "In patients with previously identified clinically significant antibodies, methods of testing shall be those that identify additional clinically significant antibodies."  No mention of just giving phenotype matched units.
Under section 5.15 "Selection of Compatible Blood and Blood Components for Transfusion", there is no mention of using phenotype matched blood in lieu of performing an antibody investigation. 
Needless to say, lol.... I'm not an advocate for just giving phenotype matched units.

You will probably need to "qualify" the vendor is some fashion, but I don't believe you have to do any serological comparisons providing you are going to use the material according to the manufacturer's directions.

Winter - in the case of DARA patients, the DTT is use to treat (panel or screening) cells rather than the serum.
SMILLER - do you enzyme-treat your own cells ? If so, have you determined their stability ?

You will probably need to "qualify" the vendor is some fashion, but I don't believe you have to do any serological comparisons providing you are going to use the material according to the manufacturer's directions.

You will probably need to "qualify" the vendor is some fashion, but I don't believe you have to do any serological comparisons providing you are going to use the material according to the manufacturer's directions.

Usually reagent antisera has FDA potency requirements.  I just run qc to make certain they react like they are supposed to.  (Plus I run a lot of mine in gel so I verify that they work in that medium also).

We use a saline method where by we use 4 drops of plasma to one drop cells, to super-saturate the cell. Incubate 30- 60 min and use IgG at coombs.
This method has served us well in patients with warm autos. Malcom, of course, went into detail about strong bonds and titers, etc., but I tell my techs that "any self respecting allo- antibody will be detected by this method" -
and yes, I'm old school. So it was, back then, once you have discovered there is a problem, or you have actually detected an antibody, going back  to a saline method is a fine and accepted way to get around the garbage you may be detecting in GEL or other "enhancing" method.
Liz
 

We have solid phase and occasionally get these "warm auto" like reactions.  Doing a tube screen w/o enhancement ( aka 30" saline) is our problem solving method.  If the patient has been transfused we'll do AHG XM just to make sure.  Like Malcolm says, before all these new fangled but convenient techniques people were not dropping dead from every transfusion.
 

The 'DAT neg', 'auto pos', gal auto antibodies are almost always best managed by using a tube technique. The autoantibody may well bind during the tube incubation phase but is eluted away during the wash phase. You usually find that if you do a gel DAT, but add patient plasma to it and incubate like an IAT, the  cells will be IgG coated.

We use the LISS tube IAT daily in my Reference Laboratory, and, in the right hands (i.e. those who are trained to competency, and are able to demonstrate continued competency, in the technique - which, before the advent of PEG, CAT and solid phase, used to be everyone!), it is perfectly safe.  As I have said before on this site, at one stage that was all we had, and the cemeteries were not full of people who had died of transfusion reactions!
In most cases, not all by any means, but in most cases, although the avidity of the auto-antibody is strong, the titre is not that high, whereas most, not all by any means, alloantibodies that are clinically significant, have a higher titre, even if their avidity is not much to write home about.
The technique is even more useful in cases of a cold AIHA, where the cold auto-antibody tends to have a wide thermal amplitude, but rarely can be detected by tube IAT at 37oC, but, of course, clinically significant alloantibodies will be reactive at 37oC.
Of course, in one way, this technique is safer than using alloadsorbed plasma.  There is no way that alloadsorption red cells would be negative for even one high prevalence antigen (such as Vel, Jra, Ata, etc), let alone negative for multiple high prevalence antigens, and so, if the patient happens to have an antibody directed against a high prevalence antigen underlying the auto-antibody, then the antibody directed against the high prevalence antigen will be adsorbed out, just as the auto-antibody will be adsorbed out, and, hey presto, you have a compatible cross-match, and a patient with (hopefully no more than) a delayed haemolytic transfusion reaction.

Basically some labs struggle with QC and the actual intent. They also may have issues with staff not detecting weak reactions, specifically in tubes. Manufacturer's in the US tend to make QC material so strong that it is less likely to be missed. The result is the manufacturer avoids product complaints and the labs do not have QC failures requiring investigation. However, the intent of QC is missed in my opinion. QC should ensure your test system is capable of detecting weak reactions. 
 
QC products manufactured where I work were developed (IgG coated control cells and Daily QC Kit) to detect if there is a weakness rather than just checking a box that QC has been done.