On 4/19/2019 at 8:30 AM, AMcCord said:

Those things are not big budget items. Once they come, new thermometers go into service, old ones are removed and discarded, new certificate goes in notebook, old certificate goes into archive file. I decided a couple of years ago that I am too hard pressed for time to check calibrations on things like thermometers.

Do you use liquid-in-glass thermometers ? If so, spirit (alcohol) or mercury ?

1 hour ago, Malcolm Needs said:

exlimey, again I agree, but it depends where Jennifer G is based.

NHSBT used to give out units of blood containing anti-D (and some other antibodies, as long as they were weak), but that is no longer so.  Since variant CJD raised its ugly head, we are no longer able to take blood from donors who have themselves been transfused (there are a few strange rules about when the blood was given, etc, but that is beside the point).  Because of this, and the fact that donors cannot be relied upon to be 100% honest (or simply don't know), so that we don't know if the antibody is as a result of a transfusion, a pregnancy or "naturally occurring", we destroy any units containing antibodies of any sort (with RARE exceptions), in case the antibody is the result of a transfusion, and it gets out into our untransfused inventory.

Interesting. My perspective is from the USA. I assume then that the donors with detectable antibodies are permanently deferred ? That must put a hurt on the supply of Rh-.

Another remote possibility: Passive anti-D from one of the transfused units ?

Most facilities are shy about transfusing red cells from donors with antibodies, but some of the savvy hospitals will get "favorable pricing" on Rh- units with anti-D. Since the Rh- unit (with anti-D) is typically going to an Rh- patient, the presence of the antibody is not usually a clinical problem, but may turn up as a laboratory anomaly. The amount of residual plasma in today's red cell products is very low, but a strong anti-D might show up post-transfusion and would probably only be seen be temporarily. You would have to look the timing of the transfusions and collection/detection of the anti-D-containing specimens. If you see a pattern, your blood supplier may be able to determine if any of the transfused units were from donors with anti-D.

1 hour ago, Malcolm Needs said:

Totally agree exlimey, however, another question I have is, ws a DAT performed when the "anti-D" was detected?  I also have another suggestion, to go along with your question about platelets, and that is it could be that one of the units was from a donor with a DEL phenotype.  Unless elutions (obviously) or molecular techniques are used, this may never be known, but it is known that some types of DEL can cause primary stimulation, but that the anti-D produced in these circumstances is very weak.  As you say exlimey, as the patient is elderly (and ill), the patient's immune system could be compromised.

Excellent points. The diagnosis, i.e., the reason for transfusion, might also give a clue. I also thought about RH-IG, but I can't think of a traditional use for that product in an elderly patient.

It might be a transient autoanti-LW, only reacting with D+ cells.

Genuine examples of anti-D are usually more persistent than the situation you outline, but never say never. An elderly person's immune system may work in unpredictable ways. On a related tangent....if it is a "real" anti-D, I would wonder about the source of immunization - I'm assuming D- RBCs were transfused. You do not mention platelet transfusions.

2 hours ago, Malcolm Needs said:

If you put a drop of blood on something like a filter paper, and then add a drop of 1M NaOH, if it is adult blood, after a couple of minutes it will turn a sort of yellow/brown colour, as the Hb is denatured by the alkaline, whereas, if it is blood derived from the baby (including cord blood), the red cells will stay red, as HbF is not denatured by the alkaline for much longer.

It is rather like doing a Kleihauer, but by "bucket chemistry", as it is known!  

Nice !!! Old School.

12 hours ago, SMILLER said:

I think the idea that there is a odd antigen on the reverse A1 cells  that is reacting with patient IgM is probably the case here.  In fact, come to think of it, I believe we have come across this sort of thing has happened before.  (The previous ABO typing was actually done 6 months ago at another hospital).

Scott

If by "odd antigen" you mean a low incidence/frequency antigen on that specific A1 cell/donor, it should be easy to resolve using another A1 cell (or set of Reverse Cells) - the forward and reverse would compliment each other. However, if everyone is having problems with this patient, it's unlikely to be the reverse cell(s).

Is the GI bleed due to ulcers ? H. pylori, perhaps. I think I read that some folks with H. pylori make cold autoantibodies.

2 hours ago, SMILLER said:

Reverse O cells are negative with this patient's plasma.  I should also note that the (tube) poly DAT was about a 1 or 2+, with a negative anti-IgG.  We don't do anti-compliment testing.

Scott

So the A1 cells are reactive, but the O cells are nonreactive. Interesting. I would have guessed autoanti-H, but that doesn't fit. Have you tested A2 cells ? Might be a weird compound antibody like anti-HI - needs the presence of both antigens to react well. Have you looked at something simpler, like anti-M, for instance ?

The DAT results suggest IgM/complement binding, but as you imply, further testing is required.

I agree - sounds like a cold auto, probably IgM. The IgG-gel cards are not exactly good at detecting IgM antibodies, Perhaps that's the reason for the nonreactive screens ?

What do O cells do in your standard version of the "reverse"?

Where are the lights ?

Along the same lines......the basis of my personal safety approach: "If it's wet, and NOT yours, don't touch it."

12 hours ago, pinktoptube said:

Bringing this back...

When a manufacturers states a product is accept for 1 month once opened. How do you calculate the expiration date? 

 - Would it always be 30 days from the day opened?

- Would you alternate between 30 and 31?

- Would you could 4 weeks?

- Do you count the date opened as day 1?

 

 

My two cents: One CALENDAR month........If you open something on the 15th, it expires on the 15th of the next month, regardless of how many days are in the current month.

But...... you have to be careful to not open something on the 29th, 30th or 31st of January..., or the 31st if the next month has 30 days....

I'm sure there are lots of variations between both Complement content of sera and the number "binding sites" on red cells. I suspect others on this site can provide references.

This is assuming you are using the same antiglobulin reagent each time: To even out the variations, I suggest you use a pool of Complement sources (3 - 5). You may also consider using a similar pool of red cells. This may help lot-to-lot consistency. Ideally, in a perfectly-controlled world, one should use the same Complement source(s)and red cell source(s) each time you prepare a batch.

7 hours ago, KBBB said:

The supplier of the panels and the storage solution is the same.  Supplier says no one else is having a problem.  If we have 2 sets of the same lot of panel, we have seen vials in one set go dark while the same vials in the other set is fine.

Interesting. I like the "no one else is having a problem" line - the implication being that the problem is a result of something done by the end user.

Random contamination (darkening) seems to be the bane of red cell manufacturers. Often, the randomness is exactly as you describe: one vial bad, another of the same batch is fine. It's very difficult to pin down a cause - could be their storage solution, could be inadequate sterilization of the containers/droppers, could be shipping, etc. I doubt there will be any resolution. I would send them pictures and ask for replacements.

Is the supplier of the affected panels the same as your source for Red Cell Storage Solution (Alsevers)?

15 hours ago, Darren said:

Do people call antibody screens negative if they are 1+ or 2+?

An EXCELLENT question Darren ! I look forward to some interesting debate.

I agree with Malcolm - the IgG/IgM nature of the antibody is not relevant, and I would avoid tests with enzyme-treated cells in patients with confirmed WAIHA, especially after adsorption procedures. I know that some workers also avoid PEG when testing adsorbed serum in these cases, opting instead for LISS or even saline antiglobulin tests on the adsorbed serum.

1 hour ago, Malcolm Needs said:

How on Earth can one body claim to "own" a procedure, if that procedure is 1) almost universal throughout the world, and 2) if the proper procedure is there to enhance patient safety?  It seems absolutely preposterous to me (if I were them, I would be very flattered that people wanted to follow my example/direction, UNLESS of course, they are unsure of what they have written vis-a-vis patient safety and are frightened of being sued if something goes wrong.

Short (facetious) answer: $$$$$$$$$

Long answer - my opinion - Facilities required or choose to follow AABB Standards (and therefore get an inspection) are required to pay for/buy said standards. At the very least, they are "institutional members" that pay an annual membership fee. The AABB Standards are very different from the Technical Manual (in which the universal, public domain procedures reside). I may be wrong, but I think the standards get some kind of tacit approval by the FDA, whereas the TM gets peer-review. Of course, both documents/books are available to anyone for a fee......

58 minutes ago, Johnv said:

You use a less sensitive assay method to reduce interference with cold and warm auto antibodies that you have shown or proven are not clinically significant, with the idea that a clinically significant allo antibody like Kell, if present, will shine through.  It's a balancing act.  

Thank you, Johnv. I know the science.

14 hours ago, AMcCord said:

Our primary method is the Echo. I use PeG for tube testing, with LISS available for working with warm autoantibodies that love PeG and solid phase too much.

Isn't it fascinating that we're "allowed" to deliberately use a less-sensitive assay when "we" feel it appropriate? Offhand, I can't think of anything similar in other path disciplines. Anyone ? Anyone ?

And..... go........

My interpretation: Users of POLYSPECIFIC antiglobulin reagents are obliged to verify performance each day of use, i.e., QC should involve use of IgG-coated cells AND Complement-coated cells. This gives the user confidence that the reagent is performing as expected.

During routine testing, addition of IgG-coated cells to negative tests is sufficient to verify that the IAT was performed correctly - correct/effective washing, the antiglobulin reagent was added and is reactive, etc.

If it were a requirement to add IgG-coated cells and complement-coated cells to every negative IAT using polyspecific antiglobulin, it would be necessary to run everything in duplicate - one set would get IgG-coated cells and the other set would get complement-coated cells. I don't think that is the case.

22 hours ago, saralm88 said:

Hi friends!

I just wanted to get a feel for what different labs are using.  We have the Echo and Neo (new) and have been using LISS for screens and xm.  I am switching to using PEG because Immucor says it is the best to use when having the machines.  What does everyone else use out there? 

I hope everyone is having a great summer!  I look forwards to hearing from you - hopefully I can get on here more and give more input of my own!

Thanks!

PEG-IAT is arguably the most sensitive tube test currently in widespread use. For this reason you're more likely to see concurrence with your Echo/Neo results if you use PEG for supplementary testing, i.e., the sensitivity of the two assays are perhaps the closest (LISS being less-sensitive). However, there's still a chance that the Echo/Neo will detect something that is not detected in PEG (or LISS).

I wonder what Immucor would say if you decided to use another manufacturer's PEG reagent ?

On 7/6/2018 at 4:35 PM, Cliff said:

Folks, please read this carefully, I suggest he is saying it is acceptable to call him Malcolm, as compared to Mr. Needs - hence informal.  He did not suggest he would find it acceptable to refer to him as a tosser, wanker, or some other (really cool sounding British) pejorative. 

I need to move to England, if only for a short time.  American English is so boring.

I think the term "Chav" has recently become popular. Even more recently, calling someone "a right old Neymar" is not very flattering.

As the Irish writer George Bernard Shaw once said: "England and America are two countries divided by a common language."

15 hours ago, TreeMoss said:

The physicians would use cold cardioplegic solution -- 4 degrees - when putting the patient on bypass.

Wow. Thank you for that information. That certainly could influence the concern some of the medics demonstrate. Is the surgical room also chilled ?

10 hours ago, rravkin@aol.com said:

Hi Scott and Exlimey, perhaps the idea of a hemolytic reaction is remote when considering cold agglutinins but if the patients body temp and OR temp are below normal body temp and room temp respectively, and, if the cold agglutinin is strong enough, either by way of concentration therein of bonding strength, does the cold agglutinin not have the capability of causing rbc agglutinins to form and remain stable long enough to cause damage to the microvasculature in the same manner as with Lupis Erythmatosis.?

That is exactly the theoretical risk that concerns the medical staff, but in my non-medical, laboratory-based opinion, the risk is extremely low. Extreme testing protocols (below 30 C) for cold-agglutinins are rarely informative, often having very specious clinical relevance. Does anyone really know what the results mean ? How high must a titration be to be significant ? If you look hard enough, you can find cold-reactive autoantibodies in most people, hence why routine testing protocols now deliberately avoid test phases below 37 C. Modern, super-sensitive test systems (PEG-IAT, CAT) don't even allow tests below 37 C and openly admit that IgM antibodies may not be detected (typically the form that "colds" take). Even with these "deficiencies" they still are licensed/approved for antibody detection and ID.

If a patient is in such a dire situation that they're undergoing radical surgery, with the selective use of hypothermia and/or by-pass procedures, the least of their worries is a cold agglutinin.

The easy fix to the transfusion of "cold blood" is a blood warmer, but obviously this would be contraindicated during hypothermic processes.