[Least Incompatible units]

We, too, have dropped using the term 'least incompatible' way back when (along with 'in vivo crossmatch', I think) ... been so long, I forgot ... 1970's, 1980's?

 

1. Not all antibodies cause RBC destruction.

2. Not all antibodies that do, cause them in the same way.

3. Grade of reactivity is dependent upon the method and for some platforms, upon the tech performing the test.

4. Grade of reactivity is not proportional to the effectiveness of destruction.

 

I think the only way to determine variations of compatibility is by using monolayer methods = specialized testing.

 

Going back to 'the letter of the law': If the patient has no clinically significant allo antibodies, there is no requirement to perform an extended crossmatch. 

 

So, once this is established either by alternate testing methods (gel is very good at picking up autoantibodies) or differential absorptions, the Immediate Spin crossmatch is all that is required.  Thus, eliminating the need for conversations about 'least incompatible'.

 

If 'no clinically significant antibodies' cannot be established, it is prudent to issue antigen-negative matched RBCs to avoid the possibilities.  Some hospitals do this regardless of the current antibody status just to avoid future antibody production.

 

Of course, if there are underlying antibodies, then an extended crossmatch is required.  This should be performed with the method that was used to circumvent the auto-antibody.  Example: Assume patient has positive DAT.

Gel: All cells positive

Albumin (or LISS or PEG or whatever): Anti-E.

Use Albumin (or LISS or PEG or whatever) to perform extended crossmatch.  If this is negative and the unit is E-neg = compatible RBCs.

 

And yes, this is what we do.

[Positive Autocontrol in gel, negative DAT]

I composed an answer to this yesterday and must have gotten 'sideswiped' before I posted it!

 

Anyway, here's what I have to add to this conversation ...

You cannot compare gel to tube testing.  Aside from the 'sensitivity' issue (DAT could be positive in gel, negative in tube), gel has a totally different premise that needs to be taken into consideration.

• Gel: Slippery RBCs will make it all the way to the bottom of the gel column during a given period of time at a given centrifugal force.
• Tube: Cells must be agglutinated.

1. Therefore, gel results are affected not only by coating of RBCs with antibodies, but also coating (roughening) with just about anything (proteins, medications).  In addition, changes in shape (e.g. sickling, acanthrocytosis, fragmentation) will cause a slower migration to the bottom. 

 

2. You cannot expect an auto control to give the same results as a DAT because the autocontrol has plasma in it.  (It's like all ladies are women but not all women are ladies.) Certain properties of the plasma will affect this downward migration (e.g. artifact, fibrin, TP ratio leading to rouleaux, cold agglutinins).

 

3. You cannot even expect the same 'DAT grade' with an auto vs DAT.  The autocontrol contains the same enhancement medium as the tests.  The presence of an enhancement medium will, ummm, enhance the antigen-antibody reaction.

 

Suggestion:  Don't mix your media.  If Auto Control is positive in gel, don't bother running DAT with tube method; run it using same method as the Auto Control (gel) and be sure to include a 'negative' control using a buffer card with patient's cells.

• If the buffer control is positive: You cannot determine if DAT is pos or neg because the 'positive result' may be due to steric interferrence rather than 'coated with antibody'; check hemo smear for sickling, acanthrocytes, etc.
• If the gel DAT is positive and the control is negative, your patient cells have a positive DAT.
• If the gel DAT is negative, the positive auto could be a result of plasma abnormalities, check protein analysis, cold agglutin, etc.

Hope I haven't overstayed my welcome ...

[Am i missing some thing ? need help]

Are you using the same method for Antibody Screen and Antibody ID?

 

If you are using MTS for the Antibody Screen and Tube Testing for your Antibody ID, the results you describe can happen simply because of the gel situation.

 

(And 0.8% cells are not in the same preservative/diluent as 3% cells.)

 

Just a thought ... some hospitals mix and match that way.

[hematolgy specimens for use in abs/abid]

"He's got a Kell" "A WHAT!?"  ;|

 

Anyway, way down on the screen on this, I forgot the subject!  Oh ... using Hemo specimens for BB tests.

 

Aside from the 'pendantics' (is that a word?) and interesting points about how reliable/contaminated these Hemo tubes may or may not be, I have a concern about the dilutional factor causing a false negative Antibody Screen/ID. 

 

Maybe I'm dating myself but I was told those little lavender top tubes used for Hemo contain liquid EDTA ... enough of which the hemo machine uses a calculation to 'correct' the values.  The pink top tubes used in BB have a 'dry' EDTA in them (concentrate sprayed on the inner walls) so the dilution factor is much less.  This was the reason presented for why BB needed to use pink tops while Hemo still uses lavendar tops when we switched to plastic.

 

No?

[AB plasma shortage]

We, too, got 'the letter' from our blood provider ... and yes, it contained the information about the use of incompatible plasma (e.g. Group A).

 

In a nutshell, we have elected to use Group A Plasma (or whatever is immediately available) instead of Group AB Plasma for the 'unknowns'.   Also, we raised the question of the use of products like Kcentra instead of plasma.  The MDs are hashing that out 'as we speak'.

 

And like others, we are issuing non-type specific Apheresis Platelets routinely (mostly Group A).

 

I think it's only fair to reserve the AB Plasma for the 4% of the population that actually needs AB plasma.

 

And, we too, are wondering just how much incompatible plasma can be tolerated.  If anyone out there knows the answer to that question, please share!

[Natural anti K]

To add another angle to this view ...

 

Has the patient EVER been transfused?

 

I'm thinking this because not only is that the first question I ask, but also because I have a tech in my BB who received 2 units RBC when she was a teenager.  When she was a student in college during her BB rotation, she tested her own plasma and found Anti-K.  Two children later ... no issues.  Now, 20+ years later, her Anti-K 'comes and goes.  It's possible it could show up now and then if her system becomes stimulated ... like maybe by an infection ... hmmm.

 

We forget that antigens are merely chemical combos ... sometimes those combos appear in nature ...

 

 

[ABID: Cold Agglutinin]

Townsend, I just cannot see what difference the cold agglutinin specificity makes due to the clinical signs and symptoms of haemolysis (with the POSSIBLE exception of anti-Pr - and I'm not convinced about that either, and, of course, anti-P in the case of PCH, but then the 2-stage DL test is better for that).

Of paramount importance is the thermal amplitude of the antibody.

Love it!

[ABID: Cold Agglutinin]

I have taught through the years that one should "never" assume something is a Cold Agglutinin unless they prove it (with a cold panel; i.e. Screening Cells, Auto, Cord and whatever Reverse Cells the patient is Negative for). I even have a story of a place with a similar protocol to what you discuss (though much worse).

When I was a Reference Lab Supervisor, we received a "very" hemolyzed specimen on a patient who had a hemolytic transfusion reaction. The Hospital sent their panel work. They did run a panel; and it was a perfect pattern of an Anti-E; but their Policy (and I can only hope they misunderstood it) was that they should try to perwarm it away and if it went away, it was not significant. A week later, we received another hemolyzed specimen from the same Hospital (different patient). This time the patient had a perfect E and c; but again, they managed to prewarm them away (which is another pet peeve of mine.....trust me, I have seen many clinically significant antibodies prewarmed away...by good Techs.; even in large, prestigious Medical Centers....so I tend to be very anti-prewarm except in the right hands). Anyway, I called their Medical Director and told her they needed to "cease and desist" with prewarming before they killed someone (not to mention, teach their Techs. how to perform basic Antibody ID).

Your Policy is not "that" bad in that your supervisor is saying you have first ruled-out major alloantibodies. But let me tell you another problem (sorry to belabor the point). If you use GEL, know that I have seen "many" instances of Kidd group antibodies that not only do not react with any heterozygous cells; but do not even react with "all" homozygous cells. So just saying you ruled everything out, doesn't necessarily mean you did. Not only have I seen that in Hospitals I have worked in; but also in work-ups sent to us at the Reference Lab from Hospitals that used GEL but did not know of this potential problem.

So, I have also taught through the years that even when you think you have ruled everything out, you need to look at your positive reactions and see "what do all of those cells have in common?" You might run into some surprises.

Brenda

 

I think pre-warm testing got it's bad reputation because in the 'old days', when we were running antibody screens that included the IS/22C phases and used polyspecific AHG, if the test was positive at AHG and also at room temp, we would rerun the AHG phase using 'Prewarm Technique' to see if we were seeing a complement fixation due to cold agglutinins or a real IgG antibody. 

 

In those days, Prewarm Technique meant using NO enhancement; albumin wasn't allowed because it was said to enhance complement uptake, which is what we were trying to avoid.  The change from Albumin to 'nothing' lowered IgG uptake, hence the sensitivity ... so yes, of course we were risking losing sight of clinically signficant warm antibodies.

 

The world has changed since then ... we don't use polyspecific AHG anymore, most places don't test at room temperature anymore and prewarming is merely just that - same test only at 37C before you mix plasma with cells.

 

In fact, if using automation (e.g. ProVue), the antibody screens are all pretty much prewarmed because they are sitting in the 37C incubator for at least a few minutes prior to adding plasma/reagents.  So, we are testing 'prewarm' by the thousands daily ... and nobody is fearful about missing antibodies due to prewarming.

 

Prewarming is no longer 'lowering sensitivity' if that is the only parameter that is changed.

 

I agree ... this hospital you cited was mistaken and hopefully has corrected their workup plan:  'Prewarming' away an antibody that is clinically signficant is a strange policy ... similar to 'just shake it harder' or 'repeat until negative'.  HOW were they 'prewarming'?  Were they using the old 'Prewarm Technique'?

 

And yes, thank you for stressing ... we, too, have seen plenty of antibodies that react with ONLY homozygous cells, even in gel. (So please no talk out there about 'eliminating with 3 heterozygous').  

 

And I agree with 'look at what positives have in common' ... we found that PEG will demonstrate a nicer Anti-Jka than gel sometimes, so if you get a hint of Kidd ... or a hint of anything significant, try PEG. 

 

More evidence that we have to carry a 'toolbox', not depend on one reagent/platform/technique. 

 

And that we cannot take all the old 'rules' and apply them to all the new processes.

[ABID: Cold Agglutinin]

I agree with the cautions ... here is what we do for your consideration:

 

Our pretransfusion testing includes a test we call 'O CELLS'.  (This is a pool of the 3 cells from the 3% Antibody Screen).  It essentially replaces the old I.S. phase from tube testing so it tells us if there are 'cold agglutinins' or 'rouleaux' that would need to be considered during crossmatching.

Test: 2 drops patient plasma + 1 drop 'O cells' ... mix, spin, read, grade and record. (Immediate Spin Phase). 

If results are questionable, incubate at 22C for 15 minutes and respin (22C Inc Phase).

 

The result is helpful information when we see mixed reactivity in the Antibody Screen (using 37C with gel) ... both cold agglutinins and rouleaux can look the same in gel.

 

Because gel is somewhat acidic, we have seen many more Anti-M's than we saw using tube testing.  If we identify Anti-M and the Ocells were also positive due to cold agglutinin, we rerun plasma vs M-pos cells prewarmed to 37C to determine the thermal amplitude of the Anti-M. 

 

No reactivity at 37C = Cold Agglutinin: Anti-M. (No antigen testing but use a blood warmer.)

Reactivity at 37C = Anti-M (Reactive at 37C) ... this one is classified as clinically signficant.

 

Ditto for others, e.g. Lewis.

 

It's simple and it works for us.

 

 

[Whose responsible for Removing Typenex Bands?]

Our BB Band is 'per sample' (idea is that it identifies/links the sample to the patient actually wearing the corresponding band), therefore it remains on the patient until a new BB Sample is drawn. 

 

In other words, only the person drawing a new BB Sample removes the old BB Band because he/she is going to attach a new BB Band that corresponds to the new BB Sample.

 

Everyone else is instructed to leave them alone.

 

[Transfusing a 25yr old patient with an auto anti-e]

I would probably recommend AHG compatible or least incompatible units. There is the risk of them developing the anti-E, but also e negative blood is hard to come by and I'd rather save it for people with a true anti-e.

Problem is, giving 'least incompatible' just makes the tech feel better.  Patient-wise, grade of compatibility doesn't always correspond to clinical significance (that's a whole 'nother conversation).

 

Knowing that, if we have a patient whose auto antibody cannot be either removed (e.g. autoabsorption or differential absorption) or circumvented by other methods (e.g. less sensitive method, prewarming, etc.) so we can see 'what is under there', then we transfuse antigen-negative for the antigens that the patient does not possess.  In other words, we avoid potential antibodies/antibody formation and we 'ignore' auto-antibodies.

 

I say 'ignore' in semi-quote because if the patient is overtly hemolyzing (not all are fulminent), then it may be best to transfuse antigen-negative for the so named auto-antibody.

 

If we had this patient ... if we can't clear away the auto-antibody, we'd give antigen 'identical'.  (Noticing comments above, give E-neg only if he/she is E-neg.)  If he/she is in an acute hemolysis situation (i.e. rapidly hemolyizing and dropping hct, severely low hct) then we'd consider giving e-neg RBCs.

[Use of an anti-A,B test result]

Ok, is my memory corrupted or was I really taught way back in the 20th century that we had to use Anti-A,B because it would pick up subgroups of A and/or B?

 

And then when monoclonal antibodies became available (yes, it was that far back!), we didn't need to be concerned about that for routine ABO Grouping anymore? 

 

Assuming that ... we do not use Anti-A,B for our routine testing.  But, we DO use it for ABO Discrepancy workups ... guess I'm still searching for that Ax or Bx patient ...

[Clinically Insignificant Panagglutinin]

We do see antibodies, as Malcolm mentioned, that are directed against some component of the Gel test system.  We suspect that they are directed at some antibiotic in the reagent cell suspending medium.  They often give that characteristic “mixed field-ish” looking agglutination typical of IgM antibodies.  Some are quite strong (even 4+).  The Auto Control in Gel is typically negative because the patient cells are in MTS diluent and not exposed to the same antibiotics that are in the reagent cells.  It seems like the 0.8% cells manufactured by Ortho for Gel testing have the offending ingredient and the 3% cells do not.  When we see this pattern of all screening and panel cells positive, autocontrol negative we will prepared our own 0.8% dilutions of 3% screening cells to test in Gel and get negative Gel reactions.  Of course all of this does not help with solid phase but the mechanism may be similar.

 

So true ... the reagent antibiotic antibody issue has been around for years, too.  This is covered by my 'interferring substance' interpretation. 

 

I guess I'm taking the attitude 'I'm looking for clinically significant antibodies.'  All the rest is academically interesting but doesn't change how we choose the units from the refrigerator.

[Complement Control]

Since they are all too pricey (this item used to cost about $16 years ago ... until they became required by the CAP!) so we make our own ... every 2 weeks.  Sugar packet from the cafeteria, fresh donor cells from our therapeutic phlebotomy patients, saline and Alsever's Solution ... you do the math.

 

We run these as Pos (Anti-C3bd) and Neg (no reagent) controls each time we run the test (gel) to show that the reagent works for that test at that time.  (We don't run many Anti-Complement DATs.)

[Clinically Insignificant Panagglutinin]

Maybe I'm taking the simplistic approach but when we see mixed cell reactivity, we consider the 3 reasons given by the manufacturer for causing such results ...

1. Mixed population - this is not the case for screening/panel cells so that out.

2. Cold Agglutinin - you investigated that and got negative results so no cold agglutinin there.

3. Rouleaux - I'll assume you checked that out as well and found none otherwise you would have said differently. n.b. Logic tells us that rouleaux should be seen with all cells, but experience tells us that it doesn't always happen that way.

 

In addition, the premise for reactivity in gel is essentially that the cells that are 'not smooth' don't make it to the bottom.  Anything that causes the surface to be 'rough' causes a 'positive result'.  Irregular shape (e.g. sickle, acanthrocytes), abnormal immunoglobulin coating, etc. etc. so those things need to be added to that list.  (Keeping in mind that reagent cells are aged.)

 

Also, gel is acidic, so we see more Anti-M than we did with tube testing.  I'll assume you checked that out.

 

Anti-Pr ... aren't all human cells Pr positive?  However, if I remember correctly, isn't Anti-Pr also enhanced by acidity?  Again, your patient doesn't have a cold agglutinin.

 

Gel is also great at picking up HLA/HTLA antibodies.

 

Currently, with no cold agglutinin demonstrated, no rouleaux and a negative DAT, and 'some pos with some neg results', we'd run the antibody screen with OES (Ortho's version of LISS/Albumin) and if that is negative, call it 'HLA/HTLA Antibodies' and move on with our lives.

 

P.S. We do have two active patients right now who's plasma reacts with everything in gel ... negative DAT, no cold agglutinin, no rouleaux and totally negative with tube testing ... calling it 'interferring substance with the method' as we'll never know what is causing this .. meds? abnormal proteins?

 

 

[New cryo SOP - have gotten questions on how to calculate a dose...?]

Ummm, yeah ... that looks right. 

 

Precisely why the MDs don't bother with the math.

 

AABB ... who's going to calculate total plasma volume?

 

Circular of Info (2013!?):  So for an average sized person (70kg) with a 50mg/dL Fibrinogen (our transfusion audit trigger), the math says to give 7 bags to raise the level to 100-125mg/dL.

 

Since the pools are 5 bags each, we have to give 2 pools to accomplish this ... even if the math said give 6 ... or 8 ... or 9 ... we'd still give 2 pools ... and that seems to be the trend 'policy' around here.

 

We are just starting up with pools, too.  I'm planning on putting in our SOP 'if patient weighs less than 50kg, give 1 pool.'  ... if 70kg or greater, give 2 pools'.  Of course, here in the USA, we have to translate that to pounds!

 

Ok, now WHO decided that a pool should be only 5 bags!? 

[Extra "just in case" specimens - How do you handle them]

We have a BB HOLD 'test' ... no testing is done but the information (e.g. BB Wristband #, Phlebotomist) is recorded as a 'test result' in our LIS.  This provides documentation that there is a usable sample, when it was drawn, when it was recieved in the lab, and when the BB Tech addressed the sample. 

 

The main lab has similar.

 

And we do have a policy that we (BB and the Lab) do not accept specimens with no orders ... so, either order a real test or order a 'HOLD'.

[Consolidating Antibody ID]

We perform testing for two hospitals.  FDA required we have a 'contract' on file with them ... that is all.

[transfusion reaction and requesting more products]

We have in place the following:

1. If the patient exhibits signs/symptoms related to transfusion reactions (there's a list), there is no choice ... the transfusion is discontinued and a Transfusion Reaction Investigation is ordered.  Period. 

• This is because the transfusion is under the license of the BB Medical Director who is thereby responsible for it. 
• Besides, if MDs have the powers to 'instantly know' whether the symptoms are due to the transfusion or not and that the blood was completely compatible or not causing any allergic, TRALI, Overload, etc. without any testing/rechecking/investigation, then  why do we need the Blood Bank investigations at all?  It is safer to stop and do the investigation than to rely on a variety of MD 'instincts'.  As much as they like to think they are, they (especially the residents) prove over and over again that they are not the experts in these matters.  (e.g. some of them are not aware of the symptoms or how to treat TRALI.)  I always think about 'how would this look in court?' 
• The only exception is 'Hives Only'.  If this happens, the infusionist is instructed by SOP to pause the transfusion, see if the hives subside, confer with MD to see if they want to administer medication, and then continue the transfusion.

 

2. When a Transfusion Reaction Investigation is ordered, a specimen is drawn that becomes a) the 'Post Reaction' specimen for comparison studies (color, DAT, etc.) and the new pretransfusion specimen for subsequent transfusions.

• All units that were crossmatched with the original specimen are released (i.e. not allocated to the patient anymore.) (n.b. we are on a BB Band system so each specimen is a separate entity)
• During the investigation, no units are issued unless the attending MD documents that there is a life/death situation where only the continuance of the transfusions will sustain life.  We haven't had this happen yet, but when it does, we plan to issue the prior compatible units with this documentation ... not sure if we should call this 'Emergency Release' or not ... now that I'm focusing on it, we probably should.

[Blood Bank ID# =LIS Specimen # - Stroke of genius or stupidity?]

You would have different number for every specimen is the way I see this.  We use a bb id code which, theoretically, stays with the pt for their entire stay.  It is a separate wrist band and only it has the code AND the BB specimen.  Nursing cannot infuse red cells if the codes do not match (BloodLoc system - this is also considered a barrier system so that 2 separate blood types are not essential for transfusions).  I have seen Nursing be complacent with BBID#s - in my experience, since "they always match" pts receive blood which is not set up on their specimen (thank God everyone was O+).  When Nursing is forced to be attentive to the entire transfusion process there is increased compliance = increased pt safety.  If you have a system of multiple checks and balances you had better make certain that the first one works because, since it usually does, the secondary systems are usually ignored.  Human nature.

 

The purpose of a BB Band is to assign a unique number to the specimen that is definitively associated with the body wearing the matching number.  The idea is that no matter what we call the patient  (e.g. Mary vs Jane), the blood in the tube is that of the body wearing the band.  It is really the only true link between patient and sample because the band was applied at the time of draw.  Remove that band and you've removed the link = no transfusion.

 

To have a consistent BB# does not serve this purpose, i.e. multiple specimens bear the same 'unique' number, which can be argued is no different than using the hospital #.

 

I want to know that the specimen being used for pretransfusion testing truely belongs to the body that it came from because that body is the body that will be transfused with blood crossmatched using that very specimen.  A one-time-use-only unique number on the patient matching the specimen matching the Unit Tag is my only assurance of that.

[what is the frequency of the C, E antigens on D negative red blood cells?]

I would check your SOPs as to what to do next, but looks like you need to run a few more panel cells to rule in/out anti-C and anti-E. You can't just say the patient probably won't make the antibody, you have to prove that it is not there. Many places will allow rule outs with 3 D-C+c+ and 3 D-E+e+ cells.

 

Ruling out with only heterozygous cells (with few exceptions, e.g. Anti-K) is risky business.  I don't allow my staff to do that and I don't recommend it.

• There are plenty of examples of antibodies that react with homozygous cells only (due to sensitivity of the test and concentration of the antibody) ... so you will get a negative result with heterozygous cells whether you run 1, 3 or 999 of them.
• Sure, if you miss such an antibody, it is weak and will likely not cause a noticeable 'reaction' ... you'll likely see it better next time around.  Oooor maybe you won't, some patients never pass that threshold and continue to react with only homozygous cells ... so you'll just keep wondering why the patient keeps coming back for more transfusions and perhaps rising chemistries, positive DAT, etc.

The 3+3 rule is often misinterpreted/simplfied.  In reality, we 'rule out' with 1 cell every time an antibody screen is deemed negative (e.g.. no antibody identification is performed, 2 more negative cells for each antigen is not sought, etc.).  This is ok as long as you are testing using homozygous cells for 'all', i.e. most 3-cell screening kits. 

 

As far as finding 'D-neg, C-pos and/or E-pos' reagent cells to determine if the Anti-D is masking Anti-C and/or Anti-E ... good luck!  Those are rare cells not seen often enough on panels.

 

Bottom line:  If patient is producing Anti-D (i.e. not passively acquired from a 'pure and only Anti-D' injection), we rule out Anti-C and/or Anti-E only if

a) we can locate the cells to do so ('never' happens)

or

the patient is positive for C and/or E respectively. 

If we cannot, the report is "Anti-D, Cannot rule out Anti-C and Anti-E" (whichever applies, most often they both apply). 

 

To address the original question:

Yes, we type Rh-neg (D-neg) RBCs for C and/or E as applicable.

Yes, we do perform an extended crossmatch on any sample with 'clinically significant antibodies' (including Anti-D) if for no other reason than to eliminate 'wondering if there is anything else' and/or 'mistakes'.

 

Does anyone remember 'the old days' when we used to use a reagent containing Anti-D, -C, and -E (Anti-DCE) instead of just Anti-D?  Donor units that were positive with this mixture were labeled 'Rh-Pos' ... maybe we should go back to that practice.  Hmmm ... thoughts?

[Expiration Time of Thawed Plasma]

You cannot extend an original outdate whether you are thawing, pooling, irradiating or anything else.

 

It is always 'whichever comes first', the original outdate or the 'new' outdate.

[Time Elapsed between Issue and Transfusion]

That Nurse is thinking of the time-frame a lot of Hospitals giving Nursing as to when they can "return" a unit to the Blood Bank if not used. But even that is controversial (still referenced in Technical Manual as 30 mins., but FDA wants temps. taken). So whatever your Policy for units being "returned" to the Blood Bank (whether 30 mins.; whether you take the temp. upon return to determine if still in range; etc.), I have always told Nursing (i.e. if there has been a delay in starting the transfusion for some reason) that if it is no longer acceptable back "by us," they should keep the unit because they have 4 hours from the time it left the Blood Bank, in which to transfuse. Because the reality is (and what does not make rational sense in this Nurse's response) is that the unit is out at Room Temp. for 4 hours even if the transfusion is started right away. So the fact that she did not start it within 30 mins., may only mean it cannot be returned to the Blood Bank; it does not mean it cannot still be transfused (it just means she has lost part of her 4 hour transfusion window).

And I know I have seen controversial posts here also with regard to "when" the 4 hour clock starts. But in my mind, it starts once the blood product is no longer being stored in the acceptable temperature range (so if not Issued in a Cooler, it starts when Issued from Blood Bank....in my opinion).

Brenda Hutson

Ditto, ditto, ditto! 

[Eluates in GEL]

We are using the ELUclear Kit (Hemo bioscience) and the 0.8% reagent red cells (Ortho/J&J, whoever they are now) and have no problems ... and we do a lot of eluate preps/testing.

[Glass tubes vs Polypropylene tubes]

We use exclusively polystyrene tubes.  I do not know of any polypropylene tubes cleared for use in blood bank.

I'm assuming you are talking about the little 12x75 or 10x75mm tubes used for 'Tube Testing'.

Ditto ... polystyrene, not polypropylene. 

 

We tested several tubes years ago when we made the switch from glass to plastic.  The difference has to do with the way the tubes are made (molded vs extruded) and the little micro pits and valleys caused by these differences ... pits and valleys will 'catchup' the button, etc. 

 

If you are in the US, I can pass on to you the name/# of the vendor we use for these tubes ... this company is very knowledgeable about the differences and they don't gouge their prices like some other vendors do.  Message me if you want their info.

 

And don't let vendors tell you 'they are all the same' because they a definately NOT!  Be aware that some vendors will switch you out with cheaper 'wrong' tubes without telling you!  (Yes, it happened here.) 

 

PS We do use plastic evacuated tubes for samples as well ...