Joanne P. Scannell

Ok, a list of 'agree/disagree' items here:
I agree with your supervisor on one plane: Don't write things on documents unless you are instructed to do so. It's very important that things don't 'depend on who is working this shift' ... Blood Banking is a team sport and demands consistency.
I disagree with the 'use a blood warmer only if the cold agglutinin reacts at 37C'. If that's the case, what are you circumventing if the antibody reacts at 37 and you are transfusing at 37? Nothing. The idea of using a blood warmer is to keep the temperature of the transfusion ABOVE reaction temperature. If you have a cold agglutinin with a thermal amplitude above 30C, a blood warmer is not going to change the reactivity and the MD needs to start thinking about reducing the antibody concentration and/or production (pheresis, medication) rather than a risky transfusion ... the patient will destroy the donor RBCs just as quickly as the auto RBCs and may even exacerbate the problem (introducing new antigens, stimulate the immune system).
I agree with your 'caution, best to use a blood warmer': To assure we are all applying the same rules for every patient, I have instructed my staff to issue RBCs with a blood warmer if they see a demonstrable cold agglutinin at the Immediate Spin/Room Temperature phase (we routinely perform this phase with pooled O cells during initial pretransfusion testing to look for 'room temperature/close to infusion temperature' cold agglutinins and rouleux so we have no such surprises later during crossmatching). Is a blood warmer always needed for these cases? Probably not ... but it is the safer side of caution and provides for continuity of a policy. We can do this automatically because it is written into our procedure which is in reality our Medical Director's instructions to us ... yes, she signs all our procedures ... hence, it is a physician's order.
Maybe your supervisor will consider putting such a policy/procedure in place for everyone to follow ... rather than you acting on your own.

I had an OB patient with an antibody to anti-Goa that we picked up on prenatal screening. One cell was positive on the screen and nothing showed up on 2 panels, Because it was an OB case, I sent it to the ref lab and they identified the culprit.

This may seem like an odd question, but was the screen tested using a different method than the panel? 
I only ask this because there are some hospitals that run Antibody Screens using Gel then run the panels using Tube Testing. 
One cannot expect Gel vs Tube testing to give 'identical' results for several reasons.
Incubation Timing can also make a difference.
If only 1 cell in the Screen was positive and the entire panel was negative, I'd tend toward an Antibody to a Low Incidence Antigen.  But, this case had 2 positive screening cells, correct?
Other than sampling/dispensing error, I'm just trying to think of the reasons the Screen would not correlate with the panel.
 

This may seem like an odd question, but was the screen tested using a different method than the panel? 
I only ask this because there are some hospitals that run Antibody Screens using Gel then run the panels using Tube Testing. 
One cannot expect Gel vs Tube testing to give 'identical' results for several reasons.
Incubation Timing can also make a difference.
If only 1 cell in the Screen was positive and the entire panel was negative, I'd tend toward an Antibody to a Low Incidence Antigen.  But, this case had 2 positive screening cells, correct?
Other than sampling/dispensing error, I'm just trying to think of the reasons the Screen would not correlate with the panel.
 

This may seem like an odd question, but was the screen tested using a different method than the panel? 
I only ask this because there are some hospitals that run Antibody Screens using Gel then run the panels using Tube Testing. 
One cannot expect Gel vs Tube testing to give 'identical' results for several reasons.
Incubation Timing can also make a difference.
If only 1 cell in the Screen was positive and the entire panel was negative, I'd tend toward an Antibody to a Low Incidence Antigen.  But, this case had 2 positive screening cells, correct?
Other than sampling/dispensing error, I'm just trying to think of the reasons the Screen would not correlate with the panel.
 

This may seem like an odd question, but was the screen tested using a different method than the panel? 
I only ask this because there are some hospitals that run Antibody Screens using Gel then run the panels using Tube Testing. 
One cannot expect Gel vs Tube testing to give 'identical' results for several reasons.
Incubation Timing can also make a difference.
If only 1 cell in the Screen was positive and the entire panel was negative, I'd tend toward an Antibody to a Low Incidence Antigen.  But, this case had 2 positive screening cells, correct?
Other than sampling/dispensing error, I'm just trying to think of the reasons the Screen would not correlate with the panel.
 

We always felt that least incompatible is like saying someone is a little pregnant . . .

With all due respect, if you do not trust the results given to you by your IRL, why did you send samples to them in the first place?
The other thing is that the term "least incompatible" has been "rubbished" by LaTwrie Petz almost 20 years ago now (and you can't get much better than him!) - see Petz LD.  "Least incompatible" units for transfusion in autoimmune hemolytic anemia: should we eliminate this meaningless term?  A commentary for clinicians and transfusion medicine professionals.  Transfusion 2003; 43(11): 1503-1507.  DOI: 10/1046/j.1537-2995.2003.00583.x.
I apologise if this reads as I am being personally rude to you; that is DEFINITELY NOT my intention.

I would expect the blood center to put an expiration date on that product.  You should not have to alter that as it would be a licensed/registered product in compliance with regulations.

The mechanisms of what have been termed TRALI (actually a subset of acute lung injury/acute respiratory distress syndrome) and TACO (actually something very common, congestive heart failure) have been widely misunderstood due to unjustified assumptions/dogma. There are many biologic mediators other than antibodies that can cause lung injury after venous infusion which directly subjects the lung vascular endothelium to these mediators (antibodies, activated cells, lipids, mediators such as sCD40L, DNA/histones).  Likewise there are many mediators that can cause or exacerbate cardiac failure after venous infusion (inflammatory mediators, excess volume).  Cardiac failure is not just volume overload, but can be caused by fever, inflammatory cytokines and vascular/myocardial muscle dysfunction.  The notion that these are distinct entities is also at variance with clinical experience.  Many patients have signs of both cardiac failure and pulmonary failure simultaneously.  So the definitions and pathophysiology used in reviews and texts are lacking in validity and just plain oversimplified and wrong, in my view.  There are compelling data to support these iconoclastic contentions for TRALI, and some for TACO.
Most germane (see attachment), when we introduced universal leukoreduction, we saw a sustained 83% drop in reports of TRALI and 50% in TACO over the following years.  This suggests that white cells/DNA/histones play a role in causing lung and heart inflammation and dysfunction.  This clinical observation was confirmed in animal studies from Denisa Wagner's lab at Harvard demonstrating that neutrophil extracellular traps (NETS) infused intravenously can cause acute lung injury (see attachment).  To me these observations are convincing evidence that leukoreduction alters cardiorespiratory injury and failure post-transfusion and represents one of the strongest arguments for universal leukoreduction.  Needless to say, this challenge to dogma has been ignored by the transfusion medicine community which continues, at least in the USA, to infuse deadly white cells and their degradation products (free DNA/histones) to patients, one of the great tragedies of the last 20 years in the USA blood bank field.  We got this entirely wrong and tens of thousands of patients have probably died unnecessarily due to complications of non-leukoreduced transfusions.
ULR TRALI TACO PMC version.pdf NETS and TRALI Wagner 2012.pdf

The company told us.  And really, it does make sense.
We are testing the sensitivity of the reagents in the cards by sending a coated cell from the reaction chamber down through the reagent/gel.  It shouldn't matter if the cell was coated a few minutes ago or a few days ago, the IGG Card is working.

We were told that because we prove the IgG Card is working properly with the positive and negative antibody screens, we do not have to make a specific sample for pos and neg 'DAT'.

Me too! And chasing the snowflakes back and forth.

We were told that because we prove the IgG Card is working properly with the positive and negative antibody screens, we do not have to make a specific sample for pos and neg 'DAT'.

We were told that because we prove the IgG Card is working properly with the positive and negative antibody screens, we do not have to make a specific sample for pos and neg 'DAT'.

Column Agglutination Technology (CAT) is superb at detecting IgG antibodies, and also at detecting certain "cold-reacting" antibodies (such as anti-I and (because of the pH of the column) anti-M, BUT the manufacturers themselves state quite freely, that they are not designed to detect all ABO mis-matches, because most ABO antibodies are IgM (anti-M are usually a mixture of IgM and IgG, but also react preferentially at a low pH).

There is no standard that requires a transfusion to be started within a certain time frame from release. 
the only timing that is critical is that the unit needs to be complete within 4 hours of release.

As David said there isn't a BB standard for time frame a transfusion needs to be started but for some reason this time frame is in the nursing policy, theirs is 20 minutes. Where they got this information I don't know. Anyway if blood is sent to the floor and it isn't going to be started in 20 minutes and the floor asked calls the BB (before they actually return it) we tell them if they are going to transfuse and it is will be completed within the 4 hours that it was issued to the floor keep it, otherwise it will be discarded (if temp is greater than 10 degrees)

I always 'balk' at this idea because as we all know, the probability of two patients having the same blood type is high.  We have had a few instances over the past few years where a wrong patient was drawn (we use BB Bands so it's very obvious) and they were the same blood type but one had antibodies and the other didn't.  
And yes, there are those who have had to come up with 'defensive measures' to 'assure' that there is no 'cheating', e.g. RN draws 2 samples and holds one in case the BB asks for a second, a witness (do you really think that happens as intended?), different colored tubes for the second draw (assuming they don't draw the wrong patient twice).
I could go on and on about this ... but that wasn't your question, was it?

I agree with those who 'don't bother' with the actual math ... between 'natural selection' and blood suppliers 'holding' certain antigen types, exact math is just an academic exercise. 
To be practical (considering tech time and reagents are valuable commodities):
If the patient's plasma contains demonstrable antibody, crossmatch a batch or two of units then do the antigen typing on the compatible units only.  No luck = order antigen-neg from the supplier. If the patient's plasma is negative, then screen (highest frequency first) a batch or two of units.  Again, No luck = order antigen-neg from the supplier.  

I agree with those who 'don't bother' with the actual math ... between 'natural selection' and blood suppliers 'holding' certain antigen types, exact math is just an academic exercise. 
To be practical (considering tech time and reagents are valuable commodities):
If the patient's plasma contains demonstrable antibody, crossmatch a batch or two of units then do the antigen typing on the compatible units only.  No luck = order antigen-neg from the supplier. If the patient's plasma is negative, then screen (highest frequency first) a batch or two of units.  Again, No luck = order antigen-neg from the supplier.  

I always 'balk' at this idea because as we all know, the probability of two patients having the same blood type is high.  We have had a few instances over the past few years where a wrong patient was drawn (we use BB Bands so it's very obvious) and they were the same blood type but one had antibodies and the other didn't.  
And yes, there are those who have had to come up with 'defensive measures' to 'assure' that there is no 'cheating', e.g. RN draws 2 samples and holds one in case the BB asks for a second, a witness (do you really think that happens as intended?), different colored tubes for the second draw (assuming they don't draw the wrong patient twice).
I could go on and on about this ... but that wasn't your question, was it?

I always 'balk' at this idea because as we all know, the probability of two patients having the same blood type is high.  We have had a few instances over the past few years where a wrong patient was drawn (we use BB Bands so it's very obvious) and they were the same blood type but one had antibodies and the other didn't.  
And yes, there are those who have had to come up with 'defensive measures' to 'assure' that there is no 'cheating', e.g. RN draws 2 samples and holds one in case the BB asks for a second, a witness (do you really think that happens as intended?), different colored tubes for the second draw (assuming they don't draw the wrong patient twice).
I could go on and on about this ... but that wasn't your question, was it?

I agree with those who 'don't bother' with the actual math ... between 'natural selection' and blood suppliers 'holding' certain antigen types, exact math is just an academic exercise. 
To be practical (considering tech time and reagents are valuable commodities):
If the patient's plasma contains demonstrable antibody, crossmatch a batch or two of units then do the antigen typing on the compatible units only.  No luck = order antigen-neg from the supplier. If the patient's plasma is negative, then screen (highest frequency first) a batch or two of units.  Again, No luck = order antigen-neg from the supplier.  

We do, 'just because' ... it's easy to find K-Neg RBCs and one never knows if they are going to try it again so we don't want to deal with switching around.  We have one patient who seems to be chronically infused with this stuff!