Malcolm Needs

Thank you for you advise.  Mr. Needs.  I was hoping for something that is built into the system that could manage this.

As someone from the UK (born there, still live there and worked all my professional life there), I concur with jshepherd's post.  I, too, am an aabb individual member.

I think we would all use a serologic centrifuge for this at the usual RPMs for long enough to get all the cells to the bottom, which 30 seconds is probably adequate.

As someone from the UK (born there, still live there and worked all my professional life there), I concur with jshepherd's post.  I, too, am an aabb individual member.

My facility is not AABB accredited, just Joint Commission and FDA, and I have an individual membership. I am the supervisor, and we are a large level 1 metropolitan trauma hospital. I have gained so much from my membership. Everything Cliff mentioned about resources is true, and I can't tell you how many times we've taken advantage of the discount on books for my pathologists (none of whom are transfusion medicine specialists). 
AABB membership also opened up all the subcommittees and sections, and I now sit on 9 subsections and lead one of them. I am also a mentor in the program Cliff mentioned above. 
I would say it's worth it for at least one year, so you can try it out and see what you get from it. Pro tip: if you love it, they do offer a 3 year membership option that knocks some of the cost down.  

We frequently did this in the Reference Laboratory where I was the Manager (but you have to include both a positive and a negative from the "gel" technique into the "tube" technique - or vice versa, to ensure that the "sensitivity" of both techniques, while not being necessarily identical, are reasonably close).

Column agglutination technology is an excellent technique, but does have a tendency to detect antibodies that react at temperatures well below 37oC, even after fairly prolonged incubation at 37oC.  However, the fact that the blood group, including the "reverse grouping" is clear of atypical agglutination suggests that this may not necessarily be the case for this patient.

Just to be on the safe side though, and if you can, I would either treat the plasma from the sample with rabbit erythrocyte stroma (which will adsorb out most "cold" agglutinins), treat the plasma with 0.01M dithiothreitol (which will denature the J-chains of IgM molecules, meaning that, although they can still sensitise the red cells, they are no longer able to agglutinate the red cells) or, and my personal favourite, is to pre-warm the plasma and red cells to 37oC before mixing, perform the IAT at strictly 37oC in glass tubes, wash with saline warmed to 37oC and use monospecific AHG.  If any, or all, of these techniques lead to negative results, the chances are that the antibody is a clinically insignificant "cold" IgM antibody, such as an auto-anti-HI (given that the patient is group A, and the test cells are all group O)..

Failing the above, send a sample to a red cell reference laboratory.

I hope that helps a little bit.

We frequently did this in the Reference Laboratory where I was the Manager (but you have to include both a positive and a negative from the "gel" technique into the "tube" technique - or vice versa, to ensure that the "sensitivity" of both techniques, while not being necessarily identical, are reasonably close).

Can you convert the tube panel cells from 3% to 0.8% and test in gel?  We primarily do that to run selected cells that are not already diluted to 0/8%

We do that.  You could also use LISS (or PEG) to complement your SIAT.  Make it more sensitive. sandra

We frequently did this in the Reference Laboratory where I was the Manager (but you have to include both a positive and a negative from the "gel" technique into the "tube" technique - or vice versa, to ensure that the "sensitivity" of both techniques, while not being necessarily identical, are reasonably close).

Column agglutination technology is an excellent technique, but does have a tendency to detect antibodies that react at temperatures well below 37oC, even after fairly prolonged incubation at 37oC.  However, the fact that the blood group, including the "reverse grouping" is clear of atypical agglutination suggests that this may not necessarily be the case for this patient.

Just to be on the safe side though, and if you can, I would either treat the plasma from the sample with rabbit erythrocyte stroma (which will adsorb out most "cold" agglutinins), treat the plasma with 0.01M dithiothreitol (which will denature the J-chains of IgM molecules, meaning that, although they can still sensitise the red cells, they are no longer able to agglutinate the red cells) or, and my personal favourite, is to pre-warm the plasma and red cells to 37oC before mixing, perform the IAT at strictly 37oC in glass tubes, wash with saline warmed to 37oC and use monospecific AHG.  If any, or all, of these techniques lead to negative results, the chances are that the antibody is a clinically insignificant "cold" IgM antibody, such as an auto-anti-HI (given that the patient is group A, and the test cells are all group O)..

Failing the above, send a sample to a red cell reference laboratory.

I hope that helps a little bit.

That's interesting because I was a long time user of Immucor products.  Thanks for looking that up.  Now I know something I didn't know yesterday. 

Column agglutination technology is an excellent technique, but does have a tendency to detect antibodies that react at temperatures well below 37oC, even after fairly prolonged incubation at 37oC.  However, the fact that the blood group, including the "reverse grouping" is clear of atypical agglutination suggests that this may not necessarily be the case for this patient.

Just to be on the safe side though, and if you can, I would either treat the plasma from the sample with rabbit erythrocyte stroma (which will adsorb out most "cold" agglutinins), treat the plasma with 0.01M dithiothreitol (which will denature the J-chains of IgM molecules, meaning that, although they can still sensitise the red cells, they are no longer able to agglutinate the red cells) or, and my personal favourite, is to pre-warm the plasma and red cells to 37oC before mixing, perform the IAT at strictly 37oC in glass tubes, wash with saline warmed to 37oC and use monospecific AHG.  If any, or all, of these techniques lead to negative results, the chances are that the antibody is a clinically insignificant "cold" IgM antibody, such as an auto-anti-HI (given that the patient is group A, and the test cells are all group O)..

Failing the above, send a sample to a red cell reference laboratory.

I hope that helps a little bit.

Column agglutination technology is an excellent technique, but does have a tendency to detect antibodies that react at temperatures well below 37oC, even after fairly prolonged incubation at 37oC.  However, the fact that the blood group, including the "reverse grouping" is clear of atypical agglutination suggests that this may not necessarily be the case for this patient.

Just to be on the safe side though, and if you can, I would either treat the plasma from the sample with rabbit erythrocyte stroma (which will adsorb out most "cold" agglutinins), treat the plasma with 0.01M dithiothreitol (which will denature the J-chains of IgM molecules, meaning that, although they can still sensitise the red cells, they are no longer able to agglutinate the red cells) or, and my personal favourite, is to pre-warm the plasma and red cells to 37oC before mixing, perform the IAT at strictly 37oC in glass tubes, wash with saline warmed to 37oC and use monospecific AHG.  If any, or all, of these techniques lead to negative results, the chances are that the antibody is a clinically insignificant "cold" IgM antibody, such as an auto-anti-HI (given that the patient is group A, and the test cells are all group O)..

Failing the above, send a sample to a red cell reference laboratory.

I hope that helps a little bit.

Rabbit Erythrocyte Stroma (RESt) kits are available commercially, but for the life of me, right at this second I CANNOT remember from which company.  I'll get in touch with some of my colleagues who still work (!) and get back to you.
I have been reliably informed that the company is Immucor (Product Code 0057316).  I hope this doesn't break any rules about advertising Cliff Reeves.

Column agglutination technology is an excellent technique, but does have a tendency to detect antibodies that react at temperatures well below 37oC, even after fairly prolonged incubation at 37oC.  However, the fact that the blood group, including the "reverse grouping" is clear of atypical agglutination suggests that this may not necessarily be the case for this patient.

Just to be on the safe side though, and if you can, I would either treat the plasma from the sample with rabbit erythrocyte stroma (which will adsorb out most "cold" agglutinins), treat the plasma with 0.01M dithiothreitol (which will denature the J-chains of IgM molecules, meaning that, although they can still sensitise the red cells, they are no longer able to agglutinate the red cells) or, and my personal favourite, is to pre-warm the plasma and red cells to 37oC before mixing, perform the IAT at strictly 37oC in glass tubes, wash with saline warmed to 37oC and use monospecific AHG.  If any, or all, of these techniques lead to negative results, the chances are that the antibody is a clinically insignificant "cold" IgM antibody, such as an auto-anti-HI (given that the patient is group A, and the test cells are all group O)..

Failing the above, send a sample to a red cell reference laboratory.

I hope that helps a little bit.

Column agglutination technology is an excellent technique, but does have a tendency to detect antibodies that react at temperatures well below 37oC, even after fairly prolonged incubation at 37oC.  However, the fact that the blood group, including the "reverse grouping" is clear of atypical agglutination suggests that this may not necessarily be the case for this patient.

Just to be on the safe side though, and if you can, I would either treat the plasma from the sample with rabbit erythrocyte stroma (which will adsorb out most "cold" agglutinins), treat the plasma with 0.01M dithiothreitol (which will denature the J-chains of IgM molecules, meaning that, although they can still sensitise the red cells, they are no longer able to agglutinate the red cells) or, and my personal favourite, is to pre-warm the plasma and red cells to 37oC before mixing, perform the IAT at strictly 37oC in glass tubes, wash with saline warmed to 37oC and use monospecific AHG.  If any, or all, of these techniques lead to negative results, the chances are that the antibody is a clinically insignificant "cold" IgM antibody, such as an auto-anti-HI (given that the patient is group A, and the test cells are all group O)..

Failing the above, send a sample to a red cell reference laboratory.

I hope that helps a little bit.

Column agglutination technology is an excellent technique, but does have a tendency to detect antibodies that react at temperatures well below 37oC, even after fairly prolonged incubation at 37oC.  However, the fact that the blood group, including the "reverse grouping" is clear of atypical agglutination suggests that this may not necessarily be the case for this patient.

Just to be on the safe side though, and if you can, I would either treat the plasma from the sample with rabbit erythrocyte stroma (which will adsorb out most "cold" agglutinins), treat the plasma with 0.01M dithiothreitol (which will denature the J-chains of IgM molecules, meaning that, although they can still sensitise the red cells, they are no longer able to agglutinate the red cells) or, and my personal favourite, is to pre-warm the plasma and red cells to 37oC before mixing, perform the IAT at strictly 37oC in glass tubes, wash with saline warmed to 37oC and use monospecific AHG.  If any, or all, of these techniques lead to negative results, the chances are that the antibody is a clinically insignificant "cold" IgM antibody, such as an auto-anti-HI (given that the patient is group A, and the test cells are all group O)..

Failing the above, send a sample to a red cell reference laboratory.

I hope that helps a little bit.

Welcome to this wonderful site Saeeed.  ENJOY!

Agree with Dr Blumberg. In an abstract from way back, 1996, Ann Church studied the value of an eluate, reference and abstract below (apologies for quality of print). 
A Church, S Nance, D Kavitsky.  Assessment of Elution Studies in Cases with 37OC Reactive Serum Autoantibodies (SA).  Transfusion 1996; 36:161S (Suppl)

Many, many years ago now, when I was working at the old Westminster Hospital in London as a quite junior member of the Blood Transfusion staff, I spent quite a few hours working on a sample from a patient with a positive DAT, trying to determine the specificity, in order to see whether the antibody was an allo- or an auto-antibody.  This included the use of several very rare red cells that I had frozen down and also examining the eluate.  After many happy hours, I had got precisely nowhere, and so sent a sample to my former colleges at the International Blood Group Reference Laboratory.
I received a somewhat "spicy" report from my heroine Joyce Poole, who explained to me, in words of one syllable, that I had rather been wasting my time, rare cell collection and the laboratory's money as, in almost all cases, the specificity would be found to be an auto-anti-Rh17 or auto-anti-Rh18!!!!!
Since then, I have reverted to doing as little as possible on such samples and, when I retired 43 years later, and, as far as I know, none of the patients ever died as a result.  There was a close one once, when I was working on a sample on a Saturday on-call in the Red Cell Reference Laboratory at NHSBT-Tooting Centre.  I was working on a sample that was overtly a case of wAIHA.  After several allo-adsorptions, I was finally able to provide "suitable blood".  It was only at the last minute that the computers came back on after an unplanned downtime, and it appeared that the patient was known, from many years previously as having an allo-anti-Vel!!!!!!!  As you can imagine, I did several more tests before I released the blood (on Pathologist's orders), as there was absolutely no evidence of an anti-Vel (auto- or allo-) in the present sample - but it did give me a bit of a turn!!!!!!!!!!!!
I would recommend a thorough reading of Petz LD, Garratty G.  Immune Hemolytic Anemias.  2nd edition, 2004, Churchill-Livingstone. ISBN  978-0-443-08559-8.
Other than that and, possibly, looking at the patient's sample at a more molecular level (as noelrbrown suggests above), I really wouldn't do much else, except that I would put a little note with the blood to be transfused to remind the doctors and nurses on the ward to be vigilant with their patient observations.
ALL OF THE ABOVE HAVING BEEN SAID, I AM NOT, AND NEVER HAVE BEEN, MEDICALLY QUALIFIED!!!!!!

Many, many years ago now, when I was working at the old Westminster Hospital in London as a quite junior member of the Blood Transfusion staff, I spent quite a few hours working on a sample from a patient with a positive DAT, trying to determine the specificity, in order to see whether the antibody was an allo- or an auto-antibody.  This included the use of several very rare red cells that I had frozen down and also examining the eluate.  After many happy hours, I had got precisely nowhere, and so sent a sample to my former colleges at the International Blood Group Reference Laboratory.
I received a somewhat "spicy" report from my heroine Joyce Poole, who explained to me, in words of one syllable, that I had rather been wasting my time, rare cell collection and the laboratory's money as, in almost all cases, the specificity would be found to be an auto-anti-Rh17 or auto-anti-Rh18!!!!!
Since then, I have reverted to doing as little as possible on such samples and, when I retired 43 years later, and, as far as I know, none of the patients ever died as a result.  There was a close one once, when I was working on a sample on a Saturday on-call in the Red Cell Reference Laboratory at NHSBT-Tooting Centre.  I was working on a sample that was overtly a case of wAIHA.  After several allo-adsorptions, I was finally able to provide "suitable blood".  It was only at the last minute that the computers came back on after an unplanned downtime, and it appeared that the patient was known, from many years previously as having an allo-anti-Vel!!!!!!!  As you can imagine, I did several more tests before I released the blood (on Pathologist's orders), as there was absolutely no evidence of an anti-Vel (auto- or allo-) in the present sample - but it did give me a bit of a turn!!!!!!!!!!!!
I would recommend a thorough reading of Petz LD, Garratty G.  Immune Hemolytic Anemias.  2nd edition, 2004, Churchill-Livingstone. ISBN  978-0-443-08559-8.
Other than that and, possibly, looking at the patient's sample at a more molecular level (as noelrbrown suggests above), I really wouldn't do much else, except that I would put a little note with the blood to be transfused to remind the doctors and nurses on the ward to be vigilant with their patient observations.
ALL OF THE ABOVE HAVING BEEN SAID, I AM NOT, AND NEVER HAVE BEEN, MEDICALLY QUALIFIED!!!!!!

Many, many years ago now, when I was working at the old Westminster Hospital in London as a quite junior member of the Blood Transfusion staff, I spent quite a few hours working on a sample from a patient with a positive DAT, trying to determine the specificity, in order to see whether the antibody was an allo- or an auto-antibody.  This included the use of several very rare red cells that I had frozen down and also examining the eluate.  After many happy hours, I had got precisely nowhere, and so sent a sample to my former colleges at the International Blood Group Reference Laboratory.
I received a somewhat "spicy" report from my heroine Joyce Poole, who explained to me, in words of one syllable, that I had rather been wasting my time, rare cell collection and the laboratory's money as, in almost all cases, the specificity would be found to be an auto-anti-Rh17 or auto-anti-Rh18!!!!!
Since then, I have reverted to doing as little as possible on such samples and, when I retired 43 years later, and, as far as I know, none of the patients ever died as a result.  There was a close one once, when I was working on a sample on a Saturday on-call in the Red Cell Reference Laboratory at NHSBT-Tooting Centre.  I was working on a sample that was overtly a case of wAIHA.  After several allo-adsorptions, I was finally able to provide "suitable blood".  It was only at the last minute that the computers came back on after an unplanned downtime, and it appeared that the patient was known, from many years previously as having an allo-anti-Vel!!!!!!!  As you can imagine, I did several more tests before I released the blood (on Pathologist's orders), as there was absolutely no evidence of an anti-Vel (auto- or allo-) in the present sample - but it did give me a bit of a turn!!!!!!!!!!!!
I would recommend a thorough reading of Petz LD, Garratty G.  Immune Hemolytic Anemias.  2nd edition, 2004, Churchill-Livingstone. ISBN  978-0-443-08559-8.
Other than that and, possibly, looking at the patient's sample at a more molecular level (as noelrbrown suggests above), I really wouldn't do much else, except that I would put a little note with the blood to be transfused to remind the doctors and nurses on the ward to be vigilant with their patient observations.
ALL OF THE ABOVE HAVING BEEN SAID, I AM NOT, AND NEVER HAVE BEEN, MEDICALLY QUALIFIED!!!!!!

Many, many years ago now, when I was working at the old Westminster Hospital in London as a quite junior member of the Blood Transfusion staff, I spent quite a few hours working on a sample from a patient with a positive DAT, trying to determine the specificity, in order to see whether the antibody was an allo- or an auto-antibody.  This included the use of several very rare red cells that I had frozen down and also examining the eluate.  After many happy hours, I had got precisely nowhere, and so sent a sample to my former colleges at the International Blood Group Reference Laboratory.
I received a somewhat "spicy" report from my heroine Joyce Poole, who explained to me, in words of one syllable, that I had rather been wasting my time, rare cell collection and the laboratory's money as, in almost all cases, the specificity would be found to be an auto-anti-Rh17 or auto-anti-Rh18!!!!!
Since then, I have reverted to doing as little as possible on such samples and, when I retired 43 years later, and, as far as I know, none of the patients ever died as a result.  There was a close one once, when I was working on a sample on a Saturday on-call in the Red Cell Reference Laboratory at NHSBT-Tooting Centre.  I was working on a sample that was overtly a case of wAIHA.  After several allo-adsorptions, I was finally able to provide "suitable blood".  It was only at the last minute that the computers came back on after an unplanned downtime, and it appeared that the patient was known, from many years previously as having an allo-anti-Vel!!!!!!!  As you can imagine, I did several more tests before I released the blood (on Pathologist's orders), as there was absolutely no evidence of an anti-Vel (auto- or allo-) in the present sample - but it did give me a bit of a turn!!!!!!!!!!!!
I would recommend a thorough reading of Petz LD, Garratty G.  Immune Hemolytic Anemias.  2nd edition, 2004, Churchill-Livingstone. ISBN  978-0-443-08559-8.
Other than that and, possibly, looking at the patient's sample at a more molecular level (as noelrbrown suggests above), I really wouldn't do much else, except that I would put a little note with the blood to be transfused to remind the doctors and nurses on the ward to be vigilant with their patient observations.
ALL OF THE ABOVE HAVING BEEN SAID, I AM NOT, AND NEVER HAVE BEEN, MEDICALLY QUALIFIED!!!!!!