Joanne P. Scannell

See an earlier post here about the monolayer method ... guess that doesn't pan out the way they thought it would.  And I don't know of any 'routine' Blood Bank that runs their testing using this method.
 
In my example, since gel picks up 'everything' while the lesser sensitive method does not, we use the lesser sensitive method to perform the crossmatch.  And yes, we would transfuse antigen-negative, crossmatch compatible RBCs (crossmatch compatible with Albumin).
 
BTW: In Sunquest, we add the testing we do.  XMTS for the extended crossmatch with gel (1+, Incompatible) and XALB for the extended crossmatch with 22% Albumin (0, Compatible).  Since the patient has an Anti-E, the system requires the unit be typed/recorded as 'E-neg.'  The 'test' %TS (Transfusion Status, part of the crossmatch battery) is the determining result - the techs final interpretation.  In this case, we answer it 'OK to Transfuse' because we have determined that it is.  If we answer 'Not OK to Transfuse', the system would release the unit from the patient, i.e. no unit tag, no issuing it to the floors.
 
Of note, in the days before gel/solid phase, we probably wouldn't have seen half of these warm autos.
 
Also, a related case of interest ... for your further amusement ...
We had a 19yo female present in Sickle Cell crisis last week.  She has a positive DAT (IgG only), an Auto-Anti-E (2-3+ gel and Albumin), a 'Warm Autoantibody of Undetermined Specificity' (1+gel only) aaaand is producing Anti-e (along with a history of Anti-N).  Somewhere along the way in her short life, she got transfused with E-neg/e-pos RBCs (not all hospitals give antigen-neg RBCs proactively OR someone was thinking they should avoid the E antigen because it has a name).  This is a prime example of why we should NOT honor Auto-'identified' antibodies because of the super exposure to the 'other' antigen.  Now, this young lady will be dealing with an Anti-e the rest of her life ... through multiple transfusions (due to her Dx) and through pregnancies with an Rh-antibody.  A disservice and a shame.

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.

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 ...

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 ...

See an earlier post here about the monolayer method ... guess that doesn't pan out the way they thought it would.  And I don't know of any 'routine' Blood Bank that runs their testing using this method.
 
In my example, since gel picks up 'everything' while the lesser sensitive method does not, we use the lesser sensitive method to perform the crossmatch.  And yes, we would transfuse antigen-negative, crossmatch compatible RBCs (crossmatch compatible with Albumin).
 
BTW: In Sunquest, we add the testing we do.  XMTS for the extended crossmatch with gel (1+, Incompatible) and XALB for the extended crossmatch with 22% Albumin (0, Compatible).  Since the patient has an Anti-E, the system requires the unit be typed/recorded as 'E-neg.'  The 'test' %TS (Transfusion Status, part of the crossmatch battery) is the determining result - the techs final interpretation.  In this case, we answer it 'OK to Transfuse' because we have determined that it is.  If we answer 'Not OK to Transfuse', the system would release the unit from the patient, i.e. no unit tag, no issuing it to the floors.
 
Of note, in the days before gel/solid phase, we probably wouldn't have seen half of these warm autos.
 
Also, a related case of interest ... for your further amusement ...
We had a 19yo female present in Sickle Cell crisis last week.  She has a positive DAT (IgG only), an Auto-Anti-E (2-3+ gel and Albumin), a 'Warm Autoantibody of Undetermined Specificity' (1+gel only) aaaand is producing Anti-e (along with a history of Anti-N).  Somewhere along the way in her short life, she got transfused with E-neg/e-pos RBCs (not all hospitals give antigen-neg RBCs proactively OR someone was thinking they should avoid the E antigen because it has a name).  This is a prime example of why we should NOT honor Auto-'identified' antibodies because of the super exposure to the 'other' antigen.  Now, this young lady will be dealing with an Anti-e the rest of her life ... through multiple transfusions (due to her Dx) and through pregnancies with an Rh-antibody.  A disservice and a shame.

See an earlier post here about the monolayer method ... guess that doesn't pan out the way they thought it would.  And I don't know of any 'routine' Blood Bank that runs their testing using this method.
 
In my example, since gel picks up 'everything' while the lesser sensitive method does not, we use the lesser sensitive method to perform the crossmatch.  And yes, we would transfuse antigen-negative, crossmatch compatible RBCs (crossmatch compatible with Albumin).
 
BTW: In Sunquest, we add the testing we do.  XMTS for the extended crossmatch with gel (1+, Incompatible) and XALB for the extended crossmatch with 22% Albumin (0, Compatible).  Since the patient has an Anti-E, the system requires the unit be typed/recorded as 'E-neg.'  The 'test' %TS (Transfusion Status, part of the crossmatch battery) is the determining result - the techs final interpretation.  In this case, we answer it 'OK to Transfuse' because we have determined that it is.  If we answer 'Not OK to Transfuse', the system would release the unit from the patient, i.e. no unit tag, no issuing it to the floors.
 
Of note, in the days before gel/solid phase, we probably wouldn't have seen half of these warm autos.
 
Also, a related case of interest ... for your further amusement ...
We had a 19yo female present in Sickle Cell crisis last week.  She has a positive DAT (IgG only), an Auto-Anti-E (2-3+ gel and Albumin), a 'Warm Autoantibody of Undetermined Specificity' (1+gel only) aaaand is producing Anti-e (along with a history of Anti-N).  Somewhere along the way in her short life, she got transfused with E-neg/e-pos RBCs (not all hospitals give antigen-neg RBCs proactively OR someone was thinking they should avoid the E antigen because it has a name).  This is a prime example of why we should NOT honor Auto-'identified' antibodies because of the super exposure to the 'other' antigen.  Now, this young lady will be dealing with an Anti-e the rest of her life ... through multiple transfusions (due to her Dx) and through pregnancies with an Rh-antibody.  A disservice and a shame.

See an earlier post here about the monolayer method ... guess that doesn't pan out the way they thought it would.  And I don't know of any 'routine' Blood Bank that runs their testing using this method.
 
In my example, since gel picks up 'everything' while the lesser sensitive method does not, we use the lesser sensitive method to perform the crossmatch.  And yes, we would transfuse antigen-negative, crossmatch compatible RBCs (crossmatch compatible with Albumin).
 
BTW: In Sunquest, we add the testing we do.  XMTS for the extended crossmatch with gel (1+, Incompatible) and XALB for the extended crossmatch with 22% Albumin (0, Compatible).  Since the patient has an Anti-E, the system requires the unit be typed/recorded as 'E-neg.'  The 'test' %TS (Transfusion Status, part of the crossmatch battery) is the determining result - the techs final interpretation.  In this case, we answer it 'OK to Transfuse' because we have determined that it is.  If we answer 'Not OK to Transfuse', the system would release the unit from the patient, i.e. no unit tag, no issuing it to the floors.
 
Of note, in the days before gel/solid phase, we probably wouldn't have seen half of these warm autos.
 
Also, a related case of interest ... for your further amusement ...
We had a 19yo female present in Sickle Cell crisis last week.  She has a positive DAT (IgG only), an Auto-Anti-E (2-3+ gel and Albumin), a 'Warm Autoantibody of Undetermined Specificity' (1+gel only) aaaand is producing Anti-e (along with a history of Anti-N).  Somewhere along the way in her short life, she got transfused with E-neg/e-pos RBCs (not all hospitals give antigen-neg RBCs proactively OR someone was thinking they should avoid the E antigen because it has a name).  This is a prime example of why we should NOT honor Auto-'identified' antibodies because of the super exposure to the 'other' antigen.  Now, this young lady will be dealing with an Anti-e the rest of her life ... through multiple transfusions (due to her Dx) and through pregnancies with an Rh-antibody.  A disservice and a shame.

Brilliant post.
The ONLY thing I would say is that monolayer methods, along with the chemiluminescence test, have proved to be less useful than was first thought. For example, anti-Inb gives a positive result, because it can cause a haemolytic transfusion reaction, but also gives a positive result vis-à-vis HDFN, which it does not cause. Some other antibodies also give "false positive" results by these methods.
That having been said, I repeat, a brilliant post!

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.

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.

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.

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.

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.

A paper/editorial that I have quoted many times before:
Petz LD. "Least incompatible" units for transfusion in autoimmune haemolytic anemia: should we eliminate this meaningless term? A commentary for clinicians and transfusion medicine professionals. Transfusion 2003; 43 (11): 1503-1507.

If you have a "Least Incompatible" form you must have a policy that allows its use, therefore I would assume that this is approved by your Medical Director. I would let you MD know prior to release just so they can interact with the pt's MD if they think it necessary.
(Least incompatible is like saying someone is a little pregnant).
If your pt has a WAIHA any transfused blood will be treated just like the pt's own. The risk of underlying alloabs cannot be taken lightly. I give these pts Rh phenotype specific rbcs as I have found that when I did not do so they made ab to the Rh ags which they did not possess (scary).

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 ...

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 ...

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 ...

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 ...

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 ...

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 ...

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 ...

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 ...

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 ...

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 ...