gagpinks

Quite recently this has been introduced (previously you had to scan the barcodes on the bag for the donor number, product, group and expiry). It is known as EDN - electronic distribution note. The box containing the blood has a tag with a barcode - you click a cog on the computer desktop and all units allocated your hospital download to an 'invisible' file. You then going into the hospital LIMS and barcode the tag in. This then imports all the units in the system. Some LIMS have it set up just to set the group but others to include the full Rh phenotype (genotype?), K type, any other antibodies that the units are antigen negative for, whether the unit is irradiated, methylene blue treated, and also CMV status.
 
It is a FAB system and virtually fool proof (I think)
 
ETA - hopefully I won't have offended Malcolm with my terminology this time. I'm hungry so not thinking on complete form...

I posted this question in UK Guidelines forum and Malcolm responded that isn't a requirement in UK.  UK donor centers guarantee that what is in the bag matches the label.
 
It is not an FDA requirement for transfusion services to serologically confirm the ABO/Rh type of red cell components using rbcs from a donor tubing segment, it's the CAP, AABB, etc.  
 
I'm trying to drum-up interest in the transfusion services community to push their donor centers to implement the same practice in the US that UK donor centers do!
 
Please don't tell me they can't do it!  This is 2015, not 1980...

We are the only lab doing titrations for a 150 miles.  If we change to gel we will contact all of our OB/Gyns and the perinatologist that comes here periodically to explain our change plus put interpretive information in the report comments.  This is why I have never done them in gel before.  Doing them on the Vision would be convenient but all titrations on it are carried out to 10 dilutions (plus neat and a control) so it would have to be worth using up all of the reagent cells that it would require.  The variability of the endpoint plus the comments above about proficiency testing makes me hesitate even more.  I do see that gel titers are reported separately on the PT results now.  There is even a uniform method in gel. Ipregeno, were you submitting results under the gel uniform procedure and still getting too high?

We discontinued doing titers in gel last year because we kept failing the CAP surveys (our results were always too high). After research, I found this in the Technical Manual:
"The AABB-recommended method is the use of saline antihuman globulin (AHG) incubated for 60-minutes at 370 C. Other methods, such as using albumin AHG or gel, may result in higher titers than the recommended method and should be validated with clinical findings and laboratory data to ensure appropriate interpretation by the obstetrician and avoid inappropriate referral of patients for high-risk obstetric care." We also retain the titered specimen and repeat it along with new titer requests to allow for possible operator differences.

I believe this is the main reason why we continue to do these types of titers by tube method. However, for isohemaglutinin titers (used for BMT or renal transplants, etc.) we use tube for IgM and gel for IgG. 

Question. How likely are you to be doing titers on maternity patients that might have titers performed at another location? Since the sensitivity of Gel is higher than tube methods might you give the pt's caregiver confusing information if your titer is elevated due to method vs true rise in titer?
I only ask since this was a question in our region where there are multiple hospitals that do prenatal testing and sometimes patients/physicians don't stick to one lab. The consensus was that for prenatal titers the standard of care within the area hospitals is to perform the testing by the Uniform Tube method so that there weren't variations in titer strength based solely on methodology.

I do believe that we set the review threshold ourselves at 1+ and lower.  This means a human will look at it and struggle to call it 1+ when it is barely there.  If we do convince ourselves to call any visible reactivity in gel 1+ it means that the range of the the titer endpoints being called 1+ seems very broad--everything from 5 dots above the button to half way up the column.  If anyone else has done tube to Vision titer correlations I would be very interested in how much variation there is.  I know to expect gel to run 1-2 dilutions higher but the case above would be 3 dilutions higher--from 2 to 16.  Even if you have been doing manual gel titers I would like to hear if you have been calling any visible reactivity a 1+ and using that as your endpoint.
The Vision is approved in the US and IgG titers are included with that.  It can't do ABO titrations that I know of.

We are validating an Ortho Vision and considering whether to use it for doing gel titrations.  We have been doing tube titrations up to this point.  We ran one today on which the Vision recorded the result of the last positive dilution as 1+ but if we read the gel card manually we would call it W+ not 1+.  That would change the titer result.  The reaction the machine called 1+ appears significantly weaker than the photos in the Interpretation Guide showing various 1+ reactions (but strong enough to be called a true positive).  The instrument requires results review (not necessarily manual review of the card itself) of any positive reaction 1+ or weaker.  Is anyone else using the Vision for titrations?  Have you seen anything similar?  How would you determine the titer in such a a case?
Background information: This antibody is suspected to be RhIG but they had no record of a negative screen in this pregnancy.  We suspect that they plan to follow titers to make sure they are dropping.  The saline/IgG tube titer is 2 (in gentle, experienced hands-- but the 1:4 dilution tube was W+). The Vision gave a 16 if that well was called 1+ (8 if it was changed to negative--there is no choice for W+ on the analyzer). 

I agree with you MaryPDX!!!
There was couple of times we got false negative DAT due to the technique we use. If you are using Gel DAT I would prefer to use analyser be cause transfused cell are at the bottom.  But if you are using manual technique probably you can use whole blood but that will clash with manufacturer instructions. 

We've done adult IgG DATs in gel for the over a decade.  There was an increase in the number of positives (due to gel being more sensitive), but don't remember how significant it was.
 

Have always used in vivo xm for these patients.  Don't like "least incompatible" as terminology, incompatible is incompatible.  Personally, I think that if there are no underlying allos an immediate spin xm should suffice.  I know of institutions that follow this algorhythm but I have never been able to convince my Medical Directors of such.
I only honor the pt's Rh phenotype.

Presumably, these are known patients, and this is how I am going to answer.
1.  We would ABO and D test by automation.  If this did not work, we would test manually.  These days, if there is a mixed-field reaction (ABO) we would (eventually) cross-match group O blood (even if we have known the patient's ABO type for decades! - I know, I know - this totally ridiculous rule was not written by me)!
2.  We would perform a DAT and an abbreviated IAT panel (waste of time doing either a full IAT panel or an enzyme panel).  
3.  We would not bother with an elution (waste of time and reagents, and, therefore, money) UNLESS there was a very good reason, such as clinical signs of a transfusion reaction.
4.  We would do a "quick and dirty" genotype, rather than rely on a phenotype.
5.  We would perform an alloadsorption (minimum x 2, maximum x 8) with R1R1 and rr red cells of known phenotype (and, on rare occasions, R2R2 red cells of known phenotype).
6.  See 4.
7.  Cross-match with the adsorbed plasma, honouring the Rh and K type (and, of course, any alloantibodies detected under the auto-antibodies).
8.  See 7, but, if the case is so urgent that we cannot wait for the adsorbed plasma, we would give ABO compatible blood that is honouring the Rh and K phenotype (and, of course, any alloantibodies detected under the auto-antibodies) and hope!

I agree with you all - many things we do for no other reason than to be compliant with some rule somewhere.
My advice for KB - talk to your Heme dept and see what they do for diffs.  Or Micro for what they do for gram stains.  Just similar subjective tests.  Do the least amount to be compliant and maintain your sanity.

I wish same . But I'm sure Malcolm will send us presentations. 

I wish same . But I'm sure Malcolm will send us presentations. 

Thanks to a very generous invitation from the organisers (in particular Phil Hoffman, aka Dr Pepper on this site, and Maddie Josephs, Chair) I will be attending and speaking at the 69th Annual Clinical Laboratory Science Convention - Central New England (ASCLS - CNE) taking place at the Rhode Island Convention Center between May 9th and May 11th 2017.  I will be talking on Wednesday 10th May 2017, giving a lecture entitled, "An In Depth Description of the Kell Blood Group System." and then, after a well-deserved break for the delegates, and for those that can stand it, a second lecture entitled, "King Henry Viii, McLeod Syndrome, Chronic Granulomatous Disease and Kx."
Sorry if this comes across as being "big headed", but I am really excited about coming back over to the USA.    

At least as useful as a measure of uncertainty . . . for many the KB is not a screening test but provides the data for amount of RhIg to be administered.

PathLabTalk QPathLabTalk Quantification.docxPathLabTalk Quantification.docxuantification.pptx
Hi NAN47, I (hopefully) have attached a short PowerPoint lecture of 14 slides, together with a Word document that explains the various slides.  I hope these help, but, if not, please do not hesitate to get back to me.  If my attachments don't open (or I have failed to attach them in the first place, please Private Message me with an email address, and I will send them to you by that method.
Best wishes,
Malcolm

Thanks Malcolm
We waited on the Oneg platelets. Delivered in 90 minutes despite minor snowstorm.
R

I have the initial EHCO printout which does not look grainy for the individual reactions but I will go back and check the reaction strength on the instrument for both runs to see how that compares.  You could be absolutely correct.  There has to be a break point somewhere and it could be that these samples just might have fallen into those areas. I do have techs review the reactions before reporting and I don't see anything on the printout that would have caused much alarm.   Unfortunately it is difficult to explain all of this to a physician or mid-wife to get them to understand why you "mistyped" their patient.
It is good to keep in mind  the probe sampling position in discrepancies with transfused patients. Should this occur again, it will be one of my considerations.   In this case my patient had not been transfused.  We learn  much from each other and I do appreciate this forum.

Without seeing the well images and/or the reaction strengths the Echo uses for grading reactions I can't say. Did the "0" result look at all grainy? Since the reaction strength for a "0" (Neg) is 0-2 and for a "?" is 3-9 perhaps your patient might have fallen at the upper end of "0" and the lower end of "?". I like reproducibility in instrumentation also but you will get variation at the low/high ends of cut-off ranges in all instruments. Would you have been as concerned if the difference was between a 1+ and 2+ reaction? Also remember that Immucor recommends reviewing all reactions prior to reporting your results just to make sure that it's not reporting a very weak reaction as negative. I'm not saying that happened in your case but it has been reported to happen. And remember, if the instruments were perfect all of the time they wouldn't need the techs LOL!

Anti-ce is a so-called compound antibody (and is also known as anti-f).  It is an antibody that will only react with red cells that are derived from an individual who has the RHCE:ce gene, or, to put it more simply, it is an antibody that will only react with red cells that express both the c and the e antigens derived from the same haplotype (i.e. in the cis position), rather than derived from different haplotypes (i.e. in the trans position).  So, for example, the anti-ce will react with red cells that are DCE/dce (Rzr), but will not react with red cells that are DCe/DcE (R1R2).  It is actually usually made by an individual with the R1R2 phenotype (or probable genotype).  It is of fairly doubtful clinical significance (BUT, NEVER trust an Rh antibody).
Anti-hrS, usually seen in individuals of Black ethnicity (who have an e variant, but who have been exposed to a "normal e antigen through pregnancy or transfusion - or both!), mimics an anti-ce.

Thanks Malcolm and exlimey.!!!!
This is what our consultants suggested. Patient is stable now.  Could you please explain bit more about anti ce.  

This is absolutely true, unless the low Hb becomes life-threatening in itself (in which case, the transfusion should be given with IVIgG and, possibly, methylprednisolone, or similar steroid, if time allows).

It is actually quite easy to do this Mabel, as long as you have the right cells available.  You split the patient's plasma sample into two, and adsorb one of these with r'r red cells (which will remove anti-C and anti-G, but leave anti-D) and test this adsorbed plasma with Ro red cells to see if there is an anti-D present.  You adsorb the other one with Ro red cells (which will remove anti-D and anti-G, but will leave anti-C) and test this adsorbed plasma with r'r red cells to see if anti-C is present.  If both adsorbed plasma samples give negative results, it is a monospecific anti-G.  If both adsorbed plasma samples give positive results, you have an anti-D and anti-C +/- an anti-G - but, in this case, the anti-G is fairly irrelevant, as the clinical advice, both for the pregnancy and for any transfusions the mother or baby may require would be the same, whether there is an anti-G present or not.