Leaderboard

This is a good solution, I would like to suggest that you do not retest them until after the due date, not just the date you reported them.

Sounds like ABO discrepancy due to a cold agglutinin which may or may not have specificity. I would run 3 M+ cells and 3 M neg cells at IS, RT and 4'C along with an autocontrol. IF only the M+ cells react at IS or RT, then I would ficin treat the A1 and B cells and repeat the reverse grouping using ficin treated cells. Just a suggestion.

Oh it is!!!!!!!!!!!!!!!!!

Do you think somebody should tell them that ABO HDFN sometimes gives a Negative DAT result in the fist two or three days of life, and that they might actually be better off looking for clinical signs, rather than performing diagnoses on the result of pathology results???????

I think that it depends upon the state of the baby. For example, if the mother is D Negative, and has been in receipt of anti-D immunoglobulin, and the baby has a positive DAT, but is showing no other signs of HDFN, then we wouldn't perform any further testing. If the baby has a lowish Hb, and the mother is group O and the baby group A or B, we may take a look at the mother's IgG ABO status, and then perform an eluate on the baby. Where we might really "go to town" is if the baby is showing overt signs of HDFN, we might well go the "whole hog" and perform an elution, just in case there is a maternal alloantibody directed against a low prevalence antigen also expressed on the red cells of the father. If this is suspected, it would be easy enough to adsorb out any IgG anti-A or anti-B on the baby's red cells, without adsorbing out the potential antigen against a paternal low prevalence antigen. The specificity of such an antibody would be interesting, but not necessarily vital, as, should the baby require a transfusion, suitable blood should be easy to obtain.

It is standard 5.1.2.4: The laboratory shall evaluate the comparability of test results obtained using different methods, instruments and if applicable testing sites. This shall be performed twice annually. We use old CAP samples or known patient samples with antibodies. Test them on the analyzer and with PEG on the bench.

We use our "old" CAP samples........... Once they've been turned in and reported, we assign them to techs using our "other" methods. SOP is gel/Ortho Vision Max Additional testing then would be manual gel, Peg, LISS, Saline. Same for titers and DAT's Seems to work pretty well for us!

Thanks Lorna. I'll have a look and see what I can provide but, as I see that you are working in the Isle of Man, may I suggest you get a copy of the BCSH Guideline "Pre-Transfusion Compatibility Procedures in Blood Transfusion Laboratories" from 2012 (which is available free on-line - just put in BCSH Guidelines), and these have a few at the end of the Guideline. In addition, have a look on this site under "Library" at the top of the page, where you might find more than one thing (probably under "Education", but not only there), that will be of use to you.

This a classic case of Sensitivity vs Specificity. Clinical assays (including those in the transfusion medicine arena) are often designed to be as sensitive as possible, especially those intended to be frontline screens. Nobody wants to miss anything. However, the downside of this approach is that sometimes specificity suffers - more positives are obtained than desired. Solid Phase, Gel and PEG assays are super-sensitive, but may detect "nuisance" antibodies like weaker autoantibodies (warm and cold), or things like anti-P1, anti-Leb, or "HTLA-like" antibodies. Less sensitive assays that employ no enhancement (saline) or thing like LISS are sometimes used strategically to avoid the nuisances. Many institutions have policies that allow the deliberate down-regulation of sensitivity to ameliorate such problems. For example, performing crossmatches in LISS rather than Gel. Certainly, there's a risk that something might be missed using a less sensitive assay, but I think it's important to realize that in years past, the use of those less sensitive assays didn't leave a trail of bodies. In patients with long-term autoantibodies, it's not unusual for the autologous cells (DAT/autocontrol) to react weaker than Screening Cells or panel cells. The appears to be some kind of weakening of native antigens to which the autoantibody is directed. Sometimes, that may even mean the DAT is negative, but still yields a reactive eluate .

I just answered this question. My Score PASS YEE- HAH!!!!!!! I got one right!

I just answered this question. My Score FAIL  

I just answered this question. My Score FAIL  

There is no evidence that cold stored platelets returned to room temperature need any change in outdating. I wouldn't go beyond 7 days for pathogen reduced platelets or 5 days for non-PRT platelets. Would just use clinical judgement. The reference above relates only to frozen platelets in any case, an entirely different critter, so not necessarily informative.

I always start with the manufacturer. They will often provide suggested plans that you can then modify.

Happy Thanksgiving to all of our Canadian Pathlabtalk members

I feel like I saw that AABB added a standard that requires us to do correlation testing twice per year between antibody screening methods. Can anyone tell me which standard it is? I would also love to hear what you do for this standard when we expect Saline, Gel, PEG etc. to react differently and use those differences to avoid weak warm autos etc.

yes, that's what we wait for...........and we usually get behind and don't end up handing them out until we've already received the results.

Can anyone explain the value of this effort to me? How do you change your tests if your results don't agree? (In Chemistry you probably recalibrate.) Do you just sign off when it is expected due to different sensitivity?

Here is the form that we use. You need to have something written in policy that accounts for the expected variability of reactions when comparing different methods. We have multiple methods for ABO/Rh, Antibody Screen, Antigen Typing, Antibody ID, and AHG Crossmatch, so we have to do method comparison on all of these. TQ-0530F03 Method Comparison__blank_copy_id_10835032.pdf

I don't have access to Standards anymore (I'm retired), and I don't recall if AABB requires them. The Joint Commission definitely does, and it asked for our 6-month correlations during every inspection.

Our "methods" are automated gel, manual gel & tube (PEG). We do not evaluate our alternate enhancements as different "methods".

Here's the SOP I used, it may be a little dated.H-1-17_Method Comparison (JPTM).docx

At our facility, the Trainee has their own log in. The Trainer is responsible for assuring that all results are entered correctly. Should something be wrong, we would hold both responsible.

Immunoglobulin This question and answer was originally published on Lab Tests Guide. They have generously permitted us to repost here on our site. Please consider visiting their site: https://www.labtestsguide.com/ Submitter Cliff Category BloodBankTalk Submitted 10/03/2024  

DAT? I would do a panel, IS, RT incubation, 4C incubation......in tube. I say this because this is where the discrepancy is happening. I see you use Vision - have you done a regular panel on the instrument? Curious if it shows clear cut reactivity - or junkie, up the side-like reactivity? I would also do an ag type on the patient - even though they've been transfused......its' only 2 units, so, IF the pt is M neg, you should see MF if the units were M pos. ( we do this but don't report......it just give you an "idea" of what may or may not be going on......) If they type 3-4+ M pos with no MF, - you can - with a decent amount of certainty - eliminate M as a possibility. Remember...........M isn't the only trouble maker in the "cold". Could be one or both Lewis's, P1, I've actually seen a K react at RT - so, ya never know!

This is a great book :)

Sorry I'm just getting use to this site and how to reply! I am wanting to start off with easier ones and get more complicated. I'm trying to prepare for exams at a higher level which will include complicated case studies. I think both serological testing and clinical would be helpful? I am at Specialist level now but never worked in a reference lab and struggle with pan reactive panels and eluates/adsorption work and want to improve my theory so I can relate to complicated questions. 😊

Thank you so much I will have a look at that! 😊

I CANNOT tell from the information you have given (not least because the phenotype of the reverse typing cells and the panel cells are unknown to me). I would very strongly suggest that you send samples to a Red Cell Reference Laboratory to get this sorted out, BEFORE the patient needs a transfusion in an emergency. From what you do tell us, I think the antibody/antibodies are unlikely to be fatally clinically significant, but it depends on the true specificity/specificities and the underlying pathology.

Hi Exlimey, this makes sense. Thank you for taking the time to explain it thoroughly. I appreciate it!

I have a book called "Antibody Identification: Art of science" . It's by the AABB, and it's chock full of case studies, over 500 pages of them, with questions for all of them.

I tend to think that there are a number of factors affecting the reaction, such as changes to the pH, rather than just dilution, that would change the equilibrium constant within the Law of Mass Action that governs antibody/antigen reactions, but pH is only one of them.

For serological testing or for clinical situations?

Are you looking for really difficult cases, or more commonplace cases?

We use un-validated lunch coolers just so that visitors/patients don't see someone walking through the halls with a bag of blood. OSHA reg is 1910.1030(g)(1)(i)(F) blood components issued for transfusion do not require a biohazard label.

Cliff: I just submitted my first question. Be easy on me