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I'll have to echo Mabel's question on this. I don't think the AABB says anything one way or the other about the need to work up a pre-transfusion DAT. Unless a DAT is suspected of being associated with a hemolytic episode (HDN, transfusion reaction, drug therapy) the information obtained from working one up is generally of little or no interest to anyone.

Just for your information Shily the minor crossmatch in the United States was eliminated many years ago. It is a waste of time and resources. You may wish to consider dropping it from your routine testing.

"Are all new lots of reagents and critical materials (e.g. blood collection sets) inspected and tested, as applicable, before use, with documentation of acceptance?" Is anyone interpreting this CAP checklist item to mean that all new lot numbers must be parallel tested against the same patient specimens with the current lot in use? Shouldn't daily reagent QC of a new lot number before use be adequate?

Thanks for the responses. To answer a few questions. 1. I'm under the impression that this particular client orders these antibody screens one week post-RhIg routinely to determine whether the product is effective. They have been advised that this is not an acceptable practice but whether they will change that is open to question. 2. There is always an outside chance that the specimen was mislabeled and not from this patient but we have requested a redraw. 3. The original "negative" antibody screen was performed by a solid-phase method and there is no sample available for retesting. As was mentioned there are numerous variables involved which determine whether anti-D will be detected post-injection. I'll fill every one in once we test the redraw. Thanks again!

We've had a client express a major concern that a patient's antibody screen was "negative" 6 days after receiving an RhIg injection. From everything that I've ever heard or read there is no correlation between a "positive" or "negative" screen and the effectiveness of RhIg. I was curious as to whether anyone has a policy addressing this. Thanks!

I know there was a long thread back in September concerning the use of anti-A,B but I had a couple of comments/questions that I wanted to throw into the mix. As far as monoclonal anti-A,B picking up A subgroups more readily than anti-A I would have to say that from our experience the monoclonal A,B reagents react better rather consistently. We test red cells which present themselves as a reverse group discrepancy (front-O, reverse-A) or react questionably or <1+ with our routine anti-A reagent with a battery of anti-A and anti-A,B reagents. These include Immucor, Ortho, Gamma and even a long outdated BCA (remember them?) product. I'm not sure why a monoclonal anti-A,B would react better than an anti-A since it's only a blend of the two clones but we have encountered the occasional very weak A subgroup which reacts only or preferably with anti-A,B. My question relates to an adsorption/elution procedure using monoclonal anti-A,B. Is your adsorption being performed only at room temperature and how long is your incubation period? Are you using any other type of elution besides a heat elution? Is your eluate tested against reagent red cells only at room temperature? I notice that the Technical Manual says that aside from room temp the eluate "may" also be tested at 37C and by the indirect Coombs test. Would anyone expect to be able to detect monoclonal anti-A,B in an indirect Coombs test? Any and all responses will be appreciated. Thanks!

Has anyone had any experience with either of these blood bank reagent vendors? Both exhibited at this year's AABB meeting. I believe that Diamed is out of Switzerland and Medion out of Germany. About two weeks ago I requested information from these companies but have thus far gotten no response. I was under the impression that their reagents were licensed in the U.S. but maybe I'm wrong. Thanks!

Any possibility this might be anti-Ce? This would react not react with the patient's own cells if his genotype was DCE/dce.

Does anyone have a good procedure to perform this with monoclonal ABO reagents? With the disappearance of polyclonal reagents I would expect that we no longer have any need for a 37C incubation either for the adsorption or for testing the eluate. Are you performing the adsorption at 4C and then eluting at 56C? Is anyone having any luck with an acid elution for this procedure? Thanks!

Do you automatically perform and report an antibody titer in the event that a prenatal patient presents with a clinically significant antibody? OR Do you require a physician's order before the titer will be done/reported ? How about billing? Is the titer included in the Antibody ID charge or is the titer billed separately? Just curious as to how this is handled! Thanks!

Several years ago (too many to mention) I was the Manager of Exam development at the ASCP in Chicago. In that capacity I worked with all the exam committees in developing their questions. This was shortly before computerized testing came to be. To get to my point, I would just like to encourage everyone who has had problems with the exam not to lose faith. Bear in mind that you are dealing with what I consider the most difficult exam put out by the ASCP. During my few years at the ASCP the pass rate for this exam was always the lowest of any other. The SBB exam committee always consistently seemed to come up with the most difficult exam questions. The mindset being that blood banking is the most critical of the laboratory disciplines that have an immediate impact on patient wellbeing. Like David I also took a practical exam for SBB certification and as he mentioned the written exam back then was quite light on patient and staff managerial issues. That's certainly not the case today. Aside from the difficulty issue I think that the low pass rate was also due to some individuals thinking that, because they were a blood bank supervisor, there was very little preparation necessary. Wrong! In any case, if you've taken the test once and not passed at least this gives you a feel as to what it's all about. Good luck, try to find others in your area to study with and keep a positive attitude even if you have to go back for a third time.

I see your point in relation to reactivity of less than 1+. But I think any reactivity of 1+ or more should indicate a titer regardless of RhIg administration. Otherwise you have no baseline for comparison. If the patient's initial post-RhIg titer is 1 and a month later is 8, there's a very good chance you're dealing with an RhIg failure. As far as gel titration is concerned we've experienced at least a couple of disgruntled physicians who have complained about significantly higher titer reports from hospitals using gel titration vs. our tube test. Of course the reference lab winds up as the bad guys. It's unfortunate that there isn't much more standardization between different facilities with the titration procedure. If everyone stuck to the AABB protocol life would be much easier.

We have a similar situation. There is a written SOP for both ABO & Rh discrepancies but we have given each tech a copy of a "work aid" which has specific examples of various discrepancies, the probable and possible reasons for them and the steps to take to resolve. This makes it a lot easier than having to sort through a formal SOP with extraneous information that is irrelevant to the problem at hand.

In my opinion a three-cell requirement for exclusions seems to be quite a bit too much. I've worked in hospitals and reference labs in which a one-cell exclusion, preferably homozygous, was sufficient and I don't recall us ever having any problems with that protocol. With the sensitivity of todays testing methods and reagents I think the chances of missing something by using less than three cells is very remote. I'd find it hard to justify the increased costs of labor and reagents using the protocol you describe.

Our reference laboratory seriously considered dropping the weak D test until we ran into a couple of roadblocks. The first was the cord blood issue. We eventually decided that we should be able to identify cord bloods so that a weak D test could be performed. The second obstacle was not so easy. How about situations in which a specimen is submitted for Rh typing on the husband of an Rh-negative prenatal patient. We have encountered a very small number of OB physicians who base Rh immune globulin candidacy on the Rh type of the husband. If we fail to recognize that this is a paternal specimen and that the husband is a weak D, the prenatal patient will not receive RhIg. I would think there would be some liability on our part if this was the case. Any thoughts?

Is anyone using the Provue or manual gel for direct Coombs' profiles? Since there is no anti-C3 gel card we have been advised that anti-C3 results can be recorded as a default result if the polyspecific is positive and the anti-IgG is negative. In other words a 2+ with polyspecific and a negative with anti-IgG automatically indicates that anti-C3 results should be recorded as 2+. I understand that part, but what if the anti-IgG results are 2+? I assume that you are then bound to perform a tube DAT with anti-C3. This somewhat defeats the purpose of using gel for DAT profiles since the great majority of polyspecific-positives will also be anti-IgG-positive and require tube testing. Also I would guess that your gel reactivity grading is routinely going to exceed what you will see in a tube test.

Thanks! May I ask what instrument you are using?

This question is for anyone using an automated instrument for Rh typing. I know most of us have eliminated the "weak D" test but I was wondering if anyone was following up their instrument Rh-negatives with a quick immediate spin tube test to confirm the Rh. I recently became aware of a couple of labs that were doing this because they didn't totally trust the instrument results. They claim that they are picking up the odd Rh-positive that the instrument is missing. In my mind this seems to be counter to the purpose of using automation. Any replies would be appreciated. Thanks!

Here's another "old schooler" opinion. I also think it's advantageous to have a microscope available for those special situations. This is especially relevant if you have techs rotating through blood bank or who cover several departments on one shift who may not feel fully comfortable turning out a "negative". Of course the other side of the coin is that they may tend to interpret two cells "holding hands" as a "positive". In any case I don't think bb techs should have no access to them at all.

Hi Cliff! Yes, I have been in touch with Immucor and they are saying that the level of mercury is too low to be of any consequence. Apparently the level is so low that they don't even mention it on the MSDS sheet. It does appear to be below detectable levels in our waste water since we are monitoring for mercury. Nevertheless our safety officer has advised us to switch to another enhancement medium since he says the EPA has been recommending that NO mercury containing products be used in situations in which the product will wind up being discarded as waste.

Immucor's ImmuAdd antibody potentiator contains thimerosol as a preservative. Since thimerosol contains mercury wouldn't there be a potential problem with the EPA since mercury would be emptying down the drain as the cellwasher decants it's wash? Has anyone heard of this being an issue? Thanks!

I posted this on the AABB website this morning but thought I would also post it here to cover both bases. A prenatal patient who we have been following monthly since July has demonstrated anti-D titers ranging from 4 to 8 and Anti-C titers ranging from 8 to 16 up until September. An October specimen gave a titers of both anti-D and anti-C at 32. Approximately 12 days later we received another specimen in which the anti-D titer was 4 and the anti-C titer 8. Three weeks later another specimen was tested and the titers were recorded as anti-D 4 and anti-C 16. Now for the problem. The patient's physician is insisting that the October results of 32 had to have been an error. We had parallel titered this with the November specimen and the same results as previously reported in November were obtained (anti-D 4 & anti-C 16). Nevertheless the physician is insisting that it is virtually impossible for a titer to drop this significantly in 12 days. Has anyone experienced a similar situation? Thanks!

This is an excellent point. I think that working this through the ACOG would probably be the most effective means along with us directly contacting clients. Unfortunately, my only experience with the ACOG was about five years ago when I wrote to offer a negative opinion on the reference to "albumin titers" in one of their bulletins. The only response I received was that my letter would be passed on to the committee. To this day the bulletin still refers to a critical albumin titer of >=16 and a critical antiglobulin titer of >=32. In any case it's worth another letter. Thanks for the suggestion.

I fully support the idea that the "weak D" test should be eliminated on prenatal patients. Unfortunately I'm coming from a national reference laboratory situation. Getting a hospital OB/GYN director to approve this is one thing. But I'm quite sure that no matter what type of physician education we might employ we would never get this concept accepted by 99% of the OB physicians nationwide.

My miscue Harry! The specimens which we are encountering are all RPR-Reactive, TP PA negative. I guess this illustrates that I'm a bit behind the times. Thanks!