johna
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Posts posted by johna
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One of our labs recently came up with a question as to whether it was acceptable to run the "weak D" test without an Rh control and accept the results if they are "negative". In a situation in which the "weak D" test is "positive" they would repeat the test along with an Rh control to validate results.
As far as I'm concerned I don't see any problem with this and the CAP inspection checklist does not seem to address the issue specifically. We do not get AABB inspected so I'm not sure if they do or not.
Any comments would be appreciated.
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Our reference laboratory occasionally notices very weak, apparently non-specific Coombs reactivity with an antibody screen which seems to have some association with a reactive RPR (negative MHATP). I recently managed to get a copy of a few pages from the latest edition of Petz & Garratty's "Immune Hemolytic Anemias" which describes a report of anticardiolipin antibodies in 22% of SLE patients. The presence of these antibodies caused both positive direct and indirect Coombs tests. We have also noted that some of these RPR-reactive patients have unexplained weakly-positive DATS.
As far as we know none of the patients that we have seen demonstrate this phenomenon have SLE, but we are rarely privy to this type of information. I was wondering if anyone else has seen anything similar to this. Look forward to your comments.
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We would only recognize an A2 if there was a reverse group discrepancy due to anti-A1. In that case we would issue a comment in the report indicating: "The patient appears to belong to the subgroup A2 and has anti-A1 present". Any subgroups lower than A2 should be easily recognized because of their very weak reactivity which is occasionally mixed-field (A3).
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I'm not in a hospital situation at this time but the hospital where I formerly worked had a policy that the antibody screen specimen be drawn prior to the injection but the test did not have to be completed beforehand. This seems reasonable to me from both a patient and laboratory convenience perspective. The patient doesn't have to wait around for results and the blood bank doesn't have to deal with a stat.
The chances of the patient being immunized at 34 weeks is remote and even if she was the pre-RhIg specimen would serve as a baseline for future testing. The anti-D in the injection would have a negligible effect on future titers and the only loss would be a vial of RhIg.
I realize that there's a move to eliminate these pre-RhIg antibody screens but if they are useful in identifying only one Rh-sensitized patient a year I would still support them.
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I've had several years experience in a reference laboratory but don't recall ever encountering anything that fits this description. My guess would be that it was just a fluke. Does this antibody also react in LISS and albumin? PEG is notorious for weak scratchy reactions that mean nothing.
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There have been some slings and arrows thrown at the concept of prewarming in recent years but when you're in a bind with a cold auto or allo that persists through to the AHG phase what are your other options? I've been a blood banker for many more than a few years and have never encountered a problem using the prewarm for crossmatch or screening.
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Our lab is dealing almost exclusively with prenatal patients and ABO/Rh typing is performed on the Olympus PK-7200. The Olympus automatically performs a "weak D" test in a separate channel from the initial D typing. We repeat any "weak Ds" manually as a secondary check before reporting.
I'd fully support the elimination of "weak D" testing if it wouldn't throw our docs into a turmoil. We already run into situations in which we report "Rh-positive, weak D" and a hospital reports "Rh-negative". Unfortunately we do not have the luxury of receiving social security numbers or something akin to a hospital number which would allow us to cross-reference previous with current results. Therefore by dropping "weak D" we'd wind up with a small number of reports which are in disagreement with previous ones and we wouldn't be aware of that until a nurse or OB calls screaming that we've made a miscue.
On the other side of the coin, from a hospital perspective you'd be able to track any discrepancies between past & current results through the SS# or hospital number before results were released. I don't have any solid data but I'm sure that from an economic perspective the "wastage" of RhIg is minimal compared to the reagent/labor cost savings by dropping "weak D".
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It is the opinion of some that validation of a new reagent is not required unless as long as you use it according to manufacturer's directions. Of course, QC is required.
I have to along with Dawn on this one (assuming that her "opinion of some" also refers to her opinion). Personally I can't see that a validation study related to a change from rabbit to monoclonal antiglobulin reagents is going to give you any relevant information. The reagents are strictly quality controlled by the manufacturer, FDA approved and the direction circular clearly spells out the protocol to follow. In addition the reagent is included in daily in-house QC. I'm not sure that anything more is necessary.
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I ran into a post on this forum that ran back about a year ago in which someone said, "You can't pay people differently for performing the same job!". Am I totally off base or is this statement very inaccurate.
I work for an organization that has a different salary scale for MTs and MLTs, which I would guess is pretty much par for the course in a laboratory. Many of these techs are performing exactly the same functions. Our job descriptions of the two differ to some extent since the MT is described as having some administrative responsibilities. But the bottom line is that when an MT and an MLT come to work, in some cases they sit side by side and a casual onlooker would see no difference in their performance or work duties. A few years ago I had an MLT quit because she knew that an MT with the same time in was doing the same job as her at a higher pay rate.
Is there a consensus that everything being equal, MTs should be paid more than MLTs? As far as I'm concerned it's a given.
Any comments would be appreciated.
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I am new to gel and can't get over the number of Anti-Ds we are working up on our moms. What protocols are being used to report these out? Do I need to titer each of these or sent it out for IgM/IgG determination? Is there anything to support a "negative screen at 28wks, RHIG given within last 3 mon and 1-2+ reactions" concludes "Anti-D most probably due to antepartum RHIG"?
Any responses would be most appreciated!
Debbie
Debbie,
I'm coming from a large reference lab perspective and was formerly employed as a tech rep for one of the RhIg manufacturers.
We are using solid-phase for antibody screening and encounter much the same problem that you are with post-RhIg anti-D. Since we do not have the luxury of having patient history readily available, we are simply reporting the antibodies as is, without any commentary. The docs and nurses should be aware that an antepartum RhIg injection will often result in a positive antibody screen prior to delivery. IgM/IgG determination would be of no practical use since most actively-produced anti-Ds by far would be IgG in nature, as would the antibody in the injection.
We titer all anti-Ds since the rule of thumb is that the titer of a post-RhIg antibody should never exceed 4. If the titer is 128, it's not due to the injection. As far as a "negative screen at 28 weeks" being a baseline to suggest that an anti-D post-RhIg is due only to the injection, you can suggest that but you certainly can't rule out the fact that the patient may have developed her own anti-D at some point after the antepartum RhIg was given. Hope this helps!
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We are a reference laboratory performing >100 antibody IDs a week and deal almost exclusively with prenatal patients. We've consistently noted what seems to be a significant correlation between the presence of very weakly-reactive Coombs antibodies which defy identification and the presence of false-positive reactive RPRs.
Some time ago I posted an inquiry on the AABB website and the only feedback that I received was from someone who recalled reading that the antibody involved in this phenomenon seemed to be directed against lipids on the red cell membrane as opposed to a specific red cell antigen. I've not been able to get any further information on this but was wondering if anyone else has had similar experiences and/or may know of any publication reference for this. Thanks in advance!
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--------------------------------------------Sir,
In our experience The blend which has IgG and IgM detects both D and weak D antigens and there fore it is not found necessary to do the Weak D testing separately.
Thankyou.
I would seriously question that any anti-D reagent can be touted as having the ability to detect "all" weak D antigens. From a reference laboratory perspective we've encountered occasional weak D specimens which react with some but not all IgG/IgM blends even after the weak D test is performed.
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For anyone who has changed from rabbit to monoclonal Coombs serum reagents I was wondering if you saw any need to validate the monoclonals? It seems pointless to me since they are basically generic equivalents and are quality controlled through daily reagent QC as well as the use of Coombs control cells. Any comments would be appreciated.
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Coming from a reference lab environment I generally don't get too much of a feel as to what the transfusion services are using in the area of instrumentation. Our lab branches have several locations using the Rosys Plato as well as a couple with the Olympus PK-7200 but neither of these instruments seems very applicable to a transfusion service.
Ortho's gel system automation seems to have gained some popularity but from what I understand it may be a bit pricey on a cost/test basis. Both the ABS2000 or the Galileo seem to be viable alternatives to gel.
In any case, would someone who has evaluated and/or is using automation in a transfusion service care to comment?
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Cliff,
How about using the "Forum" name preceded by some derivative of "Immunohematology". For instance: ImmunoHem, ImmHem or IH.
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I've never had to become involved with CPT codes before until I was asked by our Billing department to resolve a couple of questions.
Code #86885 (Anti-human globulin test, indirect, qualitative, each antiserum) seems to refer to an antibody screen or red cell antigen typing, however #86850 is an Antibody Screen and #86905 and #86906 seem to cover antigen typing. And what's with the "each antiserum" for #86885?
Code #86886 (Anti-human globulin test, indirect, titer, each antiserum) seems to refer to a Coombs titer. But what's with the "each antiserum"?
Any assistance would be appreciated.
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Was wondering if I could get some comments on the current use or non-use of the prewarm technique. Within the past couple of years the procedure has been the recipient of multiple slings and arrows by a few noted authors in the field.
Personally, coming from a reference lab which deals almost exclusively with prenatals, I still find it hard to believe that an anti-M which is prewarmable could possibly have any effect during pregnancy. Obviously these screens should be followed up periodically to exclude the development of a warm-reactive IgG anti-M but at what point do we simply avoid titers in these cases? The problem with reporting titers with these specimens is that unless something like DTT or 2ME are employed one is giving the physician a titer which is falsely elevated due to IgM activity. Admittedly some of this reactivity may be due to IgG antibody which is non-reactive at 37C, but how relevant would that tend to be?
In any case, any comments regarding your protocol for both prenatals and transfusion candidates would be of interest. Thanks!
In any
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Some time ago I posted a similar question on the AABB website and the consensus seemed to be that for the most part microscopes should be kept out of the blood bank. Personally, having \"grown up\" with a microscope by my side through years in both transfusion services and reference laboratory, it's difficult :cry: to break the bond. I guess my feeling is that if my staff is well trained using a microscope we should not have the \"overreading\" problems which tend to complicate matters.Basically I was wondering what the general opinion is as to whether scopes should be used to read Coombs reactivity, whether for direct or indirect Coombs testing.
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This is John Alfano reporting in.
I'm the Standardization Director/Supervisor for LabCorp's main Immunohematology facility in Burlington, NC. We perform primarily basically all the testing that a transfusion service does with the exception of any testing associated with transfusion. The Burlington location serves as the primary antibody identification site for the LabCorp system and consequently we perform roughly 40-50 IDs a day (which makes a workday very interesting).
This seems like a great website and I look forward to joining in the discussions.
Some time ago I posted a similar question on the AABB website and the consensus seemed to be that for the most part microscopes should be kept out of the blood bank. Personally, having \"grown up\" with a microscope by my side through years in both transfusion services and reference laboratory, it's difficult :cry: to break the bond. I guess my feeling is that if my staff is well trained using a microscope we should not have the \"overreading\" problems which tend to complicate matters.
How Many samples to Validate a New Method
in Education / Quality
Posted
I agree with John. What's the point in validating a procedure that's fully approved by all the regulatory agencies and is being used by well over half the blood banks in the country. The results of a validation may look nice on paper for an inspector but would have no practical value. In these hard economic times it would seem more sensible to devote the time spent in doing this evaluation to something more productive and constructive.