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Hey Liz, You may be interested in knowing that some blood component suppliers are titering Anti A, B in "O" type platelet pheresis do to an article from Transfusion Magazine where the researchers showed a connection between "O" type platelet phoresis donors and hemolyitic transfusion reactions do to elevated concentration of Anti A,B in this small population of donors. I saw a titer sticker on an type O phoresis platelet the other day. It was somewhat releiving given that ABO compatibility is not practiced strictly when transfusing platelets. However, my facility practices strict Rh compatibilty do to reasons given in previous posts.

Somewhere in the AABB Standards there is a statement that reads something to the effect that a crossmatched unit of blood should be performed only on an indate specimen. The indate specimen is only good for three days and therefore the crossmatched blood can only be good for this maximum time of three days. If the unit was crossmatched on the second day of the indate specimen then the crossmatch is only good for two days; so forth and so on.

This thread is interesting because it shows the direction of blood bank testing towards automation. Sure, today we may utilize these gel cards manually but this is just a stepping stone towards blood bank automation and I think that we should understand that we are witnessing the threshold of blood bank automation; for better or for worse. I have heard arguments from both sides, for and against automation, but as a spectator the whole process is exciting to see. One of the biggest concerns with blood bank automation is accountability; as David Saiken has posted in a previous thread CAP requires 100% correct results in blood bank; this statement pertaining mainly to ABO/Rh testing. When your patient population will continue to grow and have no prior history pertaining to ABO/Rh type accountability is a very big priority when automating a blood bank.

Mindy, I would agree with the other posters that there should be a zero tolerence for ABO/Rh mistypes, however I would also suggest further investigation into the circumstances leading to these mistypes; ie what other testing was occuring at the time, and if anything could have been done differently, this line of questioning will help gain understanding to issues pertaining to Blood Bank irganomics(spelling??) to technical practice and competence. I do not think you are being too strick; you may not be strick enough depending on your findings. Good Luck!!:)

Thanks Liz.:)

Liz, Thanks for the info. But I am still having trouble understanding how we distinguish ABO incompatibility with incompatibility based on other blood groups when our AHG crossmatch is incompatible. In practice I use GEL to perform AHG crossmatch and if it comes up incompatible the last possibility I consider is ABO incompatibility; of course we still do the IS crossmatch in parallel.

Lilym, Our procedures, practice, and most important, reagents do not identify the cause for the weak D; ie low antigen expression or altered antigen expression. When an altered antigen is expressed sensitization and production of an allo-D is possible. This is why RhoGam is administered.

Ejani, Sorry for the very late post but how can anyone tell the difference between an IVIG reaction and a hemolytic transfusion reaction based on the initial symptoms. Isn't the potential cause of the reaction decided after the transfusion reaction work-up??

Lcsmrz, It seems that if you are trying to omit the IS crossmatch when performing an AHG crossmatch your computer must be validated to catch ABO incompatiblity. In the abscence of this type of computer system it seems that your are obligated to continue with the additional IS crossmatch. So if we are performing an AHG crossmatch and we aquire incompatible results how can we distiguish the cause between ABO and other groups based soley on the AHG crossmatch. I think that this is where the IS crossmatch is beneficial because it is here that an ABO incompatibility is most probable, as opposed to the AHG crossmatch.

BorCliff, John C Staley gave good advice here but I would also add that, most probably, the majority of the 12 PC's tranfused pre-hysterectomy bleed out and now post hysterectomy, we are working with a closed system where sensitization would have a greater potential to occur. If, indeed, your O Neg PC inventory is too depleted to transfuse for this case then you would have no choice but to transfuse O Pos PC's but I don't agree that it is less likely the patient would now be sensitized because the system is now closed once again. Of course, the development of an allo-D, now, is of no relevance to a future prenancy.

Lilym, I would repeat baby's ABO/Rh type using a heal stick specimen. I would also repeat the DAT and eluate using lavender bullet specimens obtained through heal stick as well. And, as was mentioned, why is an Rh Pos mother receiving RhoGam? Additionally, what meds was the mother administered?

Malcolm, Your post here is very interesting, as most are, and it provoked so many questions. I will limit them to a few. If this enzyme is not working to full capacity does that effect the circulating life of the fetal RBC by reducing it? And if so is there potentially an overall underdevelopement of the infant and/or the fetus? And is it safe to assume that this is a genetically tramsmitted condition? As far as the specifics of the low enzyme activity, is it caused by a deviation of normal enzyme structure or is the enzyme concentration decreased from normal, or is there a deviation of normal substrate structure or a decreased substrate concentration, or some combination there of, or some other reason entirely. Boy, I think we have enough "Or's" to rowe a Vicking ship. Thank you in advance for any information and please don't feel obligated to answer all. Thank you.

Vic, Your case is an example of how mystical we all become in the face of "Non-specific reactivity. We rule out all clinically significant Ab's and yet feel some obligation to entitil this reactivity; a "Non-specific Cold" (do to RT testing despite the 37C incubation), a "Cold Auto" (do to what?? was an Auto Control run??),and an "Antibody with no apparent specificity" from Malcolm's post (is it always true that any reactivity detected using the gel card involves Ab-Ag reactions?) Your approach is the best way to call, and work with this situation. Gel cross-match compatible units are what's best for this patient, because it was in gel that you detected the non-specific reactivity in the first place. The use of a blood warmer based on these results is a precaution which doesn't seem to be entirely justified. However, I have always wondered why a blood warmer is not routinely used in tranfusion. It seems entirely logical that transfusing a warm, or body temp., liquid directly into the blood stream would be of greater benefit then a 5 to 10 degree liquid, for an obviously ill patient. Maybe this is why vital signs are taken twice within the first 30 minutes of transfusion, and, of course, the blood warms to RT during this time. Maybe the RN could take a vital sign after the first 15min of a prewarmed transfusion and then monitor the patient for the remaining transfusion time. Has it ever been shown that blood warmers are of no consequence? And, has it ever been shown that they are benefical? Are blood warmers really all that expensive and time consuming to acquire and utilize?

Hey Sunny54, Congradulations on your new position. You ask the sixty-four million dollar question. I would say that if you engage conversations that are outside the relm of work at the bench then you need to keep the idea that at some point the direction of the conversation needs to resume with work. The fact that we work in an enclosed environment aids in perpetuating all sorts of conversation but if you want your staff to focus on the work at hand and keep outside conversation to a minimum then you have to set the example by bringing that conversation back to the work. This is not easy and it takes time for a repore to build that gives you this level of control without being offensive. I wish you the very best of luck and keep us posted on how things are going.

Mary, How about just adding a word and check off box to the unit tag graphics as part of what the nursing staff would be responsible for. You could place the new graphic near where they fill out the vital signs.

Adiescast, Is it possible that if this is a brand new antibody you are seeing a predominant IgG concentration and a lesser concentration of the IgM that would have originally been generated and may be crossreacting do to it's lesser specificity?

Hey Malcolm, Thank you for clearing that up, and for the reference, and the info, and mostly for your positive influence. It is all greatly appreciated.:) But I have to ask, how can finding an antibody bound to red cells NOT be clinically significant with respect to the patient? This is what I am understanding from the first paragraph of your post.

Malcolm, What is a serologic transfusion reaction? Is it not clinically significant given the reactants involved, especially when working up a potential transfusion reaction; or is it an in-vitro induced anomally; can we tell the difference? Would it not lend to a more realistic diagnosis (for lack of better words) of the patient; and perhaps the patient's physician would want to check it again with a second specimen at a given time. You sound as if you would more readily accept a weak reaction in gel before you would accept the same weak reaction from the microscope. Do your feelings towards the use of the microscope in the blood bank revolve more around work flow as opposed to the significance of results obtained? I use the microscope sometimes in the BB and it's use can alter the workflow but only minimally for a DAT check, but much more significantly when your KHB is positive.

We had a similar situation but the conflict in Rh result was between the patient history at their doctors office and our current Rh typing using tube method. The historic Rh was Neg and our current Rh was positive; repeated on a second specimen one day apart. The patient, an L&D pt., was given RhoGam at 28 weeks gestation. The patient was now in for delivery when we acquired our findings. One interesting aspect of this case was the visual texture of the actual IS Rh Pos agglutinate. It had a somewhat rubbery or mucoid visual texture as we manipulated the tube upon reading. I beleive that this was do to the binding of the concentration of RhoGam to exposed D antigen sites. This binding would prevent our D reagent from binding to these sites causinig an incomplete or meshed agglutinate which would be limitted in it's ability to expel water potentially causing the mucoid appearence; and it did not have the more crisp texture and the clearer suppernatent background. The other interesting aspect of this case is that the patient physician still wanted the additional RhoGam that she ordered. Error on the side of caution; excellent chioce. But one complication that could occur with giving RhoGam to an Rh-Pos L&D patient would be that the Blood Bank staff would have to be alert to any orders for FMHSC using D antigen as the detection method. With this case and other like L&D cases that are encountered we need to perform KHB staining to detect any fetal maternal hemorhage. The reason I say this is because I can see the patient physician ordering an FMHSC and our staff performing the test and giving out a false Neg result do to the RhoGam binding D antigen sites and preveneting binding of the D reagent used causing the Rosette count to fall to a negative interpretation or not appearing at all; ultimately causing the generation of an allo-D in a positive D mosaic mother once the in-vivo RhoGam was overwhelmed or depleted which may not be seen until the next pregnancy and all sorts of problems to follow in a worst case situation. Of course this would be assuming that the circulating concentration of the fetal cells in the maternal system exceeded the life of that of the administered RhoGam and remained circulating long enough at a concentration capable of sensitizing the mother. I hope this helps some.

Thank you Liz for this info. I always learn something new here and I greatly appreciate it. This procedure is probably used in extreme rare cases do to the litigation potential.

Yanxia, In my post I was merely speaking of a fictious reagent cell that could be utilized as a positive control to be run with panel cells, if we were pressed to do so. The reason I brought this up is because I was understanding from the previous quoted post that an auto control was being utilized in this way, which didn't make sence to me for several reasons. I think that you would agree that if such a cell like this came up positive when running the panel any positive panel reactions would be questionable. The reality is that we do not have a control cell to run with antibody screens or panels and even though we have indirect control procedures in place to check the viability of reagent and procedure we do not really have any direct control to determine patient serum/ plasma, reagent cell, reaction viability outside of conventional serologic practices, which work real well, especially when experienced serologists like Malcolm and others are at the helm.

DR P, You have acheived an in formative and comical post here; and I am still laughing because it's true to real life! After performing all of these in-vitro manipulations the term compatibility becomes very obscure. And even if we attach the specific manipulations when reporting compatibility, at the end of the day we are still left with the same obscurity. It's amazing how complex things suddenly become. Thank you.

I should add that after reading over several other posts and reveiwing Malcolm's post from "Absorbance/ Adsorbance " thread I see how it is done very clearly. I'll try to read before I write in the future.

I have to say that I have never heard of using PEG to differentially adsord Antibodies and I am not sure that it has this capablity outside of varying the incubation time of the reaction volume, so I not surprised with "#4."

Hey Liz, You answered your own question;"PeG enhances reactions." PeG is polyetholene glicol (spelling?); that's right; anti freeze. Now what we use as a reagent in the Blood Bank is not exactly the same as what we use in our cars but the same principle is applicable; that is polyetholene glicol breaks up water. Water in our reaction volume has the ability to suppress the over mulecular charges present at the antigen epitope and the antiboby variable region by binding to individually charged particles at each site and therefore rendering the particles more nutral. PeG, by beaking up water allows these charged particles to maintain their complete charge and therefore enable stonger bonding between opposite charged particles comprising each site of the antigen epitope and the antibody variable region for both IgG, and apparently IgM class antibobies, according to the post given by David Saikin. Although it's late I hope this helps. This is a response to Liz's post to David Saikin about PeG. I overlooked the "Reply with Quote" icon.