rravkin@aol.com

Hey Donna, Would this same pattern occur in Ficin treated panel cells?:)

Hey Malcolm, Thank you for your comment. I wanted to know if you were aware of any BB instrumentation being developed around a prewarm format of testing? (and with the abscence of light) :)

I am wondering if pre-warm should be the primary technique as opposed to the RT, to 37C inc, and back to RT to finish. Pre-warm would more closely mimic the in-vivo state without any alteration of molecules from that state and thus give us better capability to prepare transfusable products. I think that our current processes being born out of RT data and techniques have created a convention for which we may not be able to break any time soon. I know that there were some previous threads that talked about the many anomaly reactions that we are forced to work up and lead to no clinically relavant solution. With the advent of automation in the BB I wonder if prewarming may soon become the convention because I believe it would be relatively simple to add heating elements such that your reactants could be prewarmed; especially when using GEL. I am no expert, and I realize that there may be some missed items but I would think it much more loggical to replicate the environment for which we want to know most about; and also with instrumentation in the BB there could also be a time when these reactions are run in the abscence of light. Let me know what you think; and thank you in advance.:)

It seems that there are certain checks that the computer makes and the manual system does not. If the manual system were designed to make these same checks and held accountable, through a form that is part of your issueing proceedure, then would this system be FDA reportable? Do we not have manual issue systems in place when, as one poster pointed out, our computers are down? So it seems that if history and attribute checks are accountable manually the why would manual issue be a reportable event?

Congradulations Heather!!!

Hey Donna, This thread seems to bring us back to another thread where the question was asked "how do we change an initial positive ABSC to negative?" Here, of course is the Rh. In practice since there is a discrepancy in the Rh result that will need to be corrected should we not just continue to give Rh-neg products? Also, I am noticing that I have not seen any posts from Malcolm on these past threads; is he on vacation? :)

Brenda, Thank you for this info and your experience. I have seen similar. Has anyone had any experience where each OR suite would have it's own refrigerator? An expence I'm sure, but I wonder if this would not be a practicle circumstance.:)

AmcCord, Your story is somewhat familiar. We would draw two specimens at different times and, preferably by different phlebotomists, on patients without any tangible history. The first specimen is for the type and screen; the second is for a confirmation of the ABO.Rh type only. In addition, we have a second tech retype the initial specimen. The key word here is "tangible history." The historical info on patients is unfortunately precarious at times and so if there is any question about viability we simply treat the patient as if they do not have a history at all. Also, determining the candidacy of a patient for RhoGam comes in the form of a questionare insert that accompanies the RhoGam and also in our policy. Usually, the mother Rh type has to be confirmed negative and the babies type does not necessarily have to be know at the same time. The date and time of the Rh negative confirmation is also required. If you want to be confused even more try checking out the thread about Du testing and it's implication in the issuence of RhoGam. Here, this thread suggests that the dicission to order RhoGam can be influenced by the result of the Du test; for example it was stated that RhoGam would be withhelded if the result was positive. I have to say that because the Du test does not have the capability of determining the orgin of a positive result making a decission to withhold RhoGam is a questionable practice; is the postive do to altered concentration or construction?? I hope this helps but there doesn't seem to be any easy answers at present do to restrictions in information exchange and associated liabilities.

We give Rh specific platelets to females of child bearing years. We try to maintain a stocked inventory.

Greetings Margaret, From the info given in the initial thread it seems that a total of three units of PC's were cleared. Also, what other testing is being done for this patient and are there any other diagnostic theories??:)

Very good Malcolm! :)

Lara, I think that the delema resides in the fact that you used a poly-specific reagent and your reference lab used a monoclonal AHG which, correct me if I'm wrong, is Anti-IgG and I beleive murine based. This case sounds like some other posts that Malcolm has addressed, and as you state as well, where we were dealing with an auto-antibody with specificity for the E antigen. However, here you may also be picking up some reactivity with the C3d component of the complement cascade as mentioned by Galvania. Please let us know what the outcome is.

Hey Judy, The practice you describe here is what I have practiced in every BB I've worked at. The reason for this practice in current times probably relates to a level of comfort amongst technical staff, nursing staff, and physician staff including the lab pathologist(s). As you know an ABO incompatablity is of the most severe type that can occur between recipient and donor. We are not just talking about a reduced circulating red cell life, we are talking about a complete and immediate demise of ABO incompatible red cells that can, and does, lead to patient demise, as seen in current literature and historic literature relating to the initial discovery of the ABO system. We also practice immediate spin crossmatch but the reactants here are not color coded and therefore one may perceive a reduction in reliability of such testing to confirm the ABO type of the patient. Considering the simplicity and second nature of this practice I think that many techs do question it but it's ability to confirm the type is sound. The impact of an ABO incompatibility is very far reaching; remember the ABO incompatible organ transplant at Duke University Hospital; that was all over the national news. Blood ABO incompatibilities doen't get as much exposure but the governing agencies that set policy for practicing blood banks keep a very close eye on this situation. So, in conclusion, we have a very sound and effective practice that avoids catastrophy. IF IT ISN"T BROKE THEN DOEN"T FIX IT! Hope this helps. :)

This case reminds me of situations where we were supporting a liver transplant and the initial PC's were type O Pos and the later PC's were ABO/Rh specific. The rational is that the initial units would bleed out during surgery and the later units would remain in the circulation. I'm not sure if this practice is applicable here. Perhaps some of our more experienced posters can comment. Additionally, Donna, fantastic advise!

Hey Malcolm, Thank you for your thoughtful response. If this case does turn out to be elicited by an immune response I will be just that much more in awe of the immune system; it is truely amazing! One side note though, I did not see a result for an auto control; this may yield more info.

Hey Margaret and Malcolm, Are the posibilities you present here capable of causing the clearence of three units of PC's within a few days with no appearent outward symptoms (only a slight fever), and no appearent serologic evidence to support an immune response ( I did not see a result of an auto control mentioned). I think that this case is very interesting. The patient had "coca-cola" urine prior to the initial ER visit and upon subsequent admission. The pre-transfusion Hgb=7.9, and after three units of PC's the hgb was only 9.2 with no appearent bleeding. With a normal, yet depleted, system the hemoglobin should have reached approx 11.9 (1gram per unit). It seems that the patient is clearing the red cells at a very rapid pace; approx. one third the total circulating volume for this patient; and this is occuring with only a slight temp noted two days later and curiously the patients hemoglobin resides there after at 7.2; the approx starting hgb. Given these facts is it not posible that we are seeing an overall upset in the isotonisty of the whole blood such that only a volume of rbc's producing a hgb of approx 7 g/dl can be supported. I think that it is very interesting that the initial hgb=7.9, post tranfusion hgb= 9.2, and after clearence the hgb is back to 7.2. It appears that this concentration of rbc's is the equilibrium piont or product there of. I guess what I am trying to ask is if an immune response can destroy approx. one third the circulating rbc's with no appearent symtoms and go undetected by conventional serologic procedures or is it equally possible that we are seeing an isotonic upset of the circulating whole blood with currently an unknown origin????? It seems that the suspition of PNH is more probable than an immune response in this case.

We do K/B staining on all shifts and on all traumas and post partum per doctor's orders. Whole blood (EDTA) specimens are used and the control consists of well mixed cord blood and adult male whole blood. One drop of cord blood to nine drops of adult male blood. We prepare the whole blood specimen and control for testing by adding two drops of each sample to their respectively labeled tubes and three drops of saline. The smear is then made as a we usually make a push smear. This ratio of whole blood specimen to saline almost always results in a monolayer of cells. But before we proceed to stain we check the smear under the microscope to ensure a monolayer. Then it's 5min of fixative, wash, dry, 10min of buffer, drain, and 3min of stain, wash, and let dry. View microscopically. The main difficulty in this procedure is simply the lack of practice. As John has stated earlier, but not this way, this procedure is based on staining fetal hemoglobin in an adult maternal system (where the fetal screen is based on detecting Rh positive cells in an Rh negative system). Therefore, many times this procure is ordered for any traumatic experience and any Rh type because, like we all said, the docs are interested in the extent of fetal bleed into the maternal system. Admittedly, the many times I've performed this procedure there have been only a very rare positive result. Once, we actually calculated a volume that was well above what the fetus' circulation could even support. We suspected that the mother may have had a subpopulation of RBC's containing fetal hemaglobin. Our TAT is approximately one hour but sometimes it can take longer. Before reporting any result a second MT will review the smears and any calculations. Both techs will initial the completed form and the result is always called to the floor. I personally enjoy performiing this procedure becuase I like the technical challenge, the microscopic work, and the mathmatical calculations, if needed.

Are there any orders for Serum and Urine Protein Electrophoresis? I think it would be interesting to see these patterns. I would also be curious to see what the rest of the CBC results looked like and the red cell morphology. Given the negative serologic results and the appearent elevated destruction of RBC's I wonder if we may be seeing something more systemic like an osmotic fragility situation, the origin of which remains to be seen.

Hey TimOz, I am not sure that I agree with your statement about the DAT test looking for in-vitro antibody binding. The DAT has the capability of detecting rbc surface bound IgG antibodies and/or the C3b or d bound product of the complement cascade depending on which reagent(s) are being used. When IgG reagent is used it specifically binds to the Fc part of the in-vivo bound IgG antibody. The auto control can detect anything in-vivo bound to the rbc's including IgM class antibodies whose specific would be detected through the eluate and panel cells, the same as IgG bound antibodies. If I have miss understood you please specify.:)

kmh76, I am writing to make a correction to my previous post. My initial understanding was that weak D testing would involve making a decision to give RHIG however I have realized that the positive weak D test would involve not giving RHIG. The real limitation of weak D testing is that it is unable to resolve the origin of the weak D; ie reduced expression of the D antigen (which would not produce an allo D, or if it did we would call it an auto D) or expression of an altered D antigen (ie D mosiac which could result in production of an allo D). As a result I think that I would agree with your view of not performing the weak D testing on L&D patients as there is little known negative effect of recieving RHIG when not truely necessary. I would also agree that if we wanted to be precise then a genetic work-up should be performed. I hope this helps in some way as I know it has helped me.

kmh76, I have always practiced performing weak D testing especially on Rh-neg L&D patients at various facilities. The testing and interpretation is really not at fault here with you situation, it is the course of action or lack of action on part of the practitioners involved with making the decission to give RhIG or not. I suspect that they are not understanding that a patient with an altered D Ag (weak D, for the most part) can develope an allo-D (against an unaltered D Ag). I am sorry to hear of your situation and you are absolutely right about the devistating effect.:raincloud Are there any policy changes on the horizon?

Hey Brenda, You are exactly right. I don't understand why the continuence of an Rh-Neg control with a historic AB Pos other than, as you say, to rule out panagglutination. Maybe you can give some insight on the relevance of panagglutination outside of the obvious distortion of the ABO/Rh type.:)

We do not use BB issued arm band ID's. We simply use the patients admission braclette for product transfusion ID purposes. I have woked at facilities which utilize the BB bracelet ID and had the same problems. There doesn't seem to be an easy fix. The patient's admission braclette is never cut off. Does anyone practice incorperating in some way the patient's admission bracelet with the BB ID bracelet??

Hey Malcolm, Absolutely fantastic!

We run an Rh Neg control once for each indated specimen to rule out panagglutination.