rravkin@aol.com

Thank you Malcolm; I was beginning to think that you weren't going to get involved with this thread. I have actually writen this book title down from a previous post. I will enjoy reading about this subject. Thank you again. Rravkin:)

Adiescast, I know the type of prewarmer you are refering to but I think that there might be a practicality issue with it's use for a syringe given the extended length of tubing involved. I have not heard of any syringe prewarming device but I am not sure if there is a practicle way to prewarm a syringe in a controlled waterbath prior to transfusion.

David, I greatly appreciate your response. What is it about the encounter with the mother's immune system that causes the shift to IgG production in the fetus? Asked another way; what is it about the encounter with maternal IgG that causes the production of IgG in the neonate? You also say that the sensitivity of the IgG that crosses the placenta is meaningless and yet this very IgG is what confers immunity for the neonate in the first three months of life. Do you mean that the aquired maternal IgG has broad specificity? When I referenced the AABB Technical Manual 15th Ed, The ABO System, it stated that O type persons produced anti A,B IgG class antibodies while A and B persons produced anti-B and anti-A respectively of IgM class. I was wondering why it is that the O type produce an IgG class while the A and B immune systems did not; because one could then speculate that an A or B mother would not pass their corresponding antibodies to the fetus if they were IgM class and, therefore, further speculate that the newborn would not have the same immune protection of that of one born of an O mother. From your statement about the ubiquitious nature of ABO antigens one could speculate that production in the noenate of corresponding antibodies does not occur as a defensive process like that of alloantibodies but rather as more of an initial filing system, perhaps, on part of the noenates immune system. I will read up on this some more and I do appreciate any further responses.

Dear Subscribers, I present this thread with some hesitation as I am not sure of it's practicle value, but I do believe it will lead to some greater understanding of Antibodies and their production through the humeral response. We have O individuals that produce Anti- A,B IgG class antibodies. We have A and B individuals that produce Anti- B and Anti- A respectively that are IgM class antibodies. The question is, What is the sensitizing event that caused the respondent production of these antibodies, and when and where did it occur? Furthermore, because the O mother produces the Anti-A,B IgG class antibodies that will cross the placent; what kind of assistance, if any, does it offer the newborn in terestial survival given the idea that from a global perspective O type individuals are of the most survived humans on earth? Additionally, why is it that the A and B individual immune systems stop with the production of the corresponding IgM class antibodies, which will not cross the placenta? Are the production of these antibodies accomplished by the immune system via regular humoral response or are they genetically predetermined and produced phenotypically like normal cellular proteins and then released into circulation. I appologize in advance if this thread is percieved as being missmatched for this site but I have a burning curiousity about this subject and I thought it would make for a fantastic topic of discussion because the ABO system is the basics for Blood Bank practice and it seems that the origin of the corresponding antibodies produced are not well understood. :)

Sona, Have you checked with the O cell manufacturer?

Malcolm, Fantastic learning experience. I hope that you are able to get another specimen.

Malcolm, Does that QC protocol apply to all BB's in England or just to reference labs there? The reason I am asking is because the frequency of QC may have to do with use. I can not see the logic behind QC'ing the panel cells twice a day in a small hospital setting.

DBritt, We have experienced this at our facility enough so that we have a protcol of washing the sceening cells in saline and reconstituting in saline as well, and repeating the screen. The repeat is usually negative. I have some reservations about this procedure because there would be a difference in buffering range between MTS and saline. And I am not sure I accept the idea that a patient is reacting specifically with the MTS diluent either. I think that the correct way to describe this anomally is to say that a reaction is taking place in the presence of MTS but not in the presence of Saline. We have had no trnsfusion problems, however. So the MTS, with respect to certain patients, does cause what appears to be clinically insignificant reactivity.

Malcolm, Forgive me if I am asking this question again but is this the first pregnacy or past the first pregnacy?

Brenda, Alright, 2 identifiers. But I think the issue with hand writen BB specimens and pre-printed lables lies with the idea that there is some assurence that the specimen is being labled at the bed side or immediately after it is aquired. Correct me if I am wrong. But in reality there realy is no assurence that the specimen is being labled immediately after being drawn weather it is hand writen or using a pre-printed lable, outside of cameras maybe. And why is this labeling of the specimen so important immediately after the draw; because specimens get placed in other areas and can potentially get mixed up and mislabled as you know. I have recieved many hand writen lables and more often then not they are legible but still a good percentage are not. But the idea behind the hand writen lable is that it is being done at the bed side or immediately after the draw assuring that a misslabled specimen is not submitted to the BB. We practice at our facility the collection of a second specimen if there is no patient history and perform an ABO/RH. This practice gives us some assurence that the initial specimen was correctly labled along with other assurences. Does anyone know of any literature that studied the habits of personel handling the specimen and specifically labling it immediately after the draw? Personly, I prefer a printed lable; they are so much easier to read and check and there is no desyfering and if the first name is trucated then you are still left with some of the letters of the first name and other none-changing identifiers which, apparently only 2 are needed; all the better.

So Malcolm, You diabolical Serologist (ha..ha..), she forwards as an A but reverses as an AB. So we have a problem with the B's. Is it spring where you are; this is when all the B's come out. I am curious to see how the resolve will distiguish between wether the forward B reaction is correct or the reverse B reaction. With the info given it would seem logical to work on both simultaneously.

DrSBright, Can you give some level of sumation of this major study?

Brenda, At our facility we encounter the same situation. We allow for the first name to be trucated but the last name, MR#, and DOB are required in addition to the phlebotomist intials, date, and time of collection. We will reject the specimen if any of this info is missing or illegible. Also, according to AABB standards the specimen sumitted for BB testing must contain three unique indentifiers; these do not change. Additionally, the same strictness with patient indentification becomes more lenient as patients become more distant from the hospital. Floor specimens require three unique indentifiers while outpatient specimens require first and last name with the exception of BB.

Heather, Thank you for the info. Do you know why these time frames are in use and how they were established?

Malcolm, If I am reading this right the patient forwards as an A but reverses as an O. The only unexpected reaction is the negative reaction for the Bcells in the reverse type. I have seen this happen before do to the specimen having been drawn above an active IV site and suffering the subsiquent contamination. At the bench, and in the absence of specimen contamination, however, I would try incubating at RT for x-time and depending on reactivity incubate further at 37C for x-time.

Thank you Malcolm and you are welcome Fiza.

Heather, I was curious to know of any advantages there were to leuko-reducing prior to centrifugation? Is it better to filter a less concentrated product? This makes sence.

Suhu, I work in a similar system as you and we practice that the BB of the hospital where the patient resides has to have a current specimen there in order to issue blood products.

Sona, Do you mean will a malarial parasite infect other blood products in addition to packed red cells; the answer is yes. Take Falciparum for example. This malarial species has several known stages within it's lifecyle that reside outside the red cell and are free flaoting in the plasma. Donors with a history of malaria are rejected for donation because it is difficult or impossible to completely irradicate or cure. Also, when one goes to donate there is a series of questions asked some of which pertain to travel to ares known for high occurance of malarial infection within a given time frame. Have you ever donated blood? If not, try sometime and you will encounter this series of questions.

Fiza, The answer you seek lies in the molecular surface of each type of vial. Plastic vials have a more open and charged molecular surface then glass. This property resides in the molecular construction of each type of tube. The open and charged surface of the plactic tubes is what generates the static electricity which causes variable attraction of what every liquids are dropped into the tube. The liquids we use are also charged so there are attracting and repelling charges which causes the variation in drop sizes and binding to the plastic. The molecular face of glass is much less charged and much more inert (ie does not react with other substances). I hope this sheds some light on your question.

Trisram, Did you run a known antisera as a control after you washed the cells 6 times? I am asking this qestion because I am wondering if after six washes you may be denaturing most of the potential antigen sites contained on the screening cells despite manufacturer's recommendations. Also, there is a reaction buffering issue. MTS diluent buffers the reaction volume within a certain pH range while normal saline may not buffer to within the same range potentially causing missed reactions.

Sonia, As you questioned intially, the whole blood to anticoagulant ratio may be altered such that the anticoagulant properties are depleted therefore unable to anticoagulate causing potential clot formation in the unit of blood. As some of the other posters stated there is a +/- 10% range for the volume collected to anticoagulant ratio ( Anyone please let me know if this understanding is incorrect). Do you know how much more than 500 ml was in the bag? 10% of 500ml = 50 ml; so if your total volume is >550ml then the unit may not be usable as it would exceed the anticoagulant capacity.

Thank you all again for your valuable posts. I am speaking about Single Donor Platlets as Aakupaku has said. I wanted to know if you utilized the SDP for only that neonate for which the initial aloquot was made or is the SDP utilized for other neonates or other patients as well? The reason I am asking is because many hospital blood banks that regularly transfuse neonates packed cells utilize the PC specifically for only that neonate for which the first aliquot was made in order to reduce the number of exposures to different donrs. Also, I would like to ask if you give ABO/Rh specific SDP's. THe reason I am asking this question is because I know that for adult transfusions of platelets ABO/Rh specificity is not always practiced and I also know that it is a rae occurence that some "O" type platelets contain abnormally elevated concentrations of anti A and B, and this has cause some noted complications. Lastly, I wonder when, where, and how we are going to start checking for bacterial growth in this product weather utilized whole or in aliquots. he biggest proble with platelets, as you know, is the fact that it being a room temp product makes it the most like candidate for bacterial contamination and this has been shown. The bartial testing perormed at the donor center has a sensitivity level even though some centers may use genetic detection sytems for thier testing. Basically, the bacteria that slips under these detection systems can still growth and at the third or forth day of shelf life may contain enough bacteria to cause a problem especially in a neonate. Do any of you know of any literature that addresses the concerns I have mentioned here? Thank you all once again, and I am sorry for the lengthy post.

Sonya, These reaction strengths are very significant. Did you retype the unit as Malcolm had suggested? To answer your question on preference; I do not have a prefernce for either procedure. I untilize the procedures as needed. The primary procedure at my facility utilizes the Gel Method. If we get scratchy reaction(s) with the gel card and see the panel as negative we will sometimes repeat the Ab screen in tube just to see if the reaction holds up. Sometimes it does and but more times it doesn't. Assuming that the DAT was perform using the Gel Cards I would suggest you check the card holders on the card centrifuge to make sure that they are in tact and are free of any obstruction. When the card spins the columns start out verticle, as you can see upon placing the card on the wheel, and then the columns are supposed to orient completely horizontal with centrifugal force. This force also causes the cells to migrate through the gel in the columb. If the card holder's movement is obstructed then card may not orient completely horizontal. When this happens the cells may not migrate to the bottom of the columb (if they are negeative of course) and the result may be what appears to be a positive reaction. While looking into this you may also want to repeat your AB Screens using freshly opened screening cells. This is a long shoot but I have seen that rarely the screening cells utilized with the gel over time sometimes do not give the same performance as when they were first opened for any number of reasons. The possibility that AB's were missed in three patients on the same day is unlikely but worth checking just the same especially since the DAT of the unit was negative. But check your card centrifuge first. Also, a question for Malcolm; Malcolm do these reaction strengths of 1+ and 3+ correlate with the posiblity of a low incidence antigen as you had suggested? And if so can you give any insight on the probability that the cause is a low incidence antigen in comparison to the other potential causes for what we are seeing?

RR1, Thank you for your insight. But let me ask you, if you are not adverse to being taught something new then aren't you a student? In fact we all are. So according to L106 an instructor has to "come down to the student level" so that we become learned. I honestly feel that there is a distinct and subjective level of condensation in that post and I find it insulting and offensive. I agree with everything you say except I really don't see humility in these words.