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And to give credit where credit is due, whatever I have achieved has been with the invaluable contributions of my collaborators, including physicians, scientists, medical technologists and nurses. In particular, my most important collaborator has been my wife, Dr. Joanna Heal MBBS, MRCP, whose brilliance and dedication to patient care made all the difference. That's her in the picture :).

I just read what I posted yesterday and would like to officially submit that post for longest sentence of the month. Scott

I have NO idea who are HFAP, but I would say that, whoever they may be, they are complete idiots. Your way of treating the patients as D Negative until proven otherwise (i.e. the patient is D Positive or is Weak D Type 1, 2 or 3) is EXACTLY what is suggested by people who actually know about the subject on both sides of the Atlantic (Daniels G. Variants of RhD – current testing and clinical consequences. British Journal of Haematology 2013; 161: 461-470, and Sandler SG, Flegel WA, Westhoff CM, Denomme GA, Delaney M, Keller MA, Johnson ST, Katz L, Queenan JT, Vassallo RR, Simon CD. It’s time to phase in RHD genotyping for patients with a serological weak D phenotype. Transfusion 2015; 55: 680-689). I have, as I said above, no idea whether this was an HFAP ruling, or the ruling of a rogue inspector from HFAP, but, either way, I would be appealing against the citation, or changing the organisation who inspects my laboratory, if the appeal is rejected. From my point-of-view (and I have a bit of experience) you have done no wrong, but the inspector/inspectors have not got a clue about the Rh Blood Group System, and, in particular, the vagaries of the RHD gene. My own wife is D Negative, and if this lot forced her to be assigned as D Positive on such minimal reactions, I would be suing immediately. Sorry about the rant!

LOL! We would send it to our reference lab! We have other things to do here... Scott

Based on an observational study of ABO grouping in Gel I reported at the 1997 AABB Annual Meeting, ABO Plasma Grouping discrepancies occurred in 0.8% (26/3183) adult ABO grouping tests in Gel. Anti-B was not detected in 24/26 patients, anti-A was not detected in 2/26 patients, and anti-A1 was not detected in 3183 patients. In comparison, anti-A and anti-B was detected in 19/26 patients by the immediate-spin tube test, and was detected in 7/26 patients after 10 minute incubation room temperature incubation and centrifugation. Based on this study and 20 years of gel testing since that time have shown me the anti-A1 is rarely detected in Gel and that 70-80% of ABO plasma grouping discrepancies are resolved using the immediate-spin tube test. Centrifugation is used quite differently in gel versus tube testing. Centrifugation is used to separate agglutinated cells from un-agglutinated cells within the gel column, but is used to enhance agglutination in standard tube tests by forcing cells together at the bottom of the tube. This may contribute to the increased sensitivity of tube testing in ABO Plasma grouping tests.

Just from a man-power standpoint, you don't always have the time to "extra" antigen type. I've seen pts with anti-E that receive products on a weekly basis (that happen to be cancer pts) that have yet to make the anti-c. What about the extended billing for antigen typing? It just seems like a gross assumption to believe a pt with an anti-E acquiring a unit of red blood cells will form an anti-c from it (going back to Malcolm, who initially replied that the anti-E could have been made for reasons other than transfusion). I agree with the serological science of why these are seen together, and why the anti-E can lead to the anti-c, but I have trouble justifying the cost of tech/time, reagents, and billing, to go off a hunch that the anti-c is probable.

Hi Logan, I am an AABB perioperative assessor (and laboratory manager )that works at a facility in Boston MA that uses cell salvage on over 3,000 cases annually. We have 11 machines, and although we are not (yet) accredited by AABB, with the work we have done with our program, we are hoping to be accredited for periop by our next BB inspection. I got involved in this because our SVP for surgical services asked me, as the resident AABB SME, LOL, to evaluate effectiveness of cell salvage at our facility. She wanted us to adhere to the AABB standards and thought I was their best candidate to lead the effort. 6 years later, the past practice is truly history. To answer your question, we do QC quarterly on each machine that we have in use--- Hgb and Albumin. AABB allows you to decide what and how much is needed, but for quality purposes, you really do need something to make sure your equipment (and operator) is obtaining the best possible product for the patient in between PM's. If you would like more information on our approach, I am happy to share what we do, just message me and I will give you my work contact information. Between Cell Salvage and other specific PBM strategies, we have reduced our organization-wide transfusion ratio per adjusted patient discharge, from 0.78 to 0.17, in ~5 years time. ( Caveat: The cell salvage program overhaul took some time and was truly implemented last). I actually like to think it is because Blood Bank is involved, but honestly, it takes a village and I had to build influence up with the surgical services team and make really good use of my role as Transfusion Committee Facilitator to make things happen. Best, Linda

If you use DDT, you won't last long either!!!!!!!!!! SORRY, I couldn't resist it!!!!!!!!!!

Someone above commented that a 2nd sample is only required in the U.S. for computer crossmatch (which used to be true). But with the 31st Edition of AABB Standards (effective April 1, 2018), this requirement was moved so that it now applies for all pretransfusion testing for allogeneic transfusions including all types of crossmatching (IS, AHG, and Computer crossmatching). This is more in line with CAP requirements and makes more sense in order to detect possible Wrong Blood In Tube (WBIT) events. AABB Standards for Blood Banks and Transfusion Services, 31st Edition 5.14.5 Pretransfusion Testing for Allogeneic Transfusion There shall be two determinations of the recipient’s ABO group as specified in Standard 5.14.1. The first determination shall be performed on a current sample, and the second determination by one of the following methods: Testing a second current sample. Comparison with previous records. Retesting the same sample if patient identification was verified using an electronic identification system or another process validated to reduce the risk of misidentification. Standards 5.11 and 5.27.1 apply. Personal Note: If you intend to retest the same sample (by a different person or the same person), be prepared to show the AABB assessor your validation proving that your "another process" is actually validated to reduce the risk of misidentification (i.e. WBITs). CAP Checklist Requirements: TRM.30575 Misidentification Risk The facility has a system to reduce the risk of mistransfusion for non-emergent red cell transfusions. NOTE: Mistransfusion occurs from misidentification of the intended recipient at the time of collection of the pretransfusion testing sample, during laboratory testing and preparation of units to be issued, and at the time of transfusion. Misidentification at sample collection occurs approximately once in every 1,000 samples, and in one in every 12,000 transfusions the recipient receives a unit not intended for or not properly selected for him/her. The laboratory is expected to have implemented a plan to reduce these risks through implementation of a risk-reduction system. Among options that might be considered are: (1) Verifying the ABO group of the intended recipient on a second sample collected at a separate phlebotomy (including the recording of the result in the institution's historical record); (2) Utilizing a mechanical barrier system or an electronic identification verification system that ensures that the patient from whom the pretransfusion specimen was collected is the same patient who is about to be transfused. Other approaches capable of reducing the risk of mistransfusion may be used. The laboratory should participate in monitoring the effectiveness of the system that it implements. The laboratory should also consider improvements in procedures and/or educational efforts as part of its program to reduce the risk of mistransfusion. TRM.40670 ABO Group and Rh(D) Type Verification The recipient's ABO group and Rh(D) type has been verified by repeat testing of the same sample, a different sample, or agreement with a historical type in the laboratory's records. NOTE: Repeat testing of the same sample may be inadequate unless the sample has been drawn using a mechanical barrier system or digital bedside patient identification system. For laboratories that employ computer crossmatching, serologic crossmatch techniques must be employed when ABO typing discrepancies are present (e.g. mixed field reactivity, missing serum reactivity, apparent change in blood type post hematopoietic stem cell transplant).

I think how rural you are also plays into this. We are the only lab that does antibody IDs in a region of rural Oregon the geographic size of a small Scandinavian country. Our blood supplier is 3.5 hours away over a mountain pass and it snows here. I am not 100% convinced that we should do this but the logic behind our policy to avoid causing production of anti-c is because 5 small hospitals with no ABID capabilities would preserve the ability to select Rh negative blood in an emergency and have very good odds of it being compatible in a patient with a known anti-E, but once they have anti-c that option is gone. We can screen for the c antigen here but if we need to find 6 units our odds get ugly and we would rather get them from the supplier--but they are not exactly across town.

In the UK, we have this (relatively new) saying, "Why give two, when one will do?" This is NOT for someone who is bleeding out, of course, but for your "Average Joe" who needs a transfusion. It is predetermined what Hb level the patient needs, and a second (or subsequent) unit will not be released unless the patient's Hb has been checked. If the Hb has reached the predetermined level, the unit will not be released. This is not something that is decided by the Consultants at the Hospital; this is something that is decided by the Chief Medical Officer (nobody above him/her except the Minister for Health)!

Testing the same specimen twice may detect some internal testing errors, but will not detect WBIT (Wrong Blood In Tube). You need to gather some data to show how many patients would be impacted by collecting a second blood sample. Ask these questions, "How many patient admits annually?", "How many patient admits required blood bank testing?" (at my facility the calculated percentage was 11%), "How many patient samples type as Group O?" (at my facility the calculated percentage was 55% and we don't draw a second blood sample on these patients), "Of the non-Group O patients, how many had an independently collected blood sample in Hematology that could be used for the second ABO blood sample" (in our facility that was calculated to be 16%). So for every 1000 patients admitted annually, 100 (I'm using 10% for sake of simple calculations) would require blood bank testing of whom 45 (100-55) would be non-group O, 7 (45 x 0.16) would have a blood sample in hematology, leaving 38 (45 - 7) or 3.8% (38/1000) patients requiring a second sample to be collected. Using this kind of data will give you a much better grasp of the impact of routine performance of a second ABO determination on all patients for whom a Type and Screen or a Type and Crossmatch is ordered.

Considering the push to using Low Titre O Whole Blood for MTP and trauma's, i'd say the benefit outweighs the risk. I have personally seen two incidents where a panicked Blood Banker accidentally issued O FFP in emergency release situations. In both cases, the patients turned out to be incompatible blood types (one A one B). Guess what, there was no adverse effect whatsoever in either case. No sign of hemolysis or transfusion reaction weeks later.

I remember John Judd once advising me to titrate an anti-M suspected to have an IgG fraction and not worry about separating the IgG from the IgM unless the titer became significant. Then we could titrate it after destroying the IgM if need be to see what the true IgG titer was. It never exceeded something like 8 so we never had to send it out for additional testing. These seems something like that--drawing a line of what is safe to save the cost of extra testing. Only do the additional testing when it is no longer safe to avoid it. You would have to determine how you will turn it out so as to not overly confuse the OB/perinatologist. "Titer against c, E, Fya, Jkb and S positive cell = 8"? Then next time when it is 16 with a cell of that phenotype, you would repeat separate titrations and results would be "titer against c & E positive cell = 8 & titer against Fya, Jkb and S positive cell = 4"? Or do you then go to separate cells for all of them but the E & c? Or turn it out as 16 and they quit using titers to monitor? I can see some logic to moving to ultrasound monitoring as soon as the cumulative titer is above 16 or so but we also like to watch how titers change over time to help us guess which antigens baby is positive for. If you already tested amniocytes for antigens that would be moot but if you have only serology to go on you could miss some clues. We titrate E & c together because they are likely to be inherited together and separate E+, c- cells are hard to find. It also depends on if you can reliably find the same phenotype of cells for the next titration (we don't have the perfect world of using the same specific donor cell for the entire pregnancy). Maybe it also matters if you know dad's phenotype/genotype. If he is R2r then baby could be c+ E- but not if he is R2R2. Sorry to ramble on; surely someone with more experience in this than I can answer with something more substantive but I've enjoyed speculating.

I agree that blood bank refrigerators in the OR (or anywhere else) are accidents waiting for a place to happen. We use a temperature monitored and controlled cooler system so that the blood for the patient in the OR is sitting right next to the anesthesiologist. Have had no mistransfusion accidents in the OR in the close to 40 years I've been here. In the hospital where I trained there was an OR refrigerator and we had mistransfusions every few months. Case closed.

Scott, you are kind of contradicting your self here. In one sentence you are advocating avoiding the production of anti-c which can only be accomplished by screening units and transfusing c= units. Then you say it would be nice if you did not have to screen for units. I see a conflict here. Bottom line, it's a gamble. Either you screen for c= units now to prevent anti-c or you take the chance they won't make anti-c and if they do you start screening units then. The latter was always my choice.

I'm sure Malcolm can give you the hard numbers and details but keep in mind that not every D- person responds the same when given D+ RBCs. Some will develop anti-D with as little as 100 microliters of cells or less while others will never develop anti-D no matter how many units of D+ RBCs they receive. Then everyone else is scattered around in between these 2 extremes. Then throw in the males and women who are beyond child bearing and it becomes even more complicated. I fall into the category believing that try to prevent the formation of anti-D after a transfusion event, especially one of multiple units is counter productive and an effort in futility.

With regard to PI with platelets, it is true you do not need to test the PI products but Babesia testing still needs to be done for RBCs collected in the 13 states of interest. Regarding test strategies, some hospitals,eg Johns Hopkins, has opted to do secondary bacterial testing on day 4 rather than the PGD test. Attached is a recent study covering the cost effectiveness of the approaches believed to be acceptable by the FDA. However, as noted the Guidance is not Final. This paper is a good starting point though. platelets Cost effectiveness methods bacteria testing Transfusion 0419.pdf

A fairly short, but very interesting interview with Neil Blumberg in the July 2019 edition of AABB News, as he his one of three new inducts into the National Blood Foundation's Hall of Fame. Congratulations Sir and, from what I know and have read, thoroughly well deserved.

1) The original antibody ID matched an anti-D, as did the eluate. 2) Just one source for anti-D testing. Its a poly-monoclonal blend. and... We are pretty sure the gentleman has NOT had any Rh immune globulin. Genomic testing is, indeed in process, as we have sent the specimen to our reference lab. The forward reaction with anti-D was a strong and clear 4+. A partial or weak D is unlikely. The rest is being processed at our reference lab this week. I will post results here... Scott

If your patient is Kell Negative (Ko) you have real problems. If your patient is K Negative, you, and your patient, have more chance!

I am sorry, but this rather proves to me that the FDA should take more advice, if they are going to claim to be the "be all and end all" in terms of ultimate authority. I, and many people much more expert in the field than me (to name one, Dr Geoff Daniels), would agree with Dr Gandhi that serological ABO typing is far superior to molecular typing, BUT, the same cannot be said for RHD typing, where molecular typing is vastly superior to serological typing (not least because no blend of monoclonal anti-D reagent can detect all weak and partial D types, and no monoclonal anti-D has yet to be found that will not react with a Partial DIII). It is also disappointing that Dr Gandhi is unable to use the internationally accepted terminology for the D antigen. Many, many moons ago, Dr Patricia Tippett, who, you will recall, did the original work on partial D categorisation, which, to a large extent, is still used,not least by the International Society of Blood Transfusion. Patricia pointed out that the correct terminology for the first of the Rh antigens was "D", and certainly not Rh(D). Obviously, Dr Gandhi is one of those who feel they are above and beyond the reaches of those who really know. Turning to Dr Park, I would again say that ABO typing is, almost universally, better done serologically (I doubt anyone would argue with that), but that the molecular testing of the RHD gene and, by inference, the fact that they are far more accurate than is D typing by serological techniques. If this were not so, people with partial D types would not still be making allo-anti-D in the numbers that they are. Similarly to the misuse of terminology by Dr Gandhi, I also note that Dr Park writes, "We use molecular-based testing for a lot of blood bank phenotyping now." Since when has a "molecular technique" in the world of blood transfusion been "phenotyping", rather than "genotyping". This is not just a mistake in terms of "blood grouping terminology", this is a very basic mistake in terms of biological science. This brings me back to my question, do these "experts" make up their rules as they go along, or do they actually take any advice from the experts in the field, who wrote those two papers I cited in my earlier post? I must say that they don't seem to be that "expert" to me.

By definition, reagent reverse grouping A1 and B cells are used to detect anti-A and anti-B antibody in patient plasma. Accordingly A1 cells should react with anti-A but not with anti-B, and B cells should react with anti-B but react with anti-A. Therefore, A1 cells should not be agglutinated by anti-B. No agglutination is a negative test result, i.e., a negative control test. Likewise, B cells should not be agglutinated by anti-A. No agglutination is a negative test result, i.e. a negative control test. Testing A1and B cells with AB plasma, Diluent, Albumin or saline may demonstrate that the test cells are not spontaneously agglutinating in their presence which serves as a negative control for those reagents, but does not serve as a negative control test for A1 cells or B cells.

If the patient has been transfused or pregnant in the last 3 mos, one has to r/i r/o significant atypical antibodies every three days. This going to involve more than a screen. Scott

Gosh, one would hope so!

https://www.nacblood.ca/resources/guidelines/CMV.html These are the Canadian National Advisory Committee Guidelines for use of CMV Negative Blood Products.

The forward type is an AB patient, your reverse type looks like you have multiple things going on. Because of the negative xm with group O donor red cells and the 1+ reactions with your group A donor red cells, I suspect an anti-A1. However, that 4+ reaction on the B cells cannot be due to the anti-A1 and I highly doubt that it is due to rouleaux; At least from my experience I don't typically see rouleaux this strong and we should have seen it with similar strength against the A1 cells. I agree that you probably have a cold reactive allo antibody going on with the B cells. In order for you to clear the ABO discrepancy I would do an IS antibody screen and see if you find a patter for a common cold antibody. Hopefully your find something; if you find a Lewis antibody I would find some random group B units and you should statistically land on one that can give you a negative result against your patient plasma to confirm it is not an ABO incompatibility issue. If you find something like an M, you could antigen type a group B unit but that will take 5-6 units before you find one, and then test it again your patient plasma to confirm negative results. The easier way out is to prove your anti-A1 and then take your reverse cell testing to the AHG phase to rule out ABO incompatibility. Consult with your pathologist of course, since this might be out of your standard operating procedure.

Exactly - patients should self identify, whenever possible, and that would be full name plus birth date. (We have had a few frequent flyers who would rattle off their MR#s when asked to identify themselves, but I think that was more about being a touch exasperated w/ our constant requests for them to tell us who they were rather than anything else.) And I agree that the birth date should be on the armband and the order for ID purposes. We do have it on the labels that go on our specimens, but it is not 'required' as an element of specimen ID. The CAP requirement for patient specimens is: "All blood samples used for compatibility testing are labeled in the presence of the patient with:1. Patient's first and last name2. Unique identification number3. Date of collection4. A method to identify the phlebotomist." AABB Stds say: "Requests: Requests for blood, blood components, tests, tissue, and derivatives and records accompanying samples from the patient shall contain sufficient information to uniquely identify the patient, including two independent identifiers. The transfusion service shall accept only complete, accurate, and legible requests." "Patient Samples: Patient samples shall be identified with an affixed label bearing sufficient information for unique identification of the patient, including two independent identifiers." They further say that the completed label has to be placed on the sample container at bedside; it has to identify the date/time of draw and the person(s) who collected the sample; that specimens have to be completely, accurately, and legibly labeled; and there should be a policy to reduce risk of misidentification of pretransfusion samples. I believe that Joint Commission recommends following AABB guidelines. So, as far as I know, the birth date is not 'required' on patient samples, but it is also not precluded from sample labeling. You can choose what your independent identifiers are and you can always have stricter requirements than standards in order to meet your needs. We choose to use full name, MR# and a separate armband ID for inpatients, giving us 3 independent identifiers - not required, but we've chosen that protocol to meet our needs.

We are also a free standing children's hospital with a level 1 trauma. Last year we changed our MTP to weight based because there was way too much wastage for the smaller patients. We are currently in the process of switching from CPDA to AS3 for all our neonates and transfusion >20cc/kg on patients < 1 year old. We will be 100% AS3 (but can still use CPD, CP2D and CPDA1 if available) by mid December (if everything works out as planned). I attached a couple of abstracts and a really nice Power Point we used to get neonatology to agree to the switch. Hope this helps. http://www.haabb.org/images/04_The_Use_of_Red_Cell_Additive_Solutions_and_Special_Attributes_in_Neonatal_Patients.pdf AS3 pediatric cardiac surgery.pdf AS-3 SurveyAbstract 2015.pdf

They most certainly DO NOT throw them out. They are an altruistic gift from our donors. The units are not marked as K+ (the hospitals are aware that the antigens that appear on the unit are those for which the is negative (except for D, D, E, c, and e) and so,if there is nothing to say that the units are K Negative, they are assumed to be K Positive. In this case, according to our Guidelines, the units should not be given to females of child bearing potential, who are not themselves K+, or to patients of either sex and any age, who are either already transfusion dependent, or likely to become transfusion dependent, unless they themselves are K Positive. That having been said, K Positive units are more likely to reach time expiry in hospitals, than are K Negative units, as might be expected.

Except that the QC manufacturer's diluent used to make a control antibody solutions is not used in any phase of patient testing--it does not need the be QC'd--it is QC. I would think the point is that the gel diluent is being controlled (which it should be), by showing it does not produce a positive reaction as a negative control. When patient or unit cells are being tested in gel, you use that gel diluent to create an 0.8% suspension--so for a positive gel control, if you are creating your own 0.8% suspension, again you want to use the manufacturer's diluent. Scott

Unless you have the right contacts......

Both. Not all reactions are caused by IgG immunoglobulins. Reactions with, for example, anti-Vel can sometimes only be detected by complement coating on the red cells.

Before you set a specific number across the board, I would suggest that you check you package inserts. Some of the human source rare antisera have positive agglutination defined as 2+ or greater and don't usually give much stronger reactions. The monoclonal rare antisera usually seems to react 3-4+. I would also expect stronger reactivity for anti-A or anti-B, depending on what you are testing them against. I would see 2+ reactivity for them as an indication that the reagent is not OK. We look for reactivity consistent w/ previous lots - +/- one grade of agglutination.

Same here, entire unit...except well over 30 years.

I believe the point of the post-transfusion H&H in this discussion is more to avoid giving another (perhaps) unnecessary unit. I think the consensus is that for a Hgb to stabilize fully, you want to look at it at 24 hrs. However, the H&H done an hour or even a half hour after a transfusion finishes is going to be close enough to make clinical decisions like whether to transfuse another unit. Scott

Ah, hang on LisaMarie. Was the patient D Positive? If so, your eluate may not contain anti-D and anti-C, but actually may contain anti-G (which would also neatly explain why you are able to elate an apparent anti-C from a C Negative patient).

Something that most people don't think about is the size of the unit. I am in a pediatric facility and we have units of all sizes. The smaller the unit, the more vulnerable it will be to temperature change. There is also the issue of the time the unit is out being made into an aliquot, and the fact that, in most institutions, the processing into an aliquot will be done close to the time of issue. So if you have an aliquot that is close to RT when it is issued, and then it comes back, what do you do? I think the only way to adhere to the spirit of the regulation is to measure the temperature directly. However, in that case, you are going to see your rate of expired units go up. There are no easy answers here, and in my experience, most inspectors know this, and many of them do not pursue it too vigourously.

Healthcare Facility Accreditation Program (HFAP). They serve a similar function as JCAHO in the United States. I mentioned this issue to Malcolm and others in another thread regarding this same issue as to how facilities can justify interpreting the presence of agglutination in the Anti-D test ( with a negative Anti-D control test) as Rh Negative! Both ORTHO and BioRad state in their direction inserts for Anti-D that agglutination is a positive test result and must be interpreted as Rh Positive. If the academic data is so compelling, why haven't the antisera manufacturers changed their directions for interpreting Anti-D test results? Why haven't the accrediting agencies changed their inspection criteria? The academic and accrediting communities are not in synch! Which has priority in the United States?

We do not have units in a fridge in OR (or anywhere else for that matter besides the BB). Our BB is just down the hall from OR, so our OR units are kept in the BB until needed for a specific patient Then they are issued in a cooler. Presumably the correct ID and read-back is done in the OR for each unit. Scott

Best patient safety care..DO NOT ALLOW NURSING TO DO THIS!

I think that this would very much depend upon whether the red cells are from a donor or a recipient. In the UK, for example, the anti-D reagents used in hospital laboratories, where they are testing (almost exclusively) patients, are designed not to detect Partial DVI, whereas those used in the NHSBT for donors and, to a certain extent, some of the reagents used in the Reference Laboratories are designed specifically to detect Partial DVI. This means that an individual could be designated as D Positive as a donor, and D Negative as a recipient. This would take a bit of explaining to the individual involved and, very often, to the doctor looking after the individual if they were not too familiar with transfusion. I would be amazed if manufacturers would make such a direction, because it is unlikely that all anti-D reagents are guaranteed to detect ALL partial D types (notably the DEL types) but WILL detect ALL Partial DIII type individuals, which can, and often do produce an allo-anti-D. I would be very confident to defend my own policy to a knowledgeable inspector, although I HOPE such an inspector would be knowledgeable enough NOT to ask about this in the first place! The attached diagram is of Partial DVI Type 1 (copied from a diagram by Geoff Daniels). Partial DVI Type 1.pptx

We have been AABB since the 70's. My manager dropped it last year. He dropped CAP also. We are just Joint Commission.

Agree with those who say that as long as it cannot be ruled as an artifact at some point, one must do a AHG crossmatch for the life of the patient. Scott

And don't forget that you will have to maintain competencies. You will probably have to send out some split samples to your reference lab or find some other means of proving that your methodology and process are good for regulatory purposes. I stopped doing even autoadsorptions because it just got too complicated and spendy to deal with those kinds of issues. Not saying don't do it, just keep an eye on the details.

If your patient doesn't type as O, then the old card can't mean anti-H. And a Bombay patient wouldn't lose their anti-H and have a negative screen now either, I don't think. Anti-HI (sometimes written IH) could likely have been identified back in the 80's when some places still did more room temperature testing. Anti-HI might have interfered then but with a negative screen you needn't worry about it now. The anti-Fya needs to be honored, of course.

We reached out to the trauma team and discussed with them. We discussed that we use non group platelets all the time, we studied the affects to these patients once we made the change in 2014 to present with no adverse concerns with the patient. When it was approved by trauma, it was made into our MTP protocol and emergency release protocol.

I am a little worried about the fact that there is no serological cross-match if the mother has made an atypical antibody. The reason I say this is because it is well-known that when a person makes one antibody, they often make more than one. If a mother makes, for example, an anti-K, which is easily detected, she may well also make another antibody specificity, such as an anti-Dia. As the Dia antigen is a low prevalence antigen in most populations, it could well be that the Dia antigen is not expressed on either the screening cells or the antibody identification panel cells - in other words, it may not be detected. Even if the baby does not express the Dia antigen on its red cells, the maternal anti-Dia will still go through the placenta, and so this anti-Dia will still be in the baby's circulation. If, the unit to be transfused is K-, but Di(a+), the baby could well have an unexpected haemolytic transfusion reaction, which could be avoided by a serological cross-match against the mother's sample. Once the unit has been cross-matched, and found to be compatible, then aliquots from the same unit of blood can be safely transfused without a further cross-match, but I feel that, for the first transfusion from any unit of blood, a serological cross-match should be performed.

I just answered this question. My Score PASS  

Thank you,Malcom!I'm finally enlightened !