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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 :).

What you are identifying is almost certainly a strong anti-H in an Oh individual. However, if the individual requires a transfusion, you will need to perform differential allo-adsorption (or something similar) to identify any other underlying clinically significant atypical antibodies (you can ignore any underlying Lewis antibodies, which are commonly also present).

Hi Rich, I am not a clinician but as far as I know IVIG can be given to obstetrical patient in diff. conditions (autoimmune disorders, recurrent pregnancy loss, ...). I thought about IVIG when I saw the DAT becoming positive plus additional reactions coming up over the time. Anti-A and Anti-B are indeed the most prevalent antibodies in plasma derived products but other specificities of low titre can be present sometimes such as anti-D, anti-K and a bunch of antibodies of undetermined specificity reacting with several to not say all RBCs. Just a thought that can be doublechecked with the clinician..? Hereunder is a very great (not recent though) paper to be read and re-read again: Problems Associated With Passively Transfused Blood Group Alloantibodies George Garratty, PhD, FRCPath American Journal of Clinical Pathology, Volume 109, Issue 6, 1 June 1998, Pages 769–777, https://doi.org/10.1093/ajcp/109.6.769

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

PLEASE do not worry. Your midwife is COMPLETELY wrong, and really should not comment about something she patently does NOT understand, and about which she has a pitiful amount of knowledge. She should never have answered your questions with her lack of knowledge, but should have left it to your Obstetrician. I note that you are a fellow "Brit"! Within the British population, the percentage of people who have the R1R1 type (which is a type within the Rh Blood Group System) is 16%. Also within the British population, the K- type (which is part of the Kell Blood Group System) is 91%. What that means is that 91% of 16% of the British population is R1R1, K-, or, give or take, a few decimal points, 15% of the British population (about an eighth of the British population). On Friday, 19th October 2018, the British population was measured as 66,690,116! Let's call that 16.5 million in round numbers. This means that, give or take, 9, 975, 000 in Britain are R1R1, K-. Now, admittedly, your midwife will only be looking after women, but, even then, that means 4, 987, 500 women will have the same Rh type and K type as you! How your midwife has only come across your "rare" type four other times in her career, is beyond belief (and I genuinely mean BEYOND belief), unless, as I say, her knowledge of blood groups and blood group serology is incredibly poor, and I repeat, she should NEVER have worried you like this. Just in case you think that I do not know what I am talking about, I have worked in the field of blood transfusion/blood group serology for 43 years, have been an internationally invited lecturer and am the Chief Examiner in Transfusion Science for the Institute of Biomedical Science in the UK, and am a co-author of the British Society of Haematology's Guidelines for Blood Grouping and Antibody Testing in Pregnancy. I don't write that to "blow my own trumpet", as it were, but to try to reassure you that I actually do know what I am talking about. I should warn you that "consulting Dr Google" is equally as useless as listening to your midwife. You should really relax. YES, it is possible for you to produce red cell antibodies during your first pregnancy, but it is INCREDIBLY RARE. It is even more rare for such an antibody to cause any problems in a first pregnancy. I notice that the report from the Blood Bank was that they detected WEAK reactions with 26 of 30 panel cells, but they could not identify a specificity. They have requested three further samples of blood to send to the Reference Laboratory. Again, to give you some comfort, I hope, I ran a Reference Laboratory in London for 16 years before I retired in 2016, and we saw, quite literally hundreds of cases like yours. For a red cell antibody to cause any problems within you pregnancy, it would have to have a titre of 32 or above (this means that it would still be detectable when it has been diluted THIRTY TWO times). I can assure you that the mere fact that the Blood Bank reports weak reactions means that there is ZERO chance that the titre will be 32 or above. If a Hospital Blood Bank, however big or famous the hospital may be, cannot identify an antibody, it is almost universal practice that samples will be sent to a Reference Laboratory for further testing - AGAIN, DO NOT WORRY ABOUT THIS. There are many, many red cell antibodies that are clinically insignificant, both in terms of transfusion reactions and haemolytic disease of the foetus and newborn (which is what your midwife has left you worried about). I KNOW it is difficult, but PLEASE do not worry. PLEASE take no notice whatsoever of your midwife on this matter (I am sure she is an excellent midwife, but she is patently no expert in the field of blood groups), but DO talk to your Obstetrician, who, I hope, will have talked to your hospital's Haematology Consultant, who, in turn, will have spoken to the Consultant in Charge of the Reference Laboratory, and I am sure that they will echo my opinion that there is NOTHING to worry about. Oh, and lastly, I am R1R1, K- myself!!!!!!!!!!!!!

The antibodies didn't read our books???

What I quickly realized was that no 2 inspectors/assessors focus on the same thing. As David noted, they seemed to focus on things they were either cited for or had cited others for recently. Over the years I had been cited for something that had passed all previous inspections because the inspector simply did not like the way we did it. When I challenged the citation with the inspecting organization the citation was often over ruled, not always but often enough to make the challenge worth while. My best advice is to prepare the best you can and consider the inspections a learning experience and hope that David is your next inspector. On a side note I was a Blood Bank inspector for CAP for 30 years so I had ample experience on both sides. One last bit of advice, never ever argue with an FDA inspector!

Probably the primary stimulation was not the fetus, but previous pregnancy, transfusion, tattooing, needle sharing, non-sterile tattooing, etc. Pregnancy is a situation in which B cells are upregulated (type 2 immunity) and T cells down regulated (roughly speaking) and pregnancy may have increased B cell activity to the point where previously undetectable antibodies are now detectable. Just a theory ;).

How many weeks pregnant was she before the fool in the office gave her RhIg? One would have hoped that, after 50 years, everyone in the office would have known NOT to give RhIg in such circumstances, but that is obviously over-optimistic.

We had a patient that seemingly converted from A Positive to A Negative. We sent the patient to our reference lab and through whatever voodoo they do, discovered that she had proteins masking her D antigens. I don't remember her specific disease process, and I don't think it was anti-D, but they reported that the patient was indeed A Positive.

If you feel that you are not being heard or appropriate action is not being taken you have the option of reporting to your accrediting agency AABB, CAP, TJC. This can also be done anonymously. The agency will contact the lab for information/investigation. If patient safety is being put at risk then you need to do everything you can to get these situations addressed which it sounds like you are doing. The other thing I would highly recommend is that you keep written/hard copy documentation of everything. You may need it sometime in the future to have proof of your diligence in trying to force compliance. Always remember the old adage "If it's not in writing, it never happened" Good luck

Have never had to do that (from 24 bed to 700+ hospitals)

I'm with David on this one. Doing both paper and computer entry just adds one more opportunity for mistakes. If you can't trust some one to put it in the computer correctly how can you trust them to write it down correctly! The key is the ability to enter the results as they see them and not have to walk over to a computer station to do it. Also, if you are entering from an instrument print out I highly suggest you get that instrument interfaced as quickly as possible. Again, you are entering results from paper and that should be avoided.

We went through this a few years ago. The problem with any kind of written worksheet is that it becomes your primary record -- the computer entry is secondary. -- resulting in both sets of records must be retained. When results are directly entered into the computer, almost all written testing records are not needed. Scott

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.

Before I attempt to answer your query, I must explain that I am NOT a doctor. I am what is called in the UK, a Biomedical Scientist and, as such, am not qualified to make a diagnosis, but I am the Chief Examiner in Transfusion Science for the Institute of Biomedical Science, and used to by the Reference Laboratory Manager in the Red Cell Reference Laboratory in the National Health Service Blood and Transplant Centre in Tooting, London, so I can claim some expertise. Although a warm auto-antibody in a person's plasma is by no means common, it is something we use to see on a daily basis at Tooting. To put it at its most basic, it results from your immune system producing an antibody directed against a red cell antigen expressed upon your own red cells, which could, under certain circumstances, lead to you becoming (usually mildly) anaemic. The "autologous adsorption" bit means that the laboratory, either at your hospital, or at a Reference Centre has been able to remove the antibody from the plasma in your blood sample by using your own red cells (thus proving beyond doubt that the antibody is indeed an auto-antibody). They have then tested this adsorbed plasma in tests to see if there are any unusual antibodies in your plasma that are directed against antigens expressed on the red cells of other individuals; so called allo-antibodies. They include in their report the caveat that concerning the "common blood group antigens" because it is all but impossible to test for antibodies against all the known antigens, of which there are well over 600, some of which are incredibly rare. Most auto-antibodies have a specificity within the Rh Blood Group System, which, at present, contains 55 different antigens (but other antigens are being found on a regular basis). Most of these auto-antibodies are directed against either the Rh antigen known as Rh17, or against that known as Rh18 (I realise these names will mean nothing to you - but bear with me). Almost everybody in the world expresses both of these antigens on there red cells, and the actual specificity of the auto-antibody is not really of any consequence. It is highly unusual, to say the least, for a maternal auto-antibody to cause any problems with a condition known as haemolytic disease of the foetus and new-born (or HDFN), particularly at an early stage of pregnancy. To me, this suggests that your early miscarriages and your auto-antibody status are coincidental, rather than the auto-antibody being the cause of your early miscarriages. Red cells are not really produced in early foetal life (indeed, there is not much in the way of blood in a foetus until about 12 weeks of gestation), so there are very few foetal red cells available to be affected by your auto-antibody. Having said all of that, I would reiterate that I am NOT a doctor, and even if I were, it would be impossible (and stupid in the extreme) to even attempt to make a diagnosis without FULL knowledge of your case. As such, I would suggest that you do discuss your case with your own physician (or your obstetrician) and be guided by what he or she suggests in terms of further testing. I hope that helps a little bit, and that I have not "blinded you with science" (which was not my intention), and I apologise for me English spelling!

Thanks ELondon. Could I just say again, even if the Reference Laboratory does detect an antibody (or more than one, come to that), it is not a particularly abnormal thing in pregnancy, but it does not mean for one minute that the pregnancy will be affected; Mother Nature has seen to that. There is another Blood Group System named Lewis. The antigens within this system are soluble in the plasma part of your blood, and are adsorbed onto the red cells from the plasma (they are not intrinsic to the red cell membrane). During pregnancy, the concentration of plasma lipoproteins (fatty proteins in the plasma) can increase enormously (about four-fold). These plasma lipoproteins "mop up" the soluble Lewis antigens, and a pregnant woman, who would normally be, for example, Le(a-b+), can become Le(a-b-), and may even, temporarily, produce antibodies against the Lewis antigens (an individual hardly ever produces antibodies against an antigen that they express - but strange things happen in pregnancy!). In addition, ALL babies are born as Le(a-b-), so any Lewis antigens Mum produces will NOT affect the baby! There are many, many other antibody specificities that will not affect the pregnancy at all. Now, I should say two things. Firstly, I cannot say, from a distance, what is the antibody in your plasma (that can only be done by the laboratories at the Hospital and the Reference Laboratory, but it does not sound at all serious). Secondly, i am what is called a Biomedical Scientist, not a doctor, and so I am, by Law, not allowed to diagnose (as far as I know, neither is the midwife), and this is why I am so glad that you are going to see an Obstetrician, who, I hope, will be able to reassure you even more. Mean while, sleep easier, and enjoy your pregnancy!

I think these bureaucratic methods corrode the trust and collegiality felt by our bedside practice colleagues. High risk patients require discussion between the medical staff of the transfusion service and the ordering provider, and a note in the medical record documenting the decision making. Signing forms is a another tip of the hat to bureaucracy and legalese that should have no role in the provision of medical care. A joint responsibility for such decisions and documentation is far more humane and in the interests of good patient care. Neither the FDA nor regulatory agencies require such divisive practices and we should abandon them for better patient care and documentation of shared decision making. I realize some of you do not have knowledgeable and enthusiastic physician support, but this responsibility needs to be taken by the transfusion service medical director, who is paid to do so, however reluctant and happy to dump this on medical technologists. Just saying.

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

You don't need to keep those records about irradiation. You are not performing it. As an inspector I almost always look at standards which I have been cited for. (I always disliked when the inspector said: "I knew I'd have to look really hard to find something in Dave's lab). That's not my style. I only dig if what I am finding merits such. I always look to verify you have corrected any prior deficiencies (these are given to us as part of the packet). I observe your staff and attempt to correlate what they are doing with what your policy/procedure says they should do. I also ask your staff (without a senior staff member accompanying me) about their work environment, employer, ability to attend CE programs. I want to see your quality stuff, especially any reports which you should have generated based on your QP. If you don't have anything it will be a long day for both of us. I will want to observe a transfusion or at least speak w a nurse about transfusions. Nursing training for transfusion and knowledge of reactions - this will be from Nursing Ed/Admin I don't want to review your procedure manual unless you ask me to look at specific items or you have added something new. I do want to see your table of contents so I can see what you do - I may take a peek at something there that piques my interest (I may also ask you if I might have a copy if it is something I'd like to bring to my own operation). There are lots of funny stories but you'll have to be inspected by me to hear them. (actually, most of them are quite sad as they involve citations). I tell your staff to relax because when I go back to work I do the same thing they do. I was an AABB inspector/assessor for 20+yrs. Still a CAP Team Leader.

Anti-Lea CAN be clinically significant, but it is very rare for it to so be, and it tends to be self-limiting. For it to be clinically significant it has to be IgG and/or complement activating, and it is self limiting because, of course, the Lewis antigens are soluble. This means that they will be in any plasma remaining on the red cells in the unit, and these soluble antigens will inhibit the patient's anti-Lea in vivo. You can usually continue to transfuse the same unit that caused the problem after a while, with no further problems. MIND YOU, you have to be ABSOLUTELY CERTAIN that it was anti-Lea that caused the reaction in the first place!

exlimey, I would most certainly agree with your first comment. In the VERY old days, when I was merely middle aged, and we only had access to tube tests and reagents, including AHG, and techniques (such as tile techniques), we didn't kill patients by the thousand, so techniques that are a little less sensitive than are available these days, will not necessarily condemn the patient to a certain and painful death, despite the deafening shouts of those who are gainfully (and, in many cases, VERY gainfully) employed within the neo-science of quality for quality's sake (we needed to pull up our socks in terms of quality, but it has got out of hand). On the other hand, having seen a fair smattering of Jk(a-b-) patients with anti-Jk3, I am unaware of "sticky" Jk(a-b-) red cells, even when they have been cryopreserved and reconstituted. I am willing to, and will freely admit to being wrong, if I am proved so.

This is an almost impossible question to answer, as it is ALWAYS the responsibility of the physician looking after the patient to perform a risk assessment as to which he or she thinks is the higher risk - viz is it a higher risk to go ahead with the transfusion, or is it a higher risk to leave the patient without a transfusion? He or she will take advice from such professionals as the Pathologist, but, in the end, only they can take the decision. That having been said, it also depends whether any or all of those antibodies listed are detectable in the present sample, or whether some are historic, and, therefore, if some of these can be "ignored" from the point-of-view of transfusion, such as the anti-N. In extremis, the clinical significance of the antibodies can be assessed by use of bioassays, such as MMA, ADCC and CLT, and even looking at the IgG subtypes of the antibodies. If it is decided that it is safer to go ahead with the transfusion, than to withhold the transfusion, it could be made safer by the use of IVIgG (see, for example, Win N, Needs M, Thornton N, Webster R, Chang C. Transfusion of least-incompatible blood with intravenous immunoglobulin plus steroids cover in two patients with rare antibody. Transfusion 2018; 58: 1626-1630 [doi: 10.1111/trf.14648], and Win N, Almusawy M, Fitzgerald L, Hannah G, Bullock T. Prevention of hemolytic transfusion reactions with intravenous immunoglobulin prophylaxis in U- patients with anti-U. Transfusion 2019; 59: 1916-1920 [doi:10.1111/trf.15230]). Finally, I MUST remind readers that I am a (retired) Biomedical Scientist, and NOT a clinician.

Yes indeed different pH, different suppliers may explain such a behavior (some anti-M are enhanced with acidification of plasma). In addition, Anti-M often shows dosage effect but I believe you have antigen M double dose cells on your panel too. What are the phenotype of the 2 cells reacting in screening and the one not reacting? Is your patient antigen M negative? It also exists the anti-M1 (the M1 antigen belongs to the MN CHO collection) that reacts with some M positive cells and stronger with M/N positive cells (M1 is expressed on M positive cells) and it can be, though rarely, produced by antigen M positive patients.

It sounds remarkably like one of your screening cells is expressing a low prevalence antigen that is not expressed on your panel cells. Antibodies directed against low prevalence antigens are actually quite common, but they are rarely detected because red cells expressing the cognate antigen are so rare. I wouldn't expend too much time or energy trying to sort out the exact specificity. In all cases of such an antibody, as long as you cross-match by the same method as you used in detecting the presence of the antibody in the first place, it would be quite safe to give cross-match compatible blood. The other thing is that the screening cell may be expressing an HLA antigen. You could treat the cell with chloroquine, and that will get rid of the HLA antigen.

I have been thinking about this and I have come, more or less, to the same way of thinking as Neil Blumberg. The first pregnancy almost certainly could not have caused sensitisation of most of the common antigens, as some would not be formed on the foetal red cells at 10 weeks of gestation, while, even with a huge foeto-maternal haemorrhage (FMH) (in terms of the ratio of the total foetal red cell mass), the actual volume of foetal red cells transferred to the maternal circulation would not be sufficient to cause sensitisation in anyone but a person who is a "super responder". The second pregnancy could easily have caused a primary response, either at partum, or as a result of a chronic FMH throughout much of the pregnancy. Unless the woman's antibody screen was performed at about six months post-partum, such antibodies may never have been detected at their peak, and then may have declined to levels where normal serological techniques would not detect them. Of course, all of this is theoretical, but, given the fact that the mother is probably an R1R1 (from information given above), it is most unlikely that an FMH estimation, such as a Kleihauer test was performed, or that the mother would have been serologically "followed up". You also do not give the woman's transfusion history. It would be helpful to know the time between the second and third pregnancy, and also, of course, if the same male was the biological father in both pregnancies. This latter piece of information may actually be very difficult indeed to ascertain, as the woman may not wish to disclose her sexual history. It is not unknown for antibodies of a particular specificity (say, purely for example, an anti-Jka) to increase in strength (as measured by serial titres) during a pregnancy that is, in this example, Jk(a-). This is more common in a pregnancy where there is at least one other specificity (let us say, again, just as an example, anti-K), where (again, just as an example) the foetal red cells do express the K antigen, but not the Jk(a) antigen. Lastly, antibodies that are forming de novo, very often seem to cross-react with antigens to which they are not actually stimulated. This is true, even in the case of some monoclonal antibodies (particularly those within the HLA system), but some antibodies (again, even monoclonal antibodies) maintain what I will call a pseudo-specificity even in the "mature state". This includes monoclonal anti-D. Thorpe et al have reported that monoclonal anti-D molecules possess a V4-34 moiety, that is also present in anti-I and anti-i, which is why these reagents should never be used straight from the fridge (Thorpe SJ, Boult CE, Stevenson FK, Scott ML, Sutherland J, Spellerberg MB, Natvig JB, Thompson KM. Cold agglutinin activity is common among human monoclonal IgM Rh system antibodies using the V4-34 heavy chain variable gene segment. Transfusion 1997; 37: 1111-1116 and Thorpe SJ, Ball C, Fox B, Thompson KM, Thorpe R, Bristow A. Anti-D and anti-i activities are inseparable in V4-34-encoded monoclonal anti-D: the same framework 1 residues are required for both activities. Transfusion 2008; 48: 930-940). I hope this helps a little.

It would behoove you to keep it. Reason being, a unit in your care was issued before all required testing was performed. Even if the blood was returned, you need to keep the documentation as to why it was released from your electronic inventory record. Now, say you issue a cooler full of an MTP pack and as the nurse is walking away, they cancel the MTP. The nurse returns the cooler, it doesn’t even make it to the floor, and you haven’t sent the slip for the physician’s signature yet. In that case, it could be a little redundant to make them sign a form for a nonexistent MTP, so I would just leave documentation of a variance from SOP document in the event of inspection with the documentation that an emergency release was initiated at the request of the physician and was canceled so you did not send a form.

if I sign out emergency release, I am keeping the request regardless if rbcs are used or not.

I would think a month is entirely adequate. Think about how the mother would have made an allo-anti-C, without making an allo-anti-D. We presume, in these cases, that the mother is the classic rr (D-, C-, E-, c+, e+), and so can make anti-D, anti-C and anti-E of the common Rh antibodies (she cannot make either anti-c or anti-e). For the mother to make an anti-C, but not an anti-D, when the mother has received a dose of prophylactic anti-D immunoglobulin, the baby/foetus has to express the C antigen, while not expressing the D antigen (ignoring anti-G for now). This almost certainly means that the father and the foetus must have the RH*Ce gene, but not the RH*D gene; an unusual, but by no means rare, situation. What would be rare, however, would be an individual who, having been given a dose of prophylactic anti-D immunoglobulin, which would, of course, "get rid of" foetal red cells expressing the D antigen (which is extremely immunogenic) but would still give her immune system time to be sensitised to the C antigen, when both the D and C antigens are expressed on the same red cells (if you see what I mean). On top of that, the C antigen is known to be nowhere near as immunogenic as the D antigen, and the likelihood gets even lower. Finally, look at the literature on anti-C causing HDFN. It is incredibly rare for anti-C (or anti-Ce) to cause clinically significant HDFN, let alone fatal, HDFN, and you will see that the chances of your pregnant women having an anti-C that will cause HDFN, particularly when it is no longer detectable in the plasma, is not so much disappearingly low, as miraculous! I really wouldn't worry about it.

My experience is that interference from rouleaux and cold autoantibodies in Gel is not unusual but this may depend on your patient population. As rouleaux is not an antibody an AHG crossmatch is not required. If you IS crossmatch you must (in my opinion) saline replace so you show any agglutination is interference and can therefore enter a negative/compatible/non-reactive result into your LISS, probably with a comment.

With attention to blood utilization, the overall red blood cell usage has gone down. Consequently blood suppliers have had to pair down the number of overall units they collect in order to avoid out dating products. Since we are drawing a population, the proportion of desired units in that population (All Rh negs and all group Os) has not changed, but the absolute number of the desired we can acquire units has dropped. Transfusion practices are still demanding nearly the same number of desired units as before blood utilization practices were implemented. About half of the Rh neg units distributed go to a non-Rh negative recipient, often because hospitals do not want to "waste" them. Perhaps if before making that decision to transfuse the blood bank contacted the blood center and asked if there was an immediate need to transfuse an Rh negative unit to an Rh negative recipient, we could better utilize the resources we have. Also I believe the merging of blood centers has contributed to the problem. Where the community blood center was usually able to manage the blood needs of the local hospitals, many are selling blood by contract to facilities miles away. This has decreased the amount of ad hoc blood available for export. The "low-titer group O" craze is also taking a toll because of the demand for repeat donors to fulfill the need to have Whole blood units with a 21-35 day out date, available for emergencies. Most blood centers are trying to recruit blood donors by blood group now in order to avoid out-dating Apos and Bpos units. This means that Rh negative and group O donors are approached to give 2-3 times more often than donors of other blood groups. The desired donors are complaining that they are being approached to give red blood cells too frequently and are starting to ignore our requests. All of these issues (and perhaps others) are contributing to the nation wide blood shortage of the most desired units. Importing products is also difficult. If they are available at all, did you know that in order to import four group O negative units a blood center might have to also purchase 50- 100 group A Pos units? Platelet utilization seems to be increasing. Where do platelet donors come from? Usually whole blood donors. Sometimes the blood center needs to decide whether to take a group O product or obtain a platelet product based on the needs of the day. Thank you to those who are excellent stewards of the products you receive! Blood centers are not shorting you because they are incompetent. Frequently it is extremely difficult to obtain the most desired products any where at any price. You can help your blood center serve you by being honest with your inventory.

This is where having a transfusion service director who knows something about clinical medicine and hematology comes in very handy. It shouldn't be the medical technologists' job to triage requests. Many transfusions do more harm than good, so it's not that difficult to figure out which patients urgently need transfusion and which can wait, but this requires a knowledgeable and tenacious physician to handle the individual requests and screen them. As a field, pathology has paid little attention to the need for those who can do such tasks, as compared with surgical pathology skills, cytopathology, etc. You may need to involve your institution's hematologist(s), intensivist(s), surgeons and anesthesiologists to help make these decisions if your lab physician(s) aren't up to the task.

The decision that a patient is in immediate risk of exsanguination and death is one that can only made at the bedside. That said, I think many trauma patients are overtransfused these days, particularly with plasma and platelets being given in most hospitals along with the first red cells. So I'd be very clear that the ordering practitioner believes that death is imminent without transfusion. And hopefully the patient would have already received tranexamic acid, and probably DDAVP as well to mitigate or even stop bleeding. These are evidence based, inexpensive, effective and safe drugs that can make the difference between surviving and not surviving, and between needing only a few units of red cells versus many more. Not all physicians have accepted these data, even trauma surgeons in some cases.

When the reason for a deviation is determined we can decide how it needs to be addressed. In some cases, the deviation was an acceptable response to a given situation. No follow up required. If education or training is required, that is provided and documented on the same form. If the deviation is the result of continued 'bad behavior', training/education issues, or egregious disregard for policy, then our next step is an 'Opportunity for Improvement'. This is something we use throughout our lab. The tech and a lead sit down together to discuss the deviations and the problems identified to determine what the tech needs to do to remedy the problem. The tech is also asked what he/she feels is needed to help him/her resolve the problem. Once the lead and the tech have come to an agreement, the resolution to the problem is spelled out, including any education/training the lead will provide and the expectations for the tech's future performance. An end date for the required improvement is also determined. When that date is reached, the lead evaluates the tech's progress. If all is well, that is documented. The End. If there are still issues, the lead can re-evalute the situation. Additional training or education can be provided, with another periord of evaluation. If need be, the problem can be referred to the lab manager for possible disciplinary action.

I would advise people to look at RH/index.htm. There are now WELL over 100 (almost 200) different weak D types, not to mention the number of Partial D types. Unless you have access to ALL of these red cells, AND use them as a control EVERY time you perform this test, you cannot QA/QC this test. There are times, even in the world of blood transfusion/blood group serology, you just have to admit defeat and keep your fingers crossed! Even if you were using molecular, rather than serological techniques, you would have to perform complete RHD sequencing each time to ensure you would detect all known mutations AND any novel mutations.

In the UK, the Guidelines say to swap to the patient's own blood group as soon as it is definitely ascertained, with no testing, whatever they have been given; it works.

The first thing to say is that the laboratory personnel cannot diagnose a transfusion reaction. This may be a delayed haemolytic transfusion reaction, where the patient is clinically compromised, or it may be a delayed serological transfusion reaction, where the sample from the patient tests for a positive DAT and a "new" antibody specificity, that can be eluted from the red cells, but where the patient is not clinically compromised. This can only be diagnosed by the physician looking after the patient. Secondly, the anti-Jka may be a de novo specificity, or may be present in the circulation as a result of an anamnestic reaction. Certainly, two weeks seems a bit quick for a de novo specificity to be detected, but it can happen (never say never in blood transfusion!), so it is more likely to be present as a result of an anamnestic reaction, although there must be a certain proportion of IgM immunoglobulin, as well as IgG. As yan xia says, Kidd antibodies can cause complement fixation, but can only so do if there is some element of IgM present (anti-Jka that is pure IgG cannot fix complement), however, it is incredibly rare for Rh antibodies to fix complement (as far as I know, there are only two examples of anti-D described in the literature that have been able to fix complement - and just think how many millions of anti-D have been detected), so the complement on your patient's red cells is much more likely to be there as a result of the anti-Jka, than the anti-E. Adding fresh serum does increase the sensitivity of the test (the so-called "two-stage IAT"), but treating the red cells with a protolytic enzyme, such as papain, and then performing the IAT is even more sensitive. An eluate can be used to "concentrate" the antibody sensitising the patient's red cells, but, be careful, as, is you are using a commercial elution kit, this may go counter to the kit instructions.

One thing I would say is that the baby should be treated on clinical symptoms, rather than on laboratory results, particularly when they are so weak that you have to do all this testing to show an abnormality in the Blood Bank. A slight rise in bilirubin is normal in a newborn baby. This situation is very similar to the difference between a haemolytic transfusion reaction, where, for example, there is a positive DAT, antibody can be eluted and there is a SIGNIFICANT rise in bilirubin and a SIGNIFICANT drop in Hb, and a serological transfusion reaction, where there may, or may not be, be a positive DAT, antibody may or may not be eluted from the red cells, a new antibody specificity may be detected in the plasma, but there is NO SIGNIFICANT rise in bilirubin and NO SIGNIFICANT drop in Hb. Your cases remind me strangely of the latter.

We supply blood to a helicopter service with a contract with our hospital system. We put Safe-T-Vue indicators on all of their units. They provide us a copy of their in-flight chart when they transfuse anyone not coming to our hospitals. If the patient doesn't come to us but has an account in our HIS, we create a bogus registration in our BBIS using a defined format account number. If they don't exist in our HIS, we create a complete registration manually in our BBIS using a defined format for MR# etc. Then we emergency issue the product in our BBIS and handle it just as we would those patients who expire before a specimen is drawn etc. We charge the helicopter service for the products which they include in their flat fee to the patient. We maintain the final disposition records for any lookbacks etc. If we got a market withdrawal or lookback, we would notify the helicopter company to follow up with the recipient. That duty is at least vaguely covered in our agreement with them, I believe. We tell the helicopter crew to return any unused products to us and not to leave them at the receiving hospital but this isn't perfect. We sometimes transfer products on paper to the receiving site if we can document handling sufficiently. It doesn't work easily if the receiving hospital doesn't use the same blood supplier.

Not all pts form antibodies each time they're transfused, and not against every antigen to which they are phenotypically negative. Futhermore, you wouldn't even know the pt is c= unless you phenotyped; otherwise, you would have only tested and found the anti-E at the time of workup, and stopped there. What prevents you from matching units that are phenotypically matched, even just the Rh group? That would require the extra resources and tech power to antigen type units. If they only have the anti-E at the date of product order, I don't see why you'd need to tack on additional testing. My lab tries to avoid extra testing if not needed

I may be mistaken, but I think the idea behind freezing an initial specimen that was titred and then thawing and running in parallel with subsequent titres, was so that if there is any variation in technique between one testing event and another, the retest of the initial specimen along with testing the subsequent specimen would eliminate any question as to how the titres have risen (or not)--in comparison to each other as they are being tested at the same time--when the subsequent specimen is received and tested, Scott

See this large study https://www.ncbi.nlm.nih.gov/pubmed/3137672 regarding use of rh positive blood for untyped trauma recipients. Abstract The emergency blood needs of 449 patients were met by supplying 1,717 uncrossmatched units of either red blood cells (RBC) type specific Whole Blood or group O RBC. The RBC were all Rh positive, and 601 units were transfused to 262 untyped patients. None of the patients presented with anti-Rh antibodies. Only 20 patients who were Rh negative received group O Rh positive RBC, and most of these patients were male. There were no acute hemolytic reactions or sensitizations of young females. Group O Rh positive RBC is our first choice to support patients with trauma who cannot wait for type specific or crossmatched blood. Those who do survive the emergency conditions can be reverted to blood of their own type without problem. Acceptance of Rh positive emergency transfusions by physicians giving emergency care can prevent unbalanced shortages in a regional blood supply system.

Awesome responses as usual Sir!

Patient Blood Management is a comprehensive, multi-modal approach to reduce/prevent anemia prevalence and reduce transfusions to only those that are life saving or absolutely essential. While the AABB has some materials and interest, they are relatively less likely to explain to you that the primary rationale is that anemia and transfusions are mostly harmful to patients in current practices. The pre-eminent organization in the USA in this matter is SABM. The founders of PBM include anesthesiologists such as Aryeh Shander at Englewood Hospital and Tim Hannon at St. Vincents, who saw that (1) Jehovah's Witnesses who refused transfusions actually had better outcomes than similar transfused patients and (2) transfused patients had dose dependent increases in nosocomial infection, thrombosis, multi-organ failure and mortality in the literature and their own practices. In other words, less is better. None is best when possible. Needless to say, the initial reaction in the blood banking and transfusion medicine community was lukewarm at best when these ideas were first put forward a couple of decades ago. But preventing anemia by doing fewer lab tests, and less frequent lab tests has begun to catch on in some places. See: https://www.sabm.org/patient-blood-management-programs/ Good place to get some initial education and join if of interest. A typical PBM program will include a part-time medical director (often an anesthesiologist, intensivist or hematologist, but also surgeons, transfusion medicine physicians, and other specialties) and one or more full-time nurses or medical technologists who focus on educating practitioners about current practices. You need a clinical champion at the bedside who other practitioners respect and will listen to. Changing practices is arduous and sometimes rather unpleasant work. When Bernard Fisher showed that the Halstead radical mastectomy for breast cancer was harmful to patients, the initial reaction was anger, disbelief and pushback. So it sometimes is with PBM. Physicians change their practices slowly or not at all. At our institution, PBM is heavily weighted towards collaborations between specialties, including, for example, an anemia management program prior to cardiac surgery, advocating restrictive transfusion practices where there is evidence (and there is tons of evidence that liberal practices are lethal at worst, wasteful at best). Happy to answer further questions.

You may have exchanged your pt by that time - then what type are you giving? I want a sample ASAP. I worked in a large tertiary care hospital, we would only give you one O= and then only if you gave us a specimen. We opened that hospital brand new and set up the rules like blood bank should be run. It was great - no one could say "we've always done it this way."

Today, We performed Kell antigen phenotyping, revealing k-, Kpb-, Jsb- (genotypically predicted as positive using SNP typing). Now, I believed his phenotype is Ko. I consider further genotyping using Sanger sequencing. Thank you for your help. Matthew Kim

It MUST be remembered that not all antibodies react by all techniques, but, equally,it MUST be remembered that not all antibodies are clinically significant. I remember way back in the 1980's, when I was working at a hospital in Croydon, Surrey, UK, we had an anti-S that we could only detect by tube technique. We sent this around to a whole bunch of other hospitals, who also used a mixture of techniques. Not one of them could detect the antibody by either microplate techniques or column agglutination techniques, both thought to be more sensitive than tube techniques, but all of those who also used tube techniques were able to detect the anti-S. I also remember having an anti-E that did not react with enzyme-treated red cells, but only reacted by IAT with untreated red cells. This was confirmed by the International Blood Group Reference Laboratory. Antibodies do not read books, particularly text books! Antibodies are only clinically significant if they react strictly at 37oC, and even then, not all are clinically significant. Think about the antibodies against antigens in either the Knops or Chido/Rodgers Blood Group Systems.

We always require an ABO/Rh for each admission, just in case someone else is using that patient's information.

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).

It is also easier to take inventory when they are standing up. If they are flat you would have to pick them up to count????