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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 :).

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!!!!!!!!!!!!!

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!

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."

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!

A - to find out the specifics of the problem - personnel may not talk in front of supervisor, so this needs to be done 1st. B - to get the other side of the story - if there is one. Don't spring a meeting on the supervisor with other personnel present without discussing problem 1st. 3 - to work things out - if possible.

The antibodies didn't read our books???

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

Just to state the obvious, if you are using pathogen reduced platelets, no testing is needed. That has been our choice due to (1) it's a superior method for preventing viral, bacterial, parasite transmission and (2) the logistics of testing 20-30 platelets per day are formidable and not without significant expense for materials, labor, QC, proficiency and competency. If your supplier provides the option of pathogen reduced, I would go that direction despite the increased expense.

Actually, if you look back at the responses you will see that the best answer is all three in the proper sequence.

3rd day at midnight, with day of draw being day zero.

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.

Congratulations! and thank you for your contributions to modern blood banking practice.

Malcolm, my sincere appreciation of your kind words. I've enjoyed and learned from your comments on this website.

Two reasons. The first is that severe HDFN caused by anti-S is very, very rare, but it does happen. The second, and much more importantly, is that a titre is a snap shot that tells the obstetrician ABSOLUTELY NOTHING in isolation. Supposing the titre is, for example, 512, the pregnancy can be monitored (as it can be anyway, whatever the titre) and there can be clinical intervention, if required. On the other hand, supposing the titre is 2, what does that mean prior to conception? Again, the answer is ABSOLUTELY NOTHING. The baby may not inherit the GYPB*S gene from the father, so the antibody will not increase in titre, or the baby may inherit the GYPB*S gene, but that doesn't mean the titre will automatically rise during the pregnancy, although, of course it can. It sounds to me that the clinicians are fishing, but without either a rod or a net (they haven't got a clue)! I know that the UK Guidelines do not apply in the US, but it might be worthwhile suggesting that they at least read "British Committee for Standards in Haematology (BCSH): White J, Qureshi H, Massey E, Needs M, Byrne G, Daniels G, Allard S. Guidelines for blood grouping and red cell antibody testing in pregnancy. Transfusion Medicine 2016; 26: 246-263 (doi: 10:1111/tme.12299) and/or Royal College of Obstetricians and Gynaecologists (RCOG). The management of women with red cell antibodies during pregnancy. Green-top Guidelines No.65; May 2014. https://www.rcog.org.uk/globalassets/documents/guidelines/rbc_gtg65.pdf.

We perform a type and screen on all of our labor patients at admission, so we do not repeat an antibody screen after delivery; but if the patient is in our facility and they want to give her antenatal RhIG, we do one before we issue it. We have identified a few patients who had already developed an immune anti-D so the treating physician had been able to monitor their pregnancy more closely.

This is the form developed by our system transfusion managers. It was based on a sample document shown in a CAP Focus on Compliance webinar a few years back. Transfusion competency-final.xlsx

An important aspect of this conundrum to remember is that physicians do not treat newborns just because of a positive DAT, they treat infants who are anemic or hyperbilirubinemic regardless of the DAT results.

I would think it would need a pretty significant bleed to find a macropositive DAT from a fetal bleed in utero. I've had patients pregnant develop an autoimmune process. Never impacted the baby.

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.

thank you Malcom and Scott for you responses! We spoke with the clinicians, who seem to understand the anti-S titer number will not tell them much of anything, and they had already realized the Jk and the C were useless to titer (which saved us a lot of grief). They could not provide any references or good reasons for needing the anti-S now, but pretty much insisted, and we acquiesced on this patient ONLY since her situation is quite unique. So we are treating the clinician rather than the patient this time; I've been covering clin path long enough to know that sometimes this is just the way it goes. Anyhow, we have at least opened a line of communication to the clinicians in the case and they feel we are trying to help them (even if we think it's silly), and that may be all the reassurance they need. And was better to know about this patient sooner rather than later, b/c if she does make it all the way to delivery with a chronic anemia we were gonna need to plan for her anyway. At least she's now on our radar in BB. Again, thank you all for your expert opinions! LCH

Malcolm, thanks so much for the article. It was very helpful. As it turned out, we sent mom's sample to our reference lab for MMA testing, and we also antigen typed her 2 brothers and her father. One of the brothers matched her Duffy and Kidd antigen types and was Coombs crossmatch compatible with her. He donated two units of packed red cells (at one donation) and was also confirmed to be Diego b negative. The patient's anti-Dib came back as clinically significant based on the MMA test. She did have a C-section after all and did not require any blood! The baby had a negative direct coombs so there were no issues there either!

@Malcolm Needs: Thank you very much for your response, I can not describe in words how grateful and relieved I am. I have been so incredibly worried that I've not even slept since speaking with the midwife, and that was 36 hours ago. I really wish Google had a 'Pregnancy filter' that blocks any attempt to look up medical information. I am under 'Midwife care' at the moment but will request a referral to an Obstretician for reassurance. This is my first pregnancy so I am still figuring out how the system works. I'm not familiar with the set up in other hospitals but the one I am registered with uses an app to send out test results. In my case I first had a message saying 'Abnormal blood test results, with no further details or comments" followed by a call from the midwife. I'm not sure what scared me the most, knowing that something abnormal had shown up on the blood test but not being able to see exactly what it was, or the call from the midwife saying how rare my blood type and antibodies are. I sincerely hope this is not the future of NHS medicine as I could very well have had a heart attack had a been a bit older. I went to the hospital again today and submitted three further samples. Hoping and praying that they will come back normal. Thanks again for your input. I feel like a great weight has been lifted off my shoulders just from reading it.

Most antibodies identified as "anti-C" are, in reality, a mixture of anti-C and anti-Ce (with the anti-Ce portion often being in the majority). This is because many of the antibody producers are R2R2, sensitised by the DCe or dCe haplotype - not all, of course, but many. According to my mentor, Joyce Poole, this was true even of monoclonal antibodies that are considered to be "anti-C". This is why you often get weak reactions with RzRz red cells with most examples of anti-C. As you are getting variable reactions with your panel cells, it could be that you have a rare example of a pure, monospecific anti-C, or an "anti-C", made in an R2R2 or R2r individual, who has been who has been sensitised by a DCE or dCE haplotype, and that you have an "anti-C" that is a mixture of true anti-C and anti-CE. All that having been said, I can't see that the above information would necessarily give a reason for your patient's odd reactions, but it might just be one of several reasons. What those other reasons may be, I don't know!

You may want your lab manager to talk to your trauma docs. I am pretty sure that they are going to want to know that you can provide type-specific blood ASAP before the Blood Bank runs out of O negs. Scott

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

This is not a popular concept but at some point we have to accept there are things we can not control. Once the blood leaves the blood bank we are at the mercy of other humans and as long as the human factor is involved there will be human error be it unintentional or intentional. Attempting to complicate a process will only provide inventive humans the opportunity of coming up with creative work arounds to circumvent your best of intentions. At some point you just have to step back, do your job and hope for the best. I had a corporate transfusion QA director who could not accept that human error could not be completely eliminated with out eliminating human involvement in the process. Her directives became horribly complex solutions with multiple, redundant checks and balances only resulting in increasing problems. Bottom line, pick your battles and fight those you have a reasonable chance of winning. Make suggestions, offer insight, provide training opportunities but at the end of the day realize that you have to accept some things are simply beyond your control and even your influence. On that happy note I'll step off my soap box and stop my philosophical ramblings.

Particularly if the massive transfusion event is a major incident, and during a time when there is only a minimum number of people working, we used to have a list of telephone numbers for, primarily, people who work in blood transfusion, but also those who work in blood transfusion as a sort of secondary discipline, and we give this to the microbiologist to contact the required number of staff (on the grounds that the microbiologist, brilliant in their own discipline as they may be, are less likely to be of use in the Blood Bank when units are required urgently, than are the staff who are already running around like headless chickens). I was lucky enough (????????) to be involved with three IRA bombs and two train crashes in my time - and the system did work.

I had a similar experience when a Family Practice Dr, who was chair of the OB committee at that time, brought back the Immune Anti-A, -B test. The only 'reference' he offered was his experience with his children. We wanted to ask if those tests affected how the infants were treated, but refrained....tongue biting was involved. The pediatricians say they don't need the test.

3rd day at midnight; draw day is day 0.

Me too! He's such a fantastic source of knowledge.

I just answered this question. My Score PASS  

I just answered this question. My Score PASS  

I'm curious. Since I've never heard of a Patient Blood Management program, what is it and what is it supposed to provide?

Looks like it can be credited to Dr. Robert Beal per Google and a 2008 article in Blood.

We do the type and screen as soon as we get the sample which almost comes immediately after the patient arrives as other labs are drawn at the same time too. Not so worried about the screen part but would like the ABORH especially if it is a female of child bearing age and she is RH pos so you don't use up the O neg supply

Hmmmm. Unless that particular cell is actually a DCe/--- (which I doubt, as they are disappearingly rare), and so has hemizygous expression, where homozygous expression would be expected, this is a bit of a mystery - unless the RHCE*Ce gene contains either a homozygous mutation, or a double heterozygous mutation - but again, this would be exceedingly rare. I'll keep thinking, but hope someone else comes up with a more realistic reason!

I agree with Dr. Blumberg that pathogen inactivated platelets are probably safer than the "cultured" platelets and that the psoralin compound used in the process currently approved by the FDA crosslinks DNA/RNA thus preventing proliferation of most organisms and WBCs. However, to my knowledge the FDA has not given blessing for pathogen inactivation to supplant irradiation yet. Reading a copy of the "prescribing information" from Cereus would answer this question. However, it is expensive, $150-$200 premium on the current cost of the products. It is not yet approved for pooled platelet concentrate products. (six-pack) It is not yet approved for three products collected from a single donor (triple product). It is not yet approved as a 7 day product. There is about a 5-6 % decrease in the donors that qualify for giving two or three products at a time. This is because the pathogen inactivation process decreases the platelet count by 5-6%. This means that blood centers will need to replace this number of donors in order to keep up with current product demand. There are some who suggest the platelet efficacy of these products is diminished at as the product approaches day 5. Whether or not this is seen clinically, I do not know but this would have a bearing on whether or not the product will be approved with 7 day out-date labeling, There is a third option that can be entertained by the providers of these products. That is "delayed high volume culturing". This process makes it standard to obtain both aerobic and anaerobic cultures from each product. This process has been used quite successfully in Great Britain to interdict contaminated platelet products. I understand this process would be approved for labeling the product with a 7 day expiration date, without the need for the consignee to do point-of-release testing (Verax). I believe it is important for hospitals to discuss the product desired with their blood supplier. Opening the discussion now will make for an easier transition when the guidance becomes final. We expect to hear from the FDA on this topic later this year.

Can you get a copy of the policy from your supplier that they use to validate their shipping containers? Type up a letter for your pathologist to approve explaining it and give that to your Quality people. Then if they want something more, ask them to show you the regulatory standard they are worried about. Scott

I disagree with this statement unless pathogen reduction will prevent lymphocyte activation.

The Ko phenotype is incredibly rare in all ethnic groups, but, some cases have been published involving a transient loss of Kell antigens, and the concurrent appearance of apparent antibodies directed against one or more of the antigens within the Kell Blood Group System. "Naturally Occurring" cases of anti-K are not unknown, but, once again are very rare. A few of these have appeared in the literature, such as: Morgan P, Bossom EL. "Naturally Occurring" Anti-Kell (K1): Two Examples. Transfusion 1963; 3: 397-398. Marsh WL, Nichols ME, Oyen R, Thayer RS, Deere WL, Freed PJ, Schmelter SE. Naturally occurring anti-K stimulated by E. Coli enterocolitis in a 20-day-old child. Transfusion 1978; 18: 149-154. Kanel GC, Davis I, Bowman JE. "Naturally-occurring" anti-K1: Possible association with mycobacterium infection. Transfusion 1978; 18: 472-473. Algora M, Barbolla L, Contreras M. Naturally occurring anti-D, anti-K, anti-Fya and anti_Leab. Vox Sanguinis 1991; 61: 141. In each case, you will notice, there is either an accompanying infection, or, in the last case a form of neoplasm. This may fit with your patient, if the early gastric cancer has allowed the escape of, for example, E coli into his circulation. I was also interested in the fact that you tested the patient's red cells, and found them to be phenotypically K-k-, but genotypically KEL: -1, 2, -3, 4, -6, 7. Did you also test the red cells with anti-Kpa, anti-Kpb, anti-Jsa and anti-Jsb, to ensure that these antigens were not detected? I am not asking this to be facetious, but because there have been examples of an apparent lack of the k antigen due to amino acid residue substitutions either at position 193, usually threonine for the k antigen, or very close to position 193 (see Millard GM, Lopez GH, Turner EM, Lizarazu ME, Roots NM, Liew Y-W, Flower RL, Hyland CA. Modified expression of the KEL2 (k) blood group antigen attributed to p.Leu196Val amino acid change three residues from the K/k antigen polymorphism site: implications for donor screening. Transfusion 2019; 59: 1156-1158 and Yazdanbakhsh K, Lee S, Yu Q, Reid ME. Identification of a defect in the intracellular trafficking of a Kell blood group variant. Blood 1999; 94 (1): 310-318). However, the amino acid residue substitutions can be "geographically remote" from position 193 affecting the expression of the k, and other Kell antigens (see Velliquette RW, Hue-Roye K, Lomas-Francis C, Gillen B, Schierts J, Gentzkow K, Peyrard T, von Zabern I, Flegel WA, Rodberg K, Debnath AK, Lee Soohee, Reid ME. Molecular basis of two novel and related high-prevalence antigens in the Kell blood group system, KUCI and KANT, and their serological and spatial association with K11 and KETI. Transfusion 2013; 53: 2872-2881)). To complicate matters further, some anti-k reagents may give weak or negative reactions, while others give apparently normal reactions. I remember a case I was involved in myself. We were following a woman with anti-D during her pregnancy. She was K+k+, and her partner was D+, K-. Upon delivery, her baby typed as K+k- in our hands (which excluded the father, unless he had a Ko haplotype). Sadly, he was no longer available to check his red cells again. I sent a sample of the baby's blood down to the IBGRL, and they made the baby a straightforward K+k+. Anyway, to cut a long story short, they were using an anti-k from a different clone to the one we were using, so I sent Joyce Poole some of the anti-k we were using, and Lo and Behold, they also got a negative reaction! I asked if they would perform a KEL gene sequence, and they did find a mutation, miles away from where the KEL2 locus was found, and yet it affected the expression of the k antigen. Sadly, I can't remember exactly the location of the mutation, and, because we couldn't type Dad again (or sequence his KEL gene, we couldn't prove it was inherited, and so could not write up the case. So, what to do? 1. Retest the patient's k antigen using a selection of anti-k reagents with different clones. 2. If you haven't already done this, test for the expression of the Kp(a), Kp(b), Js(a) and Js(b) antigens, to see if the patient is, at a phenotypic level either a Ko or a Kmod. 3. It might be worthwhile performing adsorption and elution tests, IF these are negative. 4. It COULD, POSSIBLY, be worthwhile just checking that the patient has a normal XK gene at position XP21.1, as, of course, it is possible to have the McLeod phenotype without having McLeod syndrome (in other words, these people do not have Chronic Granulomatous Disease [CGD]) - we had a donor like this where I worked (the only one in the UK). 5. If transfusion is required in the meantime, give K- IAT cross-match compatible blood. SORRY FOR THE VERY LONG POST.

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).

We instituted the practice of retyping the patients if their histories could not be proven. To do so, we instituted the practice of performing the retypes on a different specimen collected at a different time within the previous 24 hrs or within 1 hr of the blood type verification in the LIS. The histories are checked on every patient in the blood bank, if they do not have a historical type, the phlebotomist is sent to the patient room to collect a new lavender top tube. It does not matter the type of the patient, if they have no history, they get retyped. This practice ties into CAP TRM.30575. We have actually "caught" incorrect collections by the RN's that collected the incorrect patient and labeled the specimen with the wrong patient information. This is our practice and we are sticking to it! The other Scott

I agree that, in the case of an emergency, of course group O blood should be given - I have never argued against that and would be completely mad to so do. No, my argument was purely that, in a normal situation, a second sample should be taken from ALL patients.

I suggest you take a moment and determine exactly why you want a second type. Is it simply to be able to meet some outside requirement? Is it to detect the possibility of a testing or clerical error at the bench or is it to determine if the blood in the tube did not come from the patient the test was ordered for? While each of these is a worthy goal, by my way of thinking only one way will achieve all 3 and that is a second sample collected at a different draw. Now you can get even more complicated if you want depending on your level of paranoia. Must that second sample be collected specifically for this purpose or can you "borrow" one from hematology? Must that sample be collected by a second individual or does that matter? Must that 2nd collecting individual be left handed because the original collector was right handed? Lastly you must determine what are the actual limitations imposed by your facility for each shift. Are you a small facility without the staff on all shifts to actually have a second sample drawn by a second person? Take the time to really consider all of this and then keep it as simple as you possibly can. No one ever improved anything by making it more complicated.

If documentation of proper blood handling for transfusion is not appropriate, I am pretty sure that the inspectors will not care whether it's happening in the Blood Bank in the Lab or in OR. This is healthcare, after all, and this is my hospital. I do think it is worthwhile to try to correct deficiencies. It make seem like a sisyphean task at times, but one cannot just give up on this stuff just because we "are at the mercy of human beings". (We should all be used to that by now!) I do think that efforts should be concentrated on making things as simple as possible, not only for ourselves, but for those other humans in all the other departments that we work with everyday. I do think its worth the effort. Scott

i do not think anyone issues blood based on a previous admission's history. People are not always who they say they are. Scott

I am going to be REALLY unpopular here, but I'm going to say it anyway (because I am a pedant)!!!!!!!!!!! Antigens CANNOT be either heterozygous or homozygous; only genes can be heterozygous or homozygous. An antigen can be described as either showing homozygous expression, or heterozygous expression. That having been said, is a red cell sample that types as K+k- phenotypically, genotypically K/K or K/Ko, or even K/k, with a mutation within the Kell gene that prevents the k antigen being expressed and detected with all anti-k grouping reagents (just in case anyone doesn't believe me - we had one!). That's got that off my chest. Now then, there is NO doubt that there are some anti-K's around that only react with K+k- red cells (dosage), but they are fairly rare, however, how many people use antibody screening red cells that are K+k-? I doubt if there are any. Therefore, we are all ruling out anti-K using red cells with apparent K antigen heterozygous expression on every single sample that (apparently) has no atypical alloantibodies present. Am I wrong about this? It follows, therefore, that, over the years, there MUST have been occasions when a patient with a very weak anti-K (one that is only detected using red cells that are apparently showing homozygous expression) and who has been transfused with K+ blood (do the maths). As far as I know, there are no papers within the literature that report a case of either a delayed or an acute transfusion reaction as a result of this. Yes, this may cause the anti-K to become stronger (and, hence, be detectable using an apparent heterozygous red cell sample showing K+k+ expression), but then, if this happens, you give K- blood. So, my considered answer is that you can exclude using K+k+ red cells. I shall now go and lie down!!!!!!!!!!!!!