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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!

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.

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

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

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????

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 important to remember that inspectors are human and as John says, they can and do cite things because it's not how they do it. Don't take it personally. Their way may give you a good idea for improving your way. At the same time, don't be afraid to challenge a citation if you feel that you've met the intent of the standard and can prove it. I definitely don't recommend arguing with an FDA inspector - you are probably not going to win.

Please let me know if you would like me to do more "mock-up cases" with RHCE variants. I can look for some good ones. I think it is fun to interact with case studies here. (I mean it is quite fun to pick Malcolm's brain and learn from him... cough cough).

Agree - also, what blood type is the mother? From an operational stand-point you have a couple of options: Call the blood type "indeterminate" or "unable to determine" or call the baby AB. Either way, we would suggest repeat testing at 4-6 months and include A1 lectin typing if discrepancy still exists. In the meantime we would give group O red cells and AB plasma/platelets until resolved.

With reference to the ABO reverse grouping problems that cannot be resolved at RT, instead of incubating the tests at 4oC for 60 minutes, have you tried incubating at 30oC, or, in extreme cases, 37oC, or using cord red cells. Most of these "cold" antibodies have a specificity involving I or IH, and so, in the majority of cases these methods will resole the problems, without compromising the ABO antibodies, which, as we know from unfortunate transfusion reactions, work pretty well at 37oC! Turning to your specific questions: Q1. Firstly, we wouldn't test the plasma at 4oC. What is the point? Apart from Zombies in Holywood films, how many humans do you know who survive with a body temperature of 4oC? All we would do is test the antibody for its thermal amplitude, and if it does not react at 30oC, we ignore it (see Petz LD, Garratty G. Immune Hemolytic Anemias. 2nd edition, 2004, Churchill-Livingstone). If the antibody does react at 30oC AND is an alloantibody, we would be more proactive, identify the specificity, and give antigen negative blood. If it was an autoantibody, we would ignore it for transfusion. Q2. Apart from the above, NO! Q3. Why would you want to remove the IgM from the red cells. They will hardly ever be swamped by the autoantibody, but, if they are, we would use Rabbit Erythrocyte Stroma (RESt), which is available commercially. Unfortunately, this also adsorbs anti-B, and so the plasma adsorbed like this should never be used for cross-matching, as a group B mis-match would never be detected. Q4. I am going to be VERY cheeky here, and I say this with no evidence whatsoever, and that I will probably be slated by most members on this site, possibly rightly so, but I think that, as you are a Reference Laboratory worker, your techniques for working with these samples are more "honed" than those of the average hospital laboratory, as you see them far more often than do the hospital laboratories. I will now go and don body armour and a steel helmet!!!!!!!!

Just to confuse things a bit, there is absolutely no evidence that fresher units of red cells, or hemoglobin AA units are superior for neonates (or anyone else). The potassium can be an issue, but some fresher units have very high potassiums as well. We define fresh for everyone as 21 days of storage or less. We wash transfusions for newborns in the ICU, or others with high potassium levels, which fixes the potassium issue (I realize this isn't feasible at many hospitals). But I would not worry overly much about storage duration. If concerned, measure the supernatant potassium in a few units and give the one that is lowest. All hospitals can readily measure potassium so why not do that if you are concerned? Storage duration is a poor surrogate for actually measuring potassium. As for CMV seronegative, it's totally unnecessary if the unit is leukoreduced. Not a shred of evidence that it helps and it may preselect for donors who are infected but pre-seroconversion. Save yourself the expense and aggravation and eliminate the use of CMV seronegative units, and convert to 100% leukoreduction if you haven't done that. There are randomized trial data and many observational studies showing the clinical benefits of leukoreduction, including fewer episodes of nosocomial infection, the major cause of hospital morbidity and mortality. Sermon over :).

We don't honor phenotypically matched blood on a newborn unless the baby has a positive antibody screen due to the mother's antibody. The product that is set up for the baby is fresh ( less than 5 days old), O =/O+(depending on the babies type), irradiated (same day), leukoreduced(comes that way from supplier) and hemoglobin S negative.

Well, the high potassium is undoubtedly a factor, in particular as it is a cardiac case. All units in the UK are leukodepleted, but I wouldn't have thought that "unleukodepleted" blood should be of too much concern in this case. The difference in the Rh type would be of no concern to me whatsoever. The baby's immune system would be immature, and so it is highly unlikely that the "foreign" Rh antigens would cause immunisation. Indeed, exposure to these "foreign" Rh antigens may be advantageous in a way, as there is the possibility, as this age, that these may lead to "accomodation", meaning that the baby may never produce antibodies against these antigens, but this has not been proved, as far as I know.

We have been doing second ABO/Rh types on transfusion candidates with no previous history since 2002! We use previously drawn hematology specimens whenever possible. Since nursing does some of our draws, we send a small pink top tube to the floor to be used (we are the only department allowed to order and use these tubes) for the "confirm type". We use parafilm around the cap so we can make it "tamper proof" to some extent. Before we did this step, industrious people would draw two tubes at the same time and save one, waiting for our request of a second draw. They would pour over the saved tube into our special tube....now they can't. We do second types on all ABO types, we don't exclude type O.....they too can be WBIT.....which could affect other lab departments.....we let them know if we find mistypes. We also don't exclude emergency transfusion......that is when the most errors happen because people seem to lose their minds in high stress situations. We stick with type O until the confirm type has been drawn. We tried the two signatures on the tube route, but found they were just grabbing anyone and having them sign the tube whether they witnessed the draw or not. Fun times in the blood bank! :)

As the vast majority of hospitals (and Reference Laboratories) in the UK use column agglutination technology and automation, it is almost impossible to perform a second ABO without either a second D type or wasting a column or more than one column. But, my point was that, if a patient groups as O the first time, and A, B or AB the second time, then, it is obvious that either the first bleed or the second bleed was WBIT. Why should it be assumed that, if the person types as group O the first time, that is both correct and that it is automatically safe to give group O blood? If anyone does, I advise them to read the posts of Dr Neil Blumberg on ABO mismatched, but apparently compatible transfusions.

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

It is true that haemolysis can most easily be seen if the unit is stored in an upright position (note the phrase "most easily" - I am NOT saying that haemolysis cannot be seen if the unit is stored flat), however, more units can be stored in an upright position WITH the expiry date showing, than can be stored with them flat. If you have to move an upright unit to see an expiry date (or, in the UK, an Rh and K type - available on ALL units), you can easily do so without disturbing the red cell - plasma/SAGM interface, so that haemolysis is still easily seen, particularly as the units are usually in a cardboard box type thing to keep them upright. This is not so easy if the unit is stored flat and, in addition, it takes up more space in the average blood bank refrigerator, most of which are designed to take upright units.

The key here is they came to Linda and asked for help!

This is well known and there are indeed other threads concerning this. Transfused cells may have different densities to the patient's own cells and therefore when you spin the tubes in the centrifuge you may find that the transfused cells and the patient's cells separate. Then, depending on where you sample from in the tube, you will either get only transfused cells, only patients cells or a mixture, giving a mixed field. Typically instruments will select cells from the bottom of the tube, whereas pipetting by hand, one normally samples from the top, giving a discrepancy between the two methods.

David is completely correct. Do not forget, also, the A, B and H antigens are not direct gene products (they cannot be, as they are sugar-residue antigens). The direct gene products are transferase enzymes (proteins). These enzymes are not working at their maximum efficiency at birth (hence the weak antigen expression), but, in addition, the "A transferase" and the "B transferase" are competing against one another. Sometimes the A transferase starts by "beating" the B transferase, in which case the A antigen is expressed more strongly than the B antigen, and, sometimes the reverse is true (as in this case). They eventually "even out", as long as no true subtypes are involved. Test again at about six months.

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

In every place I have worked, the KB has been performed in Blood Bank. In every place I have worked, I have argued that the KB should be performed in Haematology, on the grounds that the staff in Haematology are far more experienced at 1) looking down a microscope (or, at least, they should be, as microscopes should not be allowed anywhere near a Blood Bank (see Issitt), and 2) looking down a microscope at minimal numbers, such as basophils and reticulocytes, whereas true positive KB's are very rare. I was consistently ignored!!!!!!!!!!!

I don't think the posters in this thread were talking about "repeating" panels - they were talking about "running" a panel with the same method when you get equivocal results on your primary method. If using solid phase - run a solid phase panel. If running gel - run a gel panel, etc. Don't just step down to tubes (or a weaker method) without giving the primary method (and usually more sensitive method) a chance to show you what it is trying to show you. For your next question - working with the specimen might have some validity if you have centrifuge problems or are running clots (red tops) for screens instead of EDTA (purple tops) specimens. Make sure your spin speeds and times will clear the white cells in a EDTA tube. Make sure you follow Immucor instructions on degrees of lipemia and hemolysis that are allowed. Otherwise - if you are running the same lot # of strips on 2 different ECHOs - I would be surprised if they give different answers. Does that help?

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

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

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

Sorry, but to my mind, these patients should also be typed twice. Yes, they can be given group O blood (almost always safely), but what if it is a WBIT, and the D typing is wrong because of it, or an antibody is missed because the "real" patient is group O with, say, an anti-K, while the other patient bled is group O, with no antibodies present. In addition, and incredibly rarely, what if the "real" patient is an Oh, while the patient bled is an ordinary group O.

No is the simple answer, however, NOTHING in blood transfusion/blood group serology is ever simple! I would thoroughly recommend you listen to the latest Podcast by BloodBankGuy (Dr Joe Chaffin) and Dr Stella Chou, which may shed light on the subject. It could well be that your patient has a Partial C (not unlike a Partial D, but not absolutely identical, as the E or e antigen is frequently also involved), particularly if your patient is of a Black ethnicity. One mutant Rh haplotype that is found not infrequently within the Black populations is (C)cdeS. With this , the C antigen is not detected by all anti-C reagents and so can appear to be C Negative. Such individuals also have a mutation causing a partial e antigen, and these people can produce an anti-hrB. Anti-hrB is relatively clinically insignificant (as opposed to anti-HrB, which is very definitely clinically significant), but mimics an anti-C+e, with the apparent anti-C element being considerably stronger than the apparent anti-e element. In addition, warm auto-antibodies classically mimic Rh specificities, and this could be such a case (the patient does not necessarily have to be diagnosed with WAIHA). While the auto-antibodies normally have a mimicking specificity within the Rh Blood Group System, this is not universal. I remember following a patient for years who was K Negative. He was never transfused with K Positive blood or blood components, and yet we were able to eluate what appeared to be an anti-K. This finding was confirmed by Joyce Poole at the International Blood Group Reference Laboratory, who was convinced that it was a mimicking specificity. I would be really grateful if you could keep us up-dated on your findings - purely because I am nosy!!!!!!!!!

Upright: so you can read the unit number plus the segments can be kept tidy to avoid getting tangled with each other, and observe hemolysis.

I agree with John. Challenge whenever you think you are in compliance. I always do - win about 60% of the time. Many inspectors can't see the forest for the trees. There are many ways to do things that comply. Just because the inspector disagrees does not always mean they are correct. I find this moreso with CAP than AABB but sometimes the latter exude hubris (doesn't mean you are wrong). Worse case scenario - you have to update something. AND NEVER ARGUE W THE FDA. I've seen those folks go to great lengths to find a needle in a haystack if you give them a hard time. I won't elaborate here but . . . take our word for it. Besides, they can take you out in handcuffs if they think you deserve it. (there is an enforcement arm). Good luck. You'll do fine.

Sorry all; I was supposed to post a paper about this myself, and forgot all about it (mind like a sieve). I also thought it derived from the Netherlands, but got that wrong too- it was a paper from the USA. Anyway, it was: Santhanakrishnan M, Tormey CA, Natarajan P, Liu J, Hendrickson JE. Clinically significant anti-KEL RBC alloantibodies are transferred by breast milk in a murine model. Vox Sanguinis 2016; 111: 79-87. DOI: 10.1111/vox.12387.

One other thing I do is to have you select 5 components which have final disposition. Then see that every person that dealt with that component had a competency for what they did - including those who transfused.

to Abstract for the Leonard paper published in Transfusion Transfusion. 2019 Apr;59(4):1183-1189. doi: 10.1111/trf.15154. Epub 2019 Feb 5. Identification of red blood cell antibodies in maternal breast milk implicated in prolonged hemolytic disease of the fetus and newborn. Leonard A1, Hittson Boal L1, Pary P2, Mo YD2, Jacquot C2, Luban NL1,2, Darbari DS1, Webb J1,2. Author information Abstract BACKGROUND: Alloantibodies against more than 50 non-ABO blood group antigens have been implicated in hemolytic disease of the fetus and newborn (HDFN) and are expected to wane within weeks after delivery. Persistent anemia leads to the hypothesis of continued exposure to red blood cell (RBC) alloantibodies via breast milk, which has been shown in a murine model and suggested in rare case reports. CASE REPORT: We report three cases of prolonged HDFN in two neonates with anti-D HDFN and one with anti-Jka HDFN. Patient 1 demonstrated 4+ anti-D serologic testing beyond 2 months; therefore, antibody testing was performed on maternal breast milk. METHODS: Maternal serum samples were tested for the presence of unexpected antibodies using standard Ortho gel card and 37 °C 60 minutes with anti-human globulin (AHG) tube saline methods. Antibody titrations were performed using the standard 37 °C 60 minutes to AHG tube saline method. Fresh breast milk samples were tested using the standard 37 °C 60 minutes to AHG tube saline method for both unexpected antibodies and titration study. Fresh breast milk from an O-positive, antibody-negative donor was used as control for any reactivity that may have been due to milk solids or proteins alone. RESULTS: Using a known methodology applied in a novel way to test breast milk for RBC alloantibodies, antibodies against fetal RBCs were identified in the maternal breast milk of three patients. CONCLUSION: Maternal RBC alloantibodies are present in breast milk and may be clinically significant in patients with prolonged recovery from HDFN. © 2019 AABB.

Here are the references. Lancet. 2016 Jun 25;387(10038):2605-2613. doi: 10.1016/S0140-6736(16)30392-0. Epub 2016 May 10. Platelet transfusion versus standard care after acute stroke due to spontaneous cerebral haemorrhage associated with antiplatelet therapy (PATCH): a randomised, open-label, phase 3 trial. Baharoglu MI1, Cordonnier C2, Al-Shahi Salman R3, de Gans K4, Koopman MM5, Brand A5, Majoie CB6, Beenen LF6, Marquering HA7, Vermeulen M1, Nederkoorn PJ1, de Haan RJ8, Roos YB9; PATCH Investigators. Author information Abstract BACKGROUND: Platelet transfusion after acute spontaneous primary intracerebral haemorrhage in people taking antiplatelet therapy might reduce death or dependence by reducing the extent of the haemorrhage. We aimed to investigate whether platelet transfusionwith standard care, compared with standard care alone, reduced death or dependence after intracerebral haemorrhage associated with antiplatelet therapy use. METHODS: We did this multicentre, open-label, masked-endpoint, randomised trial at 60 hospitals in the Netherlands, UK, and France. We enrolled adults within 6 h of supratentorial intracerebral haemorrhage symptom onset if they had used antiplatelet therapy for at least 7 days beforehand and had a Glasgow Coma Scale score of at least 8. With use of a secure web-based system that concealed allocation and used biased coin randomisation, study collaborators randomly assigned participants (1:1; stratified by hospital and type of antiplatelet therapy) to receive either standard care or standard care with platelet transfusion within 90 min of diagnostic brain imaging. Participants and local investigators giving interventions were not masked to treatment allocation, but allocation was concealed from outcome assessors and investigators analysing data. The primary outcome was shift towards death or dependence rated on the modified Rankin Scale (mRS) at 3 months, and analysed by ordinal logistic regression, adjusted for stratification variables and the Intracerebral Haemorrhage Score. The primary analysis was done in the intention-to-treat population and safety analyses were done in the intention-to-treat and as-treated populations. This trial is registered with the Netherlands Trial Register, number NTR1303, and is now closed. FINDINGS: Between Feb 4, 2009, and Oct 8, 2015, 41 sites enrolled 190 participants. 97 participants were randomly assigned to platelet transfusion and 93 to standard care. The odds of death or dependence at 3 months were higher in the platelet transfusiongroup than in the standard care group (adjusted common odds ratio 2·05, 95% CI 1·18-3·56; p=0·0114). 40 (42%) participants who received platelet transfusion had a serious adverse event during their hospital stay, as did 28 (29%) who received standard care. 23 (24%) participants assigned to platelet transfusion and 16 (17%) assigned to standard care died during hospital stay. INTERPRETATION: Platelet transfusion seems inferior to standard care for people taking antiplatelet therapy before intracerebral haemorrhage. Platelet transfusion cannot be recommended for this indication in clinical practice. N Engl J Med. 2019 Jan 17;380(3):242-251. doi: 10.1056/NEJMoa1807320. Epub 2018 Nov 2. Randomized Trial of Platelet-Transfusion Thresholds in Neonates. Curley A1, Stanworth SJ1, Willoughby K1, Fustolo-Gunnink SF1, Venkatesh V1, Hudson C1, Deary A1, Hodge R1, Hopkins V1, Lopez Santamaria B1, Mora A1, Llewelyn C1, D'Amore A1, Khan R1, Onland W1, Lopriore E1, Fijnvandraat K1, New H1, Clarke P1, Watts T1; PlaNeT2 MATISSE Collaborators. Collaborators (124) Author information Abstract BACKGROUND: Platelet transfusions are commonly used to prevent bleeding in preterm infants with thrombocytopenia. Data are lacking to provide guidance regarding thresholds for prophylactic platelet transfusions in preterm neonates with severe thrombocytopenia. METHODS: In this multicenter trial, we randomly assigned infants born at less than 34 weeks of gestation in whom severe thrombocytopenia developed to receive a platelet transfusion at platelet-count thresholds of 50,000 per cubic millimeter (high-threshold group) or 25,000 per cubic millimeter (low-threshold group). Bleeding was documented prospectively with the use of a validated bleeding-assessment tool. The primary outcome was death or new major bleeding within 28 days after randomization. RESULTS: A total of 660 infants (median birth weight, 740 g; and median gestational age, 26.6 weeks) underwent randomization. In the high-threshold group, 90% of the infants (296 of 328 infants) received at least one platelet transfusion, as compared with 53% (177 of 331 infants) in the low-threshold group. A new major bleeding episode or death occurred in 26% of the infants (85 of 324) in the high-threshold group and in 19% (61 of 329) in the low-threshold group (odds ratio, 1.57; 95% confidence interval [CI], 1.06 to 2.32; P=0.02). There was no significant difference between the groups with respect to rates of serious adverse events (25% in the high-threshold group and 22% in the low-threshold group; odds ratio, 1.14; 95% CI, 0.78 to 1.67). CONCLUSIONS: Among preterm infants with severe thrombocytopenia, those randomly assigned to receive platelet transfusions at a platelet-count threshold of 50,000 per cubic millimeter had a significantly higher rate of death or major bleeding within 28 days after randomization than those who received platelet transfusions at a platelet-count threshold of 25,000 per cubic millimeter. (Funded by the National Health Service Blood and Transplant Research and Development Committee and others; Current Controlled Trials number, ISRCTN87736839 .). Front Immunol. 2015 Feb 2;6:28. doi: 10.3389/fimmu.2015.00028. eCollection 2015. Platelet transfusion - the new immunology of an old therapy. Stolla M1, Refaai MA1, Heal JM1, Spinelli SL1, Garraud O2, Phipps RP3, Blumberg N1. Author information Abstract Platelet transfusion has been a vital therapeutic approach in patients with hematologic malignancies for close to half a century. Randomized trials show that prophylactic platelet transfusions mitigate bleeding in patients with acute myeloid leukemia. However, even with prophylactic transfusions, as many as 75% of patients, experience hemorrhage. While platelet transfusion efficacy is modest, questions and concerns have arisen about the risks of platelet transfusion therapy. The acknowledged serious risks of platelet transfusion include viral transmission, bacterial sepsis, and acute lung injury. Less serious adverse effects include allergic and non-hemolytic febrile reactions. Rare hemolytic reactions have occurred due to a common policy of transfusing without regard to ABO type. In the last decade or so, new concerns have arisen; platelet-derived lipids are implicated in transfusion-related acute lung injury after transfusion. With the recognition that platelets are immune cells came the discoveries that supernatant IL-6, IL-27 sCD40L, and OX40L are closely linked to febrile reactions and sCD40L with acute lung injury. Platelet transfusions are pro-inflammatory, and may be pro-thrombotic. Anti-A and anti-B can bind to incompatible recipient or donor platelets and soluble antigens, impair hemostasis and thus increase bleeding. Finally, stored platelet supernatants contain biological mediators such as VEGF and TGF-β1 that may compromise the host versus tumor response. This is particularly of concern in patients receiving many platelet transfusions, as for acute leukemia. New evidence suggests that removing stored supernatant will improve clinical outcomes. This new view of platelets as pro-inflammatory and immunomodulatory agents suggests that innovative approaches to improving platelet storage and pre-transfusion manipulations to reduce toxicity could substantially improve the efficacy and safety of this long-employed therapy.

They should have, or create a policy to replace/reattach the armband. Get your pathologist and QA involved.

Check with your blood supplier. During transport (up to 8-12 hours), platelets are not agitated.

I don't think so. It's not like charging for a antibody ID after getting a positive screen. It would be more like repeating a charge for, say, a potassium because the analyzer failed on running it the first time. So I would say no, you cannot bill again. Scott

We will do a pre-darzelex blood type and antibody screen as well as antigen-type the patient for all antigens that we have anti-sera for. When transfusion is needed after the darzelex is started, we will use phenotypically-matched packed cells. If the patient specimens don't come until after the patient has received the drug, we send the specimens to our Red Cross Reference Lab buddies to work up for us. They use the DTT (not DDT!) and antigen-type the patient to provide information for our future use.

We had a patient with an antibody to one of the Bg antigens. I remember that dealing with it was not straightforward. They are (I think) HLA antigens. Issitt says that the antigen expression is variable even in the same donor or patient. I didn't see anything about sample age, but I just glanced over the entry. It is in Chapter 19 of the third edition of Applied Blood Group Serology. Be aware that this was published in 1985, and so relies on serology alone.

What are you referring to with "95% of recipients of AB plasma have antibody to the soluble antigen present"? I'm referring to the unknown ABO type patient who receives AB plasma, or the intentional use of AB plasma for all patients despite knowing the recipient's ABO type. All of those O, A and B patients have antibody that will react with the A and B soluble antigens that are present in AB plasma (even in non-secretors, albeit in smaller amounts). We and others have empirical and laboratory evidence that these immune complexes interfere with platelet and endothelial cell function/integrity leading to increased bleeding, lung injury, sepsis and mortality. Even with low titer O Pos WB units aren't you going to see just as much formation of antigen-antibody complexes as you do with a non-type specific platvelet pheresis? The volume of plasma will be about the same and will contain anti-A, anti-B and anti-A,B, correct? Don't know for sure, but a little bit of antibody in a body full of antigen may or may not be as dangerous as a little bit of antigen in the presence of lots of antibody (think about anaphylaxis versus the safety of IVIgG). The biologic and clinical consequences of immune complex formation may well be dependent on ratios of antigen to antibody, and the size of the complexes formed. In general, lots of antibody on a bit of antigen seems to more biologically active than a lot of antigen with modest amounts of antibody. What about the Trauma centers that are using A plasma - is that any better? One of the first clues is that A plasma is no worse than AB, suggesting that the antibody content makes little difference. Group A plasma is at least identical with 40% of recipients. Time will tell, but I suspect that low titer O plasma and whole blood will be no worse than our current practices where we give tons of incompatible soluble antigen (and sometimes cellular antigen with platelets).

Here is a link to excellent resources regarding studies and risks for Low Titre O Whole blood. https://www.strac.org/blood. I think this may help answer a lot of questions. Here in San Antonio, I have seen great results from pre-hospital (ambulance and helicopter) use of cold-stored LTOWB. Patients who have received units have arrived stable where, in the past, would have surely been an MTP activation. Our local trauma centers are using it, up to 8 units before switching to components. The results have been positive.

I think you will find that dichloro-diphenyl-trichloroethane will destroy a lot more than just the Kell Blood Group System antigens!!!!!!!!!!!

If you want to enhance the weak reverse, have you tried pre-treating the red cells with a proteolytic enzyme, such as papain or ficin? Obviously, this will require strict control.

You should probably get used to the DTT procedure. Hemo-BioScience offers the reagent in small aliquots that can be used easily without bothering with trying to manufacture the stuff. There are several threads on this already on this site. Do a search and see the discussions. I had posted our procedure in one - let me know if it is not accessible now and I can send it to you. The cord panel method would be nice if you are doing a lot of pts, and at least the cells will last a while. DDT treated cells will not last long at all.

No need for platelets if the whole blood is stored less than about 14-15 days. Room temperature stored platelets aren't very effective in any case, particularly if ABO mismatched, and refrigerated whole blood platelets still retain some function for considerably longer than previously thought. The main attraction for advocates is ease of use, as well as transportation simplicity to the site of traumatic injury. There are those who believe that cold stored platelets will be more effective than the customary room temperature stored platelets. There is no denying the first two points, but the third is still uncertain as far as clinical efficacy and safety. That said, we've seriously overestimated the efficacy and seriously underestimated the toxicity of current platelet products (particularly those that are not ABO identical). Two recent randomized trials show that liberal platelet transfusion worsens bleeding and increases mortality compared with no transfusion or restrictive platelet transfusion. Lancet. 2016 Jun 25;387(10038):2605-2613. doi: 10.1016/S0140-6736(16)30392-0. N Engl J Med. 2019 Jan 17;380(3):242-251. doi: 10.1056/NEJMoa1807320. In addition to logistics, one major challenge is going to be the use of so-called universal donor O whole blood in the 55% of the population that is not group O. If the whole blood is really low-titer (<50 or so) and only a few units are transfused, this practice is probably not likely to be a big problem for patients. But we may see "indication creep," and use of group O whole blood (but not so low titer, <200 :)) ) both in non-hospital situations and then in hospital treatment of patients of known ABO type (not O). This will potentially cause low grade hemolysis, bleeding, multi-organ failure and mortality if we are not careful about finding out what is both safe and effective (see references below). Fortunately for the advocates of whole blood, and hopefully, for our patients, the current practices of so-called "universal donor"group O red cells, whatever ABO type platelets and so-called "universal donor" AB plasma for all patients is highly toxic due to formation of ABO immune complexes in every patient we give this cocktail to. Leads to hemolysis, endothelial cell injury, organ failure and increased bleeding in the patients we have reported, as compared with patients receiving only ABO identical transfusions. Group O whole blood is ABO identical with 45% of recipients, which will be progress from 0% with our current protocols since 95% of recipients of AB plasma have antibody to the soluble antigen present. My predicition is that If the amount of incompatible group O plasma from whole blood transfused is modest, and the titer of anti-A/B is low enough, whole blood may indeed be safer than what we are currently transfusing. Time will tell. Vox Sang. 2011 Jul;101(1):55-60. doi: 10.1111/j.1423-0410.2010.01464.x. Anesth Analg. 2018 Jun;126(6):2135-2138. doi: 10.1213/ANE.0000000000002600.

We have all of the units listed as you mention above in the Blood Bank system but the Dr's only see the 4 main categories. If they want anything special in the unit (irradiated, washed, etc.) they have to use a special comment. This way they don't get mixed up on which product to select.

One thing I would add to Dansket's post is that the standard says group O, it does not say O Neg. If your specimen types Rh Positive, you may, according to the standard, switch to O Pos and save your O Neg inventory for actual Rh Negative patients.

Aside from the "yuck" factor, centrifuges for WB are huge and generate massive G forces, a regular centrifuge would never work. Just an option. Also, would your vendor take them back?