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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.

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

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 ;).

I can't really explain your serological findings, but I agree with Malcolm's sentiment: "That stuff'll kill ya!" Anti-Vel is notoriously slippery and infamously dangerous. Without a more detailed look at your results, I see a few remote possibilities: 1. The anti-Vel may have an IgM component that doesn't like the Gel, but does like the PEG test 2. There's possibly something underlying the anti-Vel, hence the "extra" reactivity 3. The unit you crossmatched is not actually Vel-, but another member of the Vel variant club

Anti-Vel is such a nasty antibody, I would give units that are known to be molecularly tested (SMIM-1 Negative), unless the cross-match is performed by 2-stage IAT with monospecific anti-C3d on a clotted sample, as it is renowned for complement activation, even when virtually undetectable by normal serological techniques - not that I want to be sensationalist!

We keep the signed form regardless of transfusion.

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

Platelets are in adequate supply largely due to hospitals (in my service area) enforcing restrictive transfusion measures and postponing elective surgeries. Most blood centers except in New York, Washington state, and California are treading water with respect to RBCs. As usual Rh neg units are in short supply. Most of the hospitals in my service area are also freeing up beds to treat respiratory infections. These will require fewer transfusions, although patients needing ECMO are of concern. Looking ahead, it is difficult to predict what will happen. This is a long term event. My current concern is that blood donors will be fatigued 3 weeks from now and avoid giving blood. That is what happened after 9/11. It could be that you might need that unit of O neg on your shelf 42 days from now. In my opinion the goal is to provide blood for everyone who needs blood. Measures to restrict are prudent (and the literature indicates this is good medicine). After this is all over and we are criticized for being too conservative, but no one died for lack of blood, I can live with that.

if the DAT and auto control are both negative, what are you adsorbing out? An antibody to a high freq antigen? A cold? This would need additional work/perspective. A history of WAA doesn't mean it's a WAA forever. Does the patient have a history of anti-C and anti-E or everything else? Everything but Rh antibodies seems unusual to me.

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.

There are many facets to this question. I would think each institution has a disaster plan. It is an AABB requirement and I am sure a requirement for many other accreditation firms. From the blood supplier point of view: About 60% of the blood we distribute comes from mobile collections. Businesses, churches, schools and so forth permit us to hold collection events. If the local health departments discourage "gatherings" or even isolating parts of a community, this will adversely affect the blood supply. While the FDA encourages blood donation, the local messaging is what really matters. Isolation of well donors has already happened in places like Seattle and New York and is reducing the blood supply. Will the virus penetrate the population such that blood donors become unwell? This is hard to predict but look at Italy. Also the duration is difficult to plan for but with China it has taken about 31/2 months for the number of reported cases to fall. One might hope that different parts of the country are affected at different times permitting the movement of blood from one region to another. However given the mobility of the population it is possible that multiple regions are affected simultaneously and movement of blood is not possible. Hopefully, blood suppliers have begun to communicate with their hospital customers regarding the state of the blood inventory and the future ability to collect blood. From the hospital's point of view, what would happen if the supply became critical? When would you consider postponing elective surgeries, or rationing blood. Would you consider issuing splitting a whole blood unit in half and making that the "dose" in order to extend the supply (what makes the red blood cells harvested from a 450-500mL of whole blood a dose?) When do you start rationing blood/platelets? What about those transfusion dependent? do you divert those whole blood units intended for trauma patients to the chronically transfused. What happens if the hospital is overrun by those with respiratory illness like is happening in Italy? What about unwell staff? Will there be enough well to run the institution? I understand in Italy, administrators are transporting patients and pathologists (like me god forbid) are working in the ER . Are you sure there is an adequate supplies in your supply chain chain for each of your supplies/reagents so you can carry out business as usual? Silly things like hand sanitizer and toilet paper, gowns, gloves are already at a premium in certain parts of the country. I am mostly curious about your response to different levels of blood availability. How do you decide to post pone surgeries. After that should transfusion demand outstrip the supply what do you do and what is the trigger for implementing the action. Thanks Blood Industry Joint Press Release for Website - final 3.12.20.pdf

Reminds me of a recent forum post I read elsewhere about someone who wanted to give a patient with an anti-Vel phenotypically negative units from family members that actually were still genetically variant. The consensus was molecular negative donor units only!

In that case David, I would do serial titrations "in house", otherwise you will be paying out for a load of tests that you do not need. However, do I presume that, as the first two titres were performed by ARC, and you did the third, you were unable to perform a parallel titration on the second sample, when you did the third? If this is true, then there is even more of a possibility that the change from 4 to 8 in results may, itself, be the result of a small experimental error (with no offence meant, and I hope none taken).

My best guess and it is nothing more than a guess, is that if these patient's require any support from the transfusion service it will be due to a preexisting condition and not the direct result of the corona virus. I don't recall in all my years, of any patients with pneumonia requiring a transfusion due to having pneumonia and I understand that pneumonia is the primary reason for hospitalization here. Now I may be way out there on this but only time and experience will tell.

From the management side; involve the tech. Meet with them and have a conversation about how/why the think the error occurred.. Make them feel involved in QA and PI by asking if they have any suggestions that may prevent a recurrence. Front line staff often have great PI ideas, but won't speak up. During the conversation you will also be able to get a good feel for whether the tech knows the procedure and is committed to following processes as written, needs some re-training or whether they purposely deviated because the had "a better way".

Since all elective surgeries have been postponed and restaurants/bars have closed the BB has been incredibly slow which is rather scary in itself (the calm before the storm?). Due to this we have voluntary reduced our inventory to help with the blood supply.

Blood products that were taken into isolation are never returned to us. If they are not used, they are discarded in the room.

N Engl J Med. 2010 Feb 18;362(7):600-13. doi: 10.1056/NEJMoa0904084. Dose of prophylactic platelet transfusions and prevention of hemorrhage. Slichter SJ1, Kaufman RM, Assmann SF, McCullough J, Triulzi DJ, Strauss RG, Gernsheimer TB, Ness PM, Brecher ME, Josephson CD, Konkle BA, Woodson RD, Ortel TL, Hillyer CD, Skerrett DL, McCrae KR, Sloan SR, Uhl L, George JN, Aquino VM, Manno CS, McFarland JG, Hess JR, Leissinger C, Granger S. Author information Abstract BACKGROUND: We conducted a trial of prophylactic platelet transfusions to evaluate the effect of platelet dose on bleeding in patients with hypoproliferative thrombocytopenia. METHODS: We randomly assigned hospitalized patients undergoing hematopoietic stem-cell transplantation or chemotherapy for hematologic cancers or solid tumors to receive prophylactic platelet transfusions at a low dose, a medium dose, or a high dose (1.1x10(11), 2.2x10(11), or 4.4x10(11) platelets per square meter of body-surface area, respectively), when morning platelet counts were 10,000 per cubic millimeter or lower. Clinical signs of bleeding were assessed daily. The primary end point was bleeding of grade 2 or higher (as defined on the basis of World Health Organization criteria). RESULTS: In the 1272 patients who received at least one platelet transfusion, the primary end point was observed in 71%, 69%, and 70% of the patients in the low-dose group, the medium-dose group, and the high-dose group, respectively (differences were not significant). The incidences of higher grades of bleeding, and other adverse events, were similar among the three groups. The median number of platelets transfused was significantly lower in the low-dose group (9.25x10(11)) than in the medium-dose group (11.25x10(11)) or the high-dose group (19.63x10(11)) (P=0.002 for low vs. medium, P<0.001 for high vs. low and high vs. medium), but the median number of platelet transfusions given was significantly higher in the low-dose group (five, vs. three in the medium-dose and three in the high-dose group; P<0.001 for low vs. medium and low vs. high). Bleeding occurred on 25% of the study days on which morning platelet counts were 5000 per cubic millimeter or lower, as compared with 17% of study days on which platelet counts were 6000 to 80,000 per cubic millimeter (P<0.001). CONCLUSIONS: Low doses of platelets administered as a prophylactic transfusion led to a decreased number of platelets transfused per patient but an increased number of transfusions given. At doses between 1.1x10(11) and 4.4x10(11) platelets per square meter, the number of platelets in the prophylactic transfusion had no effect on the incidence of bleeding. (ClinicalTrials.gov number, NCT00128713.)

I must admit, we always used to use polyclonal antibodies, and there is a reason for this. Even blended monoclonal antibodies will still only recognise certain epitopes within the antigen, and while the K and k antigens tend to be single amino acid substitutions of methionine at position 193 for the K antigen, and threonine at position 193 for the k antigen, this is by no means universal. A weak expression of K is seen when either an argenine or a serine residue replace the methionine residue at position 193. As with amino acid substitutions leading to weakened expression of the K antigen, so the same can happen with the k antigen, but these substitutions may not actually be at position 193. A recent publication has shown that a substitution of Leu196Val weakens the expression of the k antigen (see Uchikawa M, Onodera T, Tsuneyama H, Enomoto T, Ishijima A, Yuasa S, Murata S, Tadokoro K, Nakajima K, Juji T. Molecular basis of unusual Kmod phenotype with K+wk-. Vox Sang 2000; 78 Suppl. 1: Abstract O011, Poole J, Warke N, Hustinx H, Taleghani BM, Martin P, Finning K, Crew VK, Green C, Bromilow I, Daniels G. A KEL gene encoding serine at position 193 of the Kell glycoprotein results in expression of KEL1 antigen. Transfusion 2006; 46: 1879-1885 and 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.). Therefore, it is more likely that you may get a false negative result using a monoclonal antibody in adsorption/elution tests, than by using a polyclonal antibody, with its wider breadth of specificity to the antigen's epitopes.

Is she given plasma derived product (not talking here about anti-D prophylaxis)? Thinking more here about IVIG?

That's the truth John. Us small places are at the mercy of the blood suppliers.

Alloasorption. In fact, having worked in Reference Laboratories for most of my life, it was VERY unusual for the patient either to have NOT have a transfusion within the previous three months - meaning that they were not a candidate for auto-adsorptions - or their haematocrit is so low that there are too few autologous red cells to perform an auto-adsorption in the first place (usually because they were sent to us because they needed a transfusion in the first place!).

Exactly. And very likely to cause in vitro hemolysis in appropriate test systems (not to mention in vivo hemolyis). I remember doing many 2-stage EDTA tests, using fresh complement and poly AHG. Good times. I think I may have met Dr. Cedergren when I was working at the BGRL in Oxford during the late 1980's.

I like explanation one very much exlimey. Very many of the examples of anti-Vel I have encountered (and I have seen many, as I was working at the BGRL in London in the mid to late 1970's when Dr Bertil Cedegren was studying the percentage of Vel Negative donors in the Swedish population) had a high concentration of IgM, and a low concentration of IgG.

We've had this happen also, and in a perfect world I'd prefer the OBs resume titers in a bit (give the RhIg time to wane) to see if anti-D is shooting up. We've been burned twice in the past six months where OBs stopped checking titers and switched to Dopplers, which showed decreased risk of fetal anemia, and the babes came out with peripheral blood full of erythroid precursors - right on down to erythroblasts - requiring emergent exchange. So I personally would request a repeat titer closer to delivery, just so you know what you may be dealing with. I don't trust the Dopplers (sorry, radiology!)

Anti-Cob has rarely caused a clinically significant haemolytic transfusion reaction, and, even then, the antibody was, in both cases, extremely potent. An anti-Cob, only detected by papain-IAT is certainly not going to be clinically significant, although when the antibody can be detected by IAT, using red cells that have not been treated with a proteolytic enzyme, then Co(b-) units should be transfused. In your case, it would be quite safe to transfuse units that are found to be compatible by IAT with untreated red cells. Geoff Daniels says in his book (Daniels G. Human Blood Groups. 3rd edition, 2013, Wiley-Blackwell) that anti-Cob is quite a rare antibody and, while I am ALWAYS wary about gainsaying anything written by Geoff, I think that may be more to do with the Co(b) antigen not being expressed on most screening red cells and even on most panel cells because, when they were, anti-Cob was a comparatively common finding in the samples submitted to NHSBT-Tooting Centre's RCI Laboratory when I was Reference Service Manager there. As you are working in the UK, you might find it useful to read the specification (SPN214/4), issued by NHSBT, "The Clinical Significance of Blood Group Alloantibodies and the Supply of Blood for Transfusion.", written by my good friend Nicole Thornton, Head of Red Cell Reference at the IBGRL. You can find it on line.

I get what you are saying John, BUT, repetitive testing on high-dose RhIg doses in cases of, for example, ITP, have shown that this does not lead to high titres of cell-free anti-D, and so I'm sorry, but I still think titrations are worth doing for a while. Think about it. If the TRUE titre was 4, a titre of 2 and a titre of 8 is only one tube either side of 4. Yes, IF the true titre had gone from 2 to 4 to 8, it is a clinically significant rise, but, it could still, at this stage, be experimental error, for the reasons I gave above.

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.

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.

Yes, but the validation does not have to be exhaustive and unreasonable. All you need to do is prove that it works as advertised in your lab.

I just got a memo from the ARC. They are working on convalescent plasma supplies. No details yet.

Really sick patients needing ECMO will use blood. I don’t have a way to gauge the utilization at this time though. All the best.

I'm currently working on building the convalescent plasma product codes into our computer system in case it is needed/wanted. But I'm in a children's only hospital so the only thing we're seeing right now is the normal stuff like urgent heart, spine, cranio and orthopedic surgeries plus our chronic transfusions for the rare anemia patients. We are no longer doing non-urgent surgeries and I anticipate to slow down further but according to the news California had the first death of a child (person under 18 yo) with COVID-19 but I haven't see if that's why the patient died. It would be nice if anyone knew lab personnel in Italy, Spain, etc but I think they may be a bit busy right now!! Unfortunately for us the flu is still going strong and we have had HUS and CAHA cases from it.

They are receiving anti-cd38, specifically daratumumab.

Drucker says they used to make those for CA. Their serofuge has a different body but the same rotor and guts. FYI.

Hemo bioscience sells Polyclonal anti K and Anti Cellano, both are FDA approved potency and could probably be diluted in a 6%BSA solution to be used for this purpose. info@hemobioscience.com for pricing info... Also your local American Red Cross may have donated units of Anti Kell plasma you might use but obviously watch out for the ABO types as these are not adsorbed.....

If you have done the alloabsorption, do you not elute and test the absorbed abs? I find it hard to believe that a patient would be sensitized to all the ags except C and E. (The most abs I've ever encountered were 10).

IVIgG can contain detectable rbc alloantibodies, although it would be unusual to be anything other than anti-A and anti-B.

I can see no reason why this would not work as a method. We used to use something very similar when testing individuals expressing the "McLeod" phenotype. However, these days it would be easier (and certainly more accurate) to perform gene sequencing on both the KEL and the XK genes. Don't forget that a true Duffy null phenotype (FY/FY), as opposed to a "GATA-1" type Fy(a-b-) is, these days, established by molecular techniques.

I just answered this question. My Score PASS  

Again thank you. The phenotype is probably R1R2 which is why I opted for anti-f and not anti-c. No transfusion history. The second pregnancy delivered in March 2018. We had no sample after her 28 week routine A/N in Dec '17. The booking sample in which we found anti-f was in June '19 (approx 10 week gestation) The woman's partner in the latest pregnancy is K- but we know how much store to set by that! I will go with this. Rich

I worry about donations if people get sick in large number and they can't donate we might experience blood products shortage.

My facility's previous control was running the previous sample in tandem and the results had to agree within one dilution. This process is currently being remodeled.

Thank you very much for the responses!

No offense at all. Who knows if I do things the way the ARC does them . . . or even AABBs "modern method", which to me is a serial 1:3 dilution (1 drop cell suspension and 2 drops test plasma/dilutions)- though that is read microscopically. I don't save send out titers as we do them routinely anymore here.

I just answered this question. My Score PASS  

In that case, I have to disagree with John for once (sorry John!). The reason I disagree is that a dose of RhIg will not give a very high titre, BUT, the titre of a pre-formed anti-D can rise very rapidly, and very dangerously, in the third trimester (much higher than the titre seen with just a dose of RhIg added to a low titre of allo-anti-D), and so, despite the complete idiocy of the person who gave the shot, I would still monitor the pregnancy by titration (well, I wouldn't, but only because in the UK we monitor anti-D in pregnancy by quantification).

My first thought was, why on earth did they give the RHiG!!!! I'm with Malcolm on that. You great minds do think alike!! I really would like to hear the rational if there is any. To answer your question, I see absolutely no value in additional titers, at least not until the next pregnancy.

The DAT is easily explained, with an anti-D level that high! Even after a double exchange transfusion, there will still be approximately 5% of foetal/neonatal red cells in the circulation, which is quite sufficient to give a positive DAT, but with an IUT, you are not removing an foetal red cells from the circulation (or minimal amounts) and should be considered more as a simple top-up transfusion (with profuse apologies to people who work in the Fetal Medicine Units, as I fully realise that there is nothing remotely "simple" about an IUT). As far as the reactions with the anti-A,B, the anti-D and the control is concerned, while the anti-A and anti-B are negative, it must be remembered that there are potentiators in monoclonal antibodies, such as albumin, that will possibly lead to them giving "false positive" reactions (although, I would suggest, that the reaction with the anti-D is anything but false - unless the anti-D is blocking the D antigen sites, which, with an anti-D level of 847IUmL-1 [it is NOT 847IU, which is an amount, rather than a concentration] would not be in the realms of impossibility). The amount of potentiator in each specificity will be different, depending upon what the antibodies are designed to detect (for example, what A and B subgroups, if any). However, the anti-D will most certainly contain potentiators, to ensure that most weak, and some partial D types are detected. This means that the control, which will have the same make up as the anti-D reagent - but without the anti-D, in other words, it would contain potentiators that would detect "false positives", which is the whole point of the control.

More likely the slips must be hung onto at least until after your blood provider gets their payment. If there is any dispute over what you are charged and/or paying for, then you have their packing slip to refer to as a sort of "receipt". Doesn't seem like you would need to hang onto them forever. May be a billing department requirement. Scott