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We start with one panel (or cells 1-10 of Immucor's Panel 20 if doing tube testing). If a specificity is apparent when crossouts are done/the pattern of reactivity is reviewed, then we use selected cells (negative for the antigen the antibody reacts with) to complete rule outs OR if a number of rule outs are needed, run another panel on the Echo. If the patient has a more complex history or the antibody screen looks more complicated, we might choose to run 2 panels on the Echo right away. I require 3 antigen positive cells which are reactive and 3 antigen negative cells which are non-reactive to 'prove' specificity. The patient is antigen typed for the specificity identified if not previously typed for that antigen and if not recently transfused. Other common clinically significant alloantibodies are ruled out with 2 cells. This works well with straight forward, single specificity samples with antibodies like anti-K, anti-E, anti-Fya, etc., which are the majority of what we see. If the antibody screen on the Echo is positive in all three cells, which happens occasionally, we run a tube/PeG screen with an autocontrol plus one panel on the Echo with some questions in mind - is it an autoantibody? is it solid phase speficific? is it multiple antibodies? is it directed against a high incidence antigen? could there be a drug involved (anti-CD38, I'm looking at you!). If the auto is positive, we do a DAT. If the specificity is not readily apparent, then we run another panel, or two, or three as needed, based on what the first panel looks like. Almost all of our IDs start on the Echo and those panels are pretty well designed for rule outs of the common offenders. It is not uncommon to use only one panel for some specificities. I encourage everyone to look at the big picture, then narrow their search based on what they see. In the long run that will save them time (and reagents). And I will admit that on a busy day, we may put 2 panels on the Echo and push GO to expedite things a bit. If we are doing tube testing, running extra panels we may not need up front, is probably going to use more time and effort. Change is uncomfortable, especially for blood bankers, but give it shot. Think the steps through and work smart. You'll start to see problem solving in a way that you hadn't seen it before. Ask your work buddies for a second opinion if you're not comfortable. Review some cases with your supervisor to really get a good feel for what he/she is asking you to do. Once you've worked through the process it a few times, you'll feel better about it. And for those ugly case - the folks at the reference lab are your best friends!

At the end of the quoted policy above is this caveat: "Increase in temperature alone should not always constitute justification for a transfusion reaction work up. Nursing judgment should be used in evaluating symptoms and notification of physician." Here, we occasionally have problems with workups not being done, or direction from the blood bank to stop transfusions, against hospital policy. This is because there is sometimes a tendency to excuse reactions, such as a temp increase, to something other than an acute reaction to the transfusion. Now, every facility has to go by their own policy, but I would rephrase this as: "A significant increase in temperature, that may be attributable to some other cause, shall not constitute justification for ignoring what may be a life-threatening acute transfusion reaction. Nursing judgment should be used in evaluating symptoms only after consultation with the Laboratory Blood Bank, and attending physician." Scott

In the US we have been doing what you say is going to be the new policy for many years, except we only would do a DAT if the autocontrol was positive. I think that approach is pretty common. Orthos' panel A is for the ijnitial assessment. Most of the time, you will have a pretty good idea what you are dealing with with those results. Then, going by the 3 x 3 rule, w use other panels for rule-outs / rule-ins. Also, if there is no history, we antigen-type the patient for those antibodies that are being made. Scott

I am enormously honoured to announce that I am going to be awarded the Gold Medal of the British Blood Transfusion Society at their Annual Scientific Meeting in Brighton this year. It is awarded to an individual for their exceptional and long standing services to the Society and to the practice of blood transfusion in the UK. Sorry if this sounds egocentric, but I am very excited.

The grocery list below is what is in nursing policy at my hospital, with my notes in italics. This is their reference cited in the policy: Berman, A. & Snyder, S. (2012). Administering intravenous therapy. In Skills in Clinical Nursing (7th ed., 511-512, 516). Upper Saddle River, NJ: Pearson Education Inc. A. Recognize and report any of the following signs / symptoms of a transfusion reaction to the Physician and blood bank immediately for consideration of transfusion reaction work up: 1. An immediate hemolytic transfusion reaction may contain any or all of the following clinical presentations: a) Fever, chills, or both (specifically 1.5 F increase) b) Nausea or vomiting (also sudden onset of diarrhea) c) Headache d) Pain – localized to the back (also flanks, abdomen, chest, head, and infusion site) e) Chest constriction (also sudden onset of cough) f) Dyspnea and cyanosis g) Subjective feelings of distress – sometimes reported as a “sense of impending doom” (anxiety, agitation) h) Hypotension, tachycardia or both (significant change in BP) i) Hemoglobinuria (dark urine, anuria in extreme cases) j) Unexpected degree of anemia due to hemolysis of transfused RBC’s k) Shock l) Rash m) Feeling of heat along the vein used for infusion 2. Delayed Hemolytic Transfusion Reaction (24 hours to 2 weeks post-transfusion) may contain any or all of the following clinical presentations: a) Fever, chills, or both b) Jaundice (sclera) (increase in bilirubin) c) Pain-localized to flanks, back, abdomen, chest, head, and infusion site d) Dyspnea e) Sudden unexplained fall in hemoglobin 7-14 days post transfusion f) Continued anemia despite transfusion therapy g) Hemoglobinemia and/or hemoglobinuria 3. Febrile Nonhemolytic Transfusion Reactions (occur at the end of the transfusion or up to 2 hours later) may contain any or all of the following clinical presentations: a) Fever – occasionally b) Chills, colds c) Discomfort d) Rigors – occasionally e) Headache f) Nausea – some patients may vomit g) Dyspnea 4. Allergic Reactions (occur usually seconds to minutes after initiation of transfusion) and may contain any or all of the following clinical presentations: a) Intensely pruritic, localized or disseminated urticarial eruption (well circumscribed, discrete wheals with erythematous, raised, serpiginous borders and blanched centers) b) Generalized pruritis may precede eruption or generalized erythema or flushing of the skin. c) Angioedema, a more severe form, consisting of localized, nonpitting, deep edema of the skin. 5. Anaphylactoid and Anaphylactic reactions (occur usually seconds to minutes after initiation of transfusion) and may contain any or all of the following clinical presentations: a) Upper or lower airway obstruction or both b) Upper – laryngeal edema causing hoarseness or stridor (lump in the throat) c) Lower – Bronchospasm generates audible wheezing, tightness in the chest or substernal pain. Other associated symptoms include dyspnea, cyanosis, feelings of anxiety (“a sense of impending doom”) d) Profound hypotension e) Tachycardia f) Severe G.I. symptoms present from onset-abdominal cramps, nausea, vomiting, diarrhea. g) Erythema and urticarial eruptions are prominent and typically involve confluent areas of the trunk, face, and neck. 6. Transfusion Reaction Acute Lung Injury (TRALI) (symptoms arise in setting of recent transfusion of plasma containing blood components [ Red Cells, Whole Blood, Fresh Frozen Plasma, Cryoprecipitate, Granulocytes], always within 1-6 hours and usually within 1-2 hours of infusion): a) Acute respiratory distress which may first be manifested as dyspnea or cyanosis b) Severe bilateral pulmonary edema and severe hypoxemia c) Tachycardia d) Fever (1-2 C increase) e) Mild to moderate hypotension, usually unresponsive to IV fluid administration f) FDA regulations require all cases of TRALI to be reported. If TRALI is mentioned and/or charted by a physician as a differential diagnosis, the Blood Bank must be notified. Increase in temperature alone should not always constitute justification for a transfusion reaction work up. Nursing judgment should be used in evaluating symptoms and notification of physician.

Firstly kudos for taking the initiative and getting outside opinions to the changes you are experiencing and are uncomfortable with. The above comments (from way more experienced blood bankers than I) indicate your new supervisor is not wrong but needs to clarify the new process in context for you all. I suggest following AMcCord's advice and pulling some past work-ups (or invent them). Include patients with a new and previous single antibody, also patients with new and previous multiple antibodies. Then get the supervisor to walk through how he would resolve them and explain how each work-up would change with a negative and positive DAT. Running a DAT with each work-up is fine as long as it is clearly laid out what you are to do with the results and why. Once you have "proved" an antibody according to policy, running only negative cells for that antigen is normal practice because it is efficient (especially for the anti-e mentioned above). This is however assuming you have manual gel, as Dansket said only full panels can be run if automated. Hope this helps.

Sometimes adaptations are made depending on limiting factors. Maybe time is of the essence because the patient is bleeding or going into major surgery so more panels or methods are run at once to arrive at a conclusion more quickly. Sometimes there is only limited amount of patient plasma so fewer tests are run at a time and further testing determined based on the results of early testing. I always say that after the first panel with usual algorithm for rule-outs it ceases to be as much about the usual rules and starts to be more a matter of judgment and experience. The "rules" help newer people and generalists stay on track. If it gets complicated, they can call on more experienced people, including waking me up at 2 AM if need be.

Our stuff is stored for 10 years, with a set of notebooks for each year. The patient's records are stored alphabetically within each year, with the current year's set is found in the Blood Bank. We do not collate individual patient's records from year-to-year. We do not search for expired patients in order to clean our printed records. We just toss a year's worth when it is 10 years old. Scott

I agree with new pain. I find that the BP question is difficult because of patients being treated concomitantly for either hypo or hypertension, not to mention getting up to use the bathroom or getting riled by being visited by that annoying person who says they deserved to be sick because of something they have done. Or maybe they got the post-op cancer diagnosis during the transfusion. I have heard 30 mm Hg suggested but I think it depends on how it is applied. I look forward to someone having a clear cut answer for you.

I always considered antibody identification both art and science with a little magic thrown in for good measure.

I just answered this question. My Score PASS  

I just answered this question. My Score PASS  

You didn't say how large your laboratory is and how Transfusion Services is staffed on the night shift. When I was doing manual testing, it was consistent with your new supervisor's approach. An autocontrol was only run with the first panel only. With automated gel testing on ProVue, only full panels can be run. Rule-outs are done by entering panel test results into the AntigenPlus antibody identification software. A maximum of 3 panels would be run before sending specimen to reference lab. This standardized protocol was used in a small hospital transfusion service (<1000 rbcs transfused annually) staffed with generalists. This protocol was easily followed, even with only 1 generalist on staff at night for the entire laboratory.

Because of the rare risk of a fatal hemolytic reaction, we only use washed group O red cells for our premature newborns. For other newborns and readmits we use ABO identical unless there is detectable maternal anti-A and/or anti-B, in which case we again use washed group O's. There is about 20-40 ml of residual plasma in almost all red cell units, more than enough to cause severe hemolysis in rare instances. We should not ignore that risk for our own convenience/inventory management/etc. in my view. We only transfuse unwashed group O red cells to patients of unknown ABO type in emergencies. There is additional evidence that ABO non-identical transfusions of incompatible antibody or soluble antigen causes harm to patients, in addition to the rare risk of life-threatening hemolysis. We have published a summary of this evidence. Is It Time to Reconsider the Concepts of "Universal Donor" and "ABO Compatible" Transfusions? Refaai MA, Cahill C, Masel D, Schmidt AE, Heal JM, Kirkley SA, Blumberg N. Anesth Analg. 2018 Jun;126(6):2135-2138. doi: 10.1213/ANE.0000000000002600.

Most developing clinically significant alloantibodies still react at 37oC, and so trying to detect them at room temperature is more or less futile as, in most cases, all you will detect are antibodies that you do not want to detect, such as cold-reacting anti-M, anti-N, anti-P1, etc, which would be a waste of time, reagents and, most importantly these days it would seem, money. Most polyspecific or broad-spectrum AHG reagents these days are a mixture of anti-IgG and anti-C3d (particularly in the UK). They do not contain anything but the merest hint of an anti-IgM (certainly, they would not be CE-marked for anti-IgM). The other thing is that I am prepared to bet quite a lot of money that your laboratory is using EDTA-anti-coagulated samples. This means that the Ca++, Mg++ and Mn++ ions are all chelated from the plasma, which means that the complement pathway cannot be initiated in vitro, so, even if the de novo antibody was capable of "fixing" complement, the anti-C3d would not detect such an antibody anyway. Therefore, as the number of recently transfused patients who are developing antibodies not yet detected by normal serological techniques who have been fatally affected by a further transfusion hasn't been great (zero in fact) and the same applies to pregnant ladies, stick to trying to detect clinically significant antibodies at 37oC using monospecific anti-IgG. GOOD QUESTION THOUGH - SHOWS YOU ARE THINKING!

To my knowledge there is not a shred of evidence that titers (or titres:)) have any clinical benefit in this situation. We are treating ourselves, not the patient. I understand the need to "do something." In our case, our something is always giving ABO identical platelets, or, when this is not possible, we wash group O platelets. Titer/titre then becomes a moot point. I also get that blood bankers hate to wash anything, especially platelets, but we have randomized trial data this improves survival in younger patients with leukemia. Also avoids positive DATs, hemolysis and refractoriness to transfusion. A culture change is needed in which we accept what we've know for decades. Transfusing a group O red cell (or platelet) to a non-O patient can very rarely result in fatal hemolysis. Why we keep doing this despite the ability to avoid this rare fatal complication is a mystery to me, except for inertia and inconvenience. Of course a long standing practice that we assumed completely safe without a shred of data is hard to change. But the evidence is quite clear that group O platelets and rbc are not universal donor unless you accept a small but real risk of death for the patient. Not a practice to be defended in this day and age. As hard as it will be, I hope we will all start doing that which is best for recipients. Not what is best for inventory control or reducing wastage, which are important but lesser values.

No previous history on patient then do immediate spin crossmatch with type "O" blood until type is confirmed on 2nd specimen drawn at a different time form the original BB specimen. Once type is confirmed then electronic crossmatch with type specific units

And most of the titres quoted on this thread (if not all) are dilutions and NOT titres. A titre is the reciprocal of the dilution - not the dilution itself.

Similar, but we go a little higher, I believe 1:200.

To address this question of safety, I would like to see hard data from the AABB community as to the frequency of events where an ABO discrepancy was detected in the second ABO determination that was not detected in the first ABO determination. More importantly, did the detection of an ABO discrepancy (missed by the first ABO determination) prevent the transfusion of ABO incompatible red blood cells? My responses above assume that the ABO discrepancy was demonstrable by repeat testing of the first blood sample.

I have a copy of the book and the answers are in it. I don't have it in front of me right now, but I think they are part of the cases in my copy.

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

I'm afraid that may not work. We used to keep all of our "in-date" antisera on the top shelf, and our out-dated teaching antisera on the bottom shelf. This meant that, if any of our "in-date" antisera fell off the shelf into the out-dated teaching antisera, and we didn't notice, it didn't matter. Sadly, what I had not taken into account was the fact that one of our inspectors (I can't remember whether it was CPA or MHRA) knew much more about physics than did I, and explained to me, in huge detail, that the out-dated antisera must be kept in a separate fridge, in case the out-dated teaching antisera defied the Law of Gravity and flew up to the top shelf and secreted themselves there. So, everyone out there, be aware that the Physical Laws DO NOT APPLY to out-dated antisera, which is pretty dangerous when you think about it. In fact, I now rarely open the door of the fridge that contains our out-dated teaching, for fear of flying bottles, and NEVER without holding a stout stick, just in case!

When Rh Immune globulin is ordered in our institution's campuses: 1. The order is placed as a TS order in our computer system and is sent to the TS. 2. We do the required testing that is necessary. 3. We send the completed RhIg control form to the pharmacy with the number of RhIg vials needed. 4. The pharmacy dispenses it. The pharmacy's SOP is not fill any orders without a form from us and refers all floors to the Transfusion Service if there is an issue. We have been doing this for about 4-5 years now.

Back to the original comment about the use of expired panel cells. Here is the AABB Standard (IRL Standards 5.1.4.2): "The criteria for the use of non-FDA-licensed reagents (including expired reagents) shall be defined." The standard does not mention a specific QC requirement, only that there must be defined criteria for use. Our lab discards panel cells 2 months after expiration. We do not perform QC on these cells.