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I would most strongly advise you to send a sample, possibly even multiple samples throughout the pregnancy, to a Reference Laboratory. As the patient is pregnant, there is the possibility that the Jk(a) antigen you are detecting is actually being expressed on the red cells of the foetus, and you are detecting it as a result of a foeto-maternal haemorrhage. However, the Jk(a) antigen is not necessarily straight forward, as there are weakened forms of the antigen (and the Jk(b) antigen come to that) where there are amino acid substitutions remote from the site usually associated with the Jk(a) and Jk(b) antigens (280 of the mature protein). In addition though, you have, obviously, to consider the health of the unborn baby who, even if the antibody does turn out to be a maternal auto-anti-Jka, may cause haemolytic disease of the foetus and newborn, albeit this will usually be be very mild. I attach a PowerPoint which may, or may not help you in your decision to send a sample to your local Reference Laboratory (also tell them the ethnicity of the patient). Interesting case - please keep us informed. In Depth Lecture on The Kidd Blood Group System.pptx

The simple answer is gagpinks, but this is the answer I have just received from my friend at the IBGRL (who shall remain anonymous for now). The question I put was as follows: "Sorry to bother you yet again, but I have had a query from a friend. I think I know the answer, but I wanted to check with an expert. If a pregnant lady has an allo-anti-D, can this affect cffDNA harvesting from the mother's circulation? I don't think it does unless the anti-D knocks out all of the foetal red cells. Best wishes from this bloody nuisance, Malcolm" Answer below. "Hi, that's right, anti-D makes no difference to the cffDNA test. The two biggest problems are false negatives due to insufficient RHD gene in the test sample and mums with a RHD gene (despite pheno typing as D-) leading to strong positive results. Take it easy." As I said, the friend will remain anonymous for now, but, suffice it to say, he/she is one of the people who do the test, so I think the answer can be trusted!

Thanks for your input. I was hoping you might respond. The Daniels book says that "No case of HDFN caused by anti-Lua or -Lub and requiring any treatment other than phototherapy is reported, although raised bilirubin or a positive DAT may be detected." Does this description equal "clinical significant HDFN" by your definition or is there newer information on more severe HDFN from these since Daniels published the 3rd edition? My thought is that, if there is no evidence of any case needing any early intervention, then there is no point in running titers to determine when to begin early intervention.

Ha ha! Good thing I retired then

In the UK, NHSBT stopped performing a DAT routinely on donor units some time ago (when I was still working). If a unit was found to be DAT positive through, for example, an incompatible cross-match, and the unit was returned to the supplier, the unit was tested, and then discarded, and the hospital reimbursed. If considered necessary, the donor's GP was informed. However, of course, it is almost certain that many DAT positive units were not discovered, and were transfused to a patient as a result of electronic issue. I have NEVER heard of a patient having any serious clinical sequalae as a result of this practice.

Agreed, sounds like you're moving to a less secure option for whatever reasons, so in that case I say go low tech and put a physical lock on the fridge door. Helmer sells fridges that have built in electronic access control, but you can also drill right through the handle bit and get a combo lock put on it. No access unless they call BB for the combo..... there are definitely ways to secure this low cost, I've got experience with both of these options and they work just fine after the surgeons stop complaining about it.

I would definitely refer this patient's sample to a reference lab for JK sequencing. As my friend Malcolm mentioned above, variants of JK antigens are not uncommon. The most common variant I've seen is caused by c.130G>C, which causes weakened expression of the Jka antigen. Interestingly, some patients with this variant would make anti-Jka, but I don't think we know much about the clinical significance of this antibody.

I wouldn't bother, to be honest. Apart from the fact that the Lutheran antigens vary in strength of expression, making it difficult to ensure that the recorded titres would "match up" one to another, but the expression of the Lutheran antigens on foetal and cord erythrocytes is known to be weak. On top of that, of course, there is the problem of finding a regular source of adult erythrocytes with heterozygous expression. In addition, anti-Lua and anti-Lub can be either IgG or IgM but are more commonly IgM. It might be worth your while treating the maternal plasma/serum with a reducing agent such as 0.01M dithiothreitol, 2-mercaptoethanol or ZZAP to see how much, if any, IgG is present. Even if the antibodies are IgG, they are thought to be adsorbed on to foetal Lutheran glycoprotein on the placental tissue. Lastly, as you so rightly say, clinically significant HDFN caused by anti-Lub is incredibly rare, and so, all in all, you could be giving yourself an awful lot of work for very little return. If you do decide to test the maternal plasma/serum with reducing agent, and you find that there is an element of IgG present, it might be worthwhile just performing a titre once, in order to see that you have not got one of these incredibly rare examples that might cause clinically significant HDFN, and, as lone as the titre isn't massive. I would rest easy. If you want, I can cite references to back up what I have written above, but I haven't done so straightaway, as actually finding some of these papers to read is equally hard work!!!!!!!!!! I hope that helps.

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The fact is that we have little to no evidence that platelet transfusion of any sort will mitigate post-pump bleeding. This is expert opinion only that has driven this practice. What we have learned in the last few years is that platelet transfusion as currently practiced (ignoring ABO for one thing) actually increases bleeding and mortality in some clinical settings. I'd rather have some oozing than be transfused with platelets empirically, both as a patient and a hematologist. With life threatening bleeding and abnormal platelet function as measured by a closure time or TEG/ROTEM, platelet transfusion makes sense and has some data driven support. Oozing, no data whatever.

Sounds like total rubbish from both a clinical and scientific viewpoint. Another instance how the administrative/legal model of reality is undermining civilization :).

Refresh the page and hover over the words.

IMO AFAIK LTOWB = low titer o whole blood TXA= Tranexamic acid Its the texting, abbreviations have gone wild :-)

I should have added that I recognize that some cardiac surgeons transfuse platelets routinely post-bypass in the hope of reducing bleeding. I suggest this is a traditional practice without the slightest shred of evidence for benefit. Purely guesswork and expert opinion, for which there is now evidence of harm. So whether you give cold or room temp platelets probably doesn't matter as (1) there is likely no benefit to either approach, and (2) there is likely equivalent harm either way. So my short answer is it doesn't matter, but that platelet transfusion to non-bleeding surgical patients likely doesn't help, and may increase the risk of thrombosis, inflammation and reduced host defenses against post-operative infection.

I'm not being critical, but I don't think I understand the rationale. You have poor compliance now with a fridge designed to provide compliance, but of course, a clever person can always find a workaround. You are proposing to replace it with a regular fridge that will offer close to zero protection for the units. I understand the maintenance costs for the Hemonetics are likely high. Are you being forced to remove it?

This is from our ABID SOP (sorry the format is weird): a. Warm Autoantibody Guidelines –(Expert judgment is required on a case-by-case basis to supplement these guidelines. Contact supervisor or Reference Lab for advice) [return to top] i. Clues it’s a Warm Auto 1. Reacts with most or all cells tested—usually at a fairly consistent strength. 2. Positive DAT. 3. If it is severe enough that there is hemolytic anemia, the patient would be anemic with a high LDH or bilirubin and high reticulocyte count. The patient’s plasma sample may appear hemolyzed or icteric. Haptoglobin would be low. 4. Contact Blood Bank Supervisor for further consult if uncertain. 5. Patient has not taken anti-CD38 (daratumumab/Darzalex/DARA) or anti-CD47 drugs in prior 6 months. ii. Clues it’s NOT a Warm Auto 1. Reactivity with most or all cells in gel, usually 2+ or less, varying strength could be HTLA-like antibody or antibody to gel diluent. It’s not uncommon for patients to have a positive DAT without having a detectable warm auto antibody so the positive DAT could be present coincidentally. a. To confirm antibody to gel diluent, convert 3% screen cells to 0.8% to run in gel. If negative, turn out the 3-cell gel screen and document situation in the patient record. b. An HLTA-like antibody will usually remain detectable (although sometimes weaker) in PEG and even saline techniques. 2. Alloantibodies: a. If patient transfused in the prior 3 months, confer with the most expert person available before calling it a warm-auto. b. Elution may produce both a panagglutinin and another specificity or may show only a new alloantibody. The panagglutinin may be so strong a weak allo is undetectable. c. If the DAT looks mixed field (repeat IgG DAT in gel for clear-cut mixed field), it may be an allo. 3. Drug-induced antibody: a. Research patient’s diagnoses for multiple myeloma, amyloidosis, or other autoimmune diseases. Look for recent surgeries or infections as a clue for cephalosporin treatment. Research their drug history for cephalosporins and anti-CD38 or anti-CD47 drugs. There is variability whether these present with only a positive DAT (more common with cephalosporins) or with a negative DAT and positive screen or with both positive. b. Rarely, other drugs cause what looks like a warm autoantibody. iii. When the Auto control (AC) or DAT is positive, first check transfusion history. The AC could be positive due to a delayed serologic/hemolytic transfusion reaction and NOT a warm auto. See Positive autocontrol. iv. If not already done, perform a DAT (Direct Antiglobulin Test Procedure). Warm autoantibody patients can have RBCs coated with IgG only or IgG and complement both. Occasionally, only complement may be present. v. If not already done, perform an antibody panel in gel (or other primary testing method). vi. People who make warm autoantibodies are more likely to make allo-antibodies as well. We need to identify any allo-antibodies in the sample so we want to avoid detecting the autoantibody if possible but still be able to detect allo-antibodies (at least strong ones). vii. If reactivity in gel is < 1+ or there are some negative reactions, start a 3% tube PEG antibody screen. If reactivity in gel is ≥ 1+, start a 3% Saline (no enhancement) 30-minute tube antibody screen. If amount of specimen is minimal, skip PEG screen and only do saline or, if some negatives, rule out with negative reactions found in gel and run selected cells needed to complete ruling out the usual antibody specificities. viii. If patient has not been recently transfused and usual specificities can’t be ruled out in tube testing, a PEG Autoadsorption should be considered. PEG adsorptions should not be attempted with patients who have a strong complement coating. ix. If can’t rule out usual specificities in tube testing and the patient has been transfused in the past 3 months, send the specimen to the Reference Lab for allo-adsorptions to determine the presence/absence of underlying alloantibodies. See Red Cross (ARC) BloodHub/Connect--Standard Work. If the patient is too critical to wait for the workup, contact the on-call Pathologist and Blood Bank supervisor. Phenotypically matched units may be indicated. See Increased Risk Transfusion Release Form. x. Turn out ABID results as Warm Autoantibody plus any other specificities detected. xi. Approach to crossmatching in the presence of warm auto-antibodies: Situation Pt Hemolyzing* XM Methods XM Results Enough negs in gel to rule out all usual Ab specificities Yes Gel Incompatible Enough negs in gel to rule out all usual Ab specificities No Gel Compatible Can rule out all usual Ab specificities in PEG Yes Gel Incompatible Can rule out all usual Ab specificities in PEG No PEG Compatible Can rule out all usual Ab specificities in Saline Yes Gel Incompatible Can rule out all usual Ab specificities in Saline No Saline Compatible Alloantibodies identified or can’t rule out some Ab specificities in Saline Yes Saline** to assess compatibility with allos, then gel to turn out results Incompatible Alloantibodies identified or can’t rule out some Ab specificities in Saline No Saline Compatible Autoadsorption required and able to rule out usual Ab specificities Yes or No Gel with neat plasma Incompatible Autoadsorption required and alloantibodies identified or can’t rule out usual Ab specificities Yes or No With adsorbed sample** to assess compatibility with allos, then gel with neat sample to turn out results Incompatible *If patient is hemolyzing, no transfused unit will be truly compatible. Use “incompatible” XM result code in STTx, not “least incompatible” for these cases. **If second XM method (that’s not to be turned out) is required, record on log sheet. 1. Warm Auto Notes: a. The purpose of the PEG or Saline Antibody screen or PEG adsorption is not to be able to call the primary antibody screen negative, but to rule out underlying alloantibodies. Generally, these tube ABSC’s will NOT be reported in STTx. b. Incubation in the presence of enhancement (gel/PEG) reagents may cause reactivity in the AC that is only an in vitro phenomenon. If the DAT is negative and the AC is positive, antibodies to enhancement constituent or autoantibodies reactive only in enhancement medium should be considered. An Antibody Elution (Eluate) may help determine the presence/absence of warm autoantibody reactivity. c. If the patient is demonstrating active hemolysis, use gel or PEG to crossmatch units. The units still may suffer shortened red cell survival in vivo so calling them incompatible is justifiable. d. Consult with Blood Bank Supervisor about performing a full phenotype with the available monoclonal (non-AHG) antisera. Consider giving phenotypically similar RBCs for transfusion. If alloantibodies are ruled out in a current specimen, units that are only historically antigen-negative are acceptable. If we must transfuse before alloantibodies can be ruled out, confirmed antigen-matched units are advised if time permits. e. Warm autoantibodies can be confirmed in one of two ways: demonstrate that EGA-treated (antibody removed) pre-transfusion autologous cells react with neat plasma or prove that the antibody reactivity is adsorbed out with pre-transfusion, autologous cells. f. Patients on daratumumab (Darzalex or DARA or other anti-cd38 drugs) may appear to have a warm auto antibody but it is actually the drug reacting with the cd38 antigens on the red cells. They may have either a negative or positive DAT and AC. The only effective way to test these patients is to test against DTT treated cells, recognizing that this will miss antibodies to antigens destroyed by DTT like the Kell system. These patients benefit from having a pre-treatment antibody screen run and possibly antigen typing for K (and if K positive, for k). In most cases molecular genotyping may be indicated. See Dithiothreitol (DTT) Treatment and Anti-CD38 Drugs (daratumumab/Darzalex)--Blood Bank Testing. g. Additional anti-CD38 drug therapeutics are in clinical trials in addition to Daratumumab (Janssen Biotech) include MOR202 (MorphoSys), Sarclisa -Isatuximab (Sanofi-Aventis), and TAK-079 (Takeda) for treatment of systemic lupus erythematosus, Amyloidosis, or other autoimmune diseases. Daratumumab and Sarclisa are approved for treating multiple myeloma. h. CD47 is a glycoprotein expressed on all cells including RBCs and platelets, which usually signals to prevent phagocytosis. Anti-CD47 blocks this signal targeting cells for destruction. Samples from patients taking anti-CD47 drugs (Hu5F9-G4 or avelumab) will react with everything like a warm auto and the reverse type may be affected like a cold auto. Anti-CD47 interferes with all RBC and platelet serological tests performed including ABO reverse typing. False positive reactions can be seen in all phases of testing (immediate spin, 37°C, and IAT) and with all forms of IAT testing (i.e., tube, gel, solid phase). Reactions with D negative cells may be stronger than with other Rh phenotypes. False negative phenotyping test results can occur due to RBCs heavily coated by anti-CD47. DATs may be falsely negative due to a “blocking effect” caused by high levels of antibody present, but eluates are strongly positive. Plasma interference and strong panreactive eluates are observed as soon as 1 hour after drug infusion. CD47 antigens cannot be denatured with DDT or other common denaturing agents. It is highly recommended to perform pretransfusion testing, including blood type, antibody screen and extended phenotype (either serological or predictive genotype) before initiating treatment. Using monoclonal Gamma-clone Anti-IgG in indirect antiglobulin testing (which does not detect IgG4 immune classes like anti-CD47) may avoid most of the interference in AHG testing. Giving antigen-matched units may be an option if full phenotyping is available. [return to top] i. Additional CD47 drug therapies are also in clinical trials and include the CD47 targeting antibodies CC9002 (Celgene), which, like Hu5F9, is also an IgG4 antibody, and the human monoclonal SRF231 (Surface Oncology). CD47 agonists are also in clinical trials. These include TT1-621 (Trillium)31 and ALX148 (ALX Oncology), which are fusion proteins with the Fc region of IgG1 antibody fused to the CD47-binding domain of SIRPα with the goal of interrupting the CD47-SIRPα survival signal. Unlike CD47-targeting antibodies, TT1-621 appears to bind only minimally to human RBCs and interference in pretransfusion testing has not been observed or reported to date.

A few references you might find of interest: Management of Blood Donors and Blood Donations From Individuals Found to Have a Positive Direct Antiglobulin Test. Transfusion Medicine Reviews 2012. Volume 26, Issue 2, Pages 142-152, Garratty G. The significance of IgG on red cell surface. Transfus Med Rev. 1987;1:47–57. Petz LD, Garratty G. Immune Haemolytic Anaemias. 2nd ed. Philadelphia, PA: Churchill Livingstone; 2004.

I just answered this question. My Score PASS  

Short periods of time (<12 to 24 hours say) at refrigerator temperatures have no known deleterious effect on platelet transfusion efficacy, so I would use them as I would use any platelet component stored at room temperature. I routinely approve this at my own institution when this happens.

I always figured that, if it was benign enough in the donor that they met donor requirements, it was likely to be relatively benign in the recipient. Not perfect, of course.

We also inculed documents owner documents authorised by and effective date.

A bit late for hopping in but. Another possibility suggests from the 2+ strength typing. Yes, it might just be heterozygous expression, but some techs will call a mixed field 2+. I know you said you didn't have transfusion history, but that's where I'd go first in workup before genotype. Try retic separation and retest. If your patient had a low titer Jka, received unmatched units elsewhere either from this MVA as uncrossmatched units before transfer, or at an outside hospital between july and now, then came to you. I think it is feasible you'd see this presentation. DAT positive in c3d first as the Jka re-activates, an anomalous Jka+ result due to transfused cells but a clearly demonstrated anti-Jka. They could also have a weak expression variant of Jka, where they test positive but can form it. Or an auto Jka. But those are way less common than I think my boring scenario :-)

I just answered this question. My Score PASS  

Hello Patient has developed antiD in first pregnancy at around 32 weeks and her quantification level was 1.0 IU/ml. In 2nd pregnancy her booking blood at (12 weeks) antibody screening was negative. At 15 weeks sample sent for fetal genotype (FDS). On this Report received inconclusive due to all Anti D. Because patients was on file for historical antibody therefore sample sent for quantification in 2nd pregnancy and Report received antibody not quantified since it reacted weakly in enzyme IAT only. My understanding standing is if patients once developed Allo antiD her titre level does not go down. Why was her antibody screen was negative in 2nd pregnancy at 12 weeks?

Yes. Another thought do you think in 1st pregnancy anti-D could be in IgM nature and therefore level might be slightly raised?

Thanks Malcolm. I checked it she was not given large dose of anti -D in her first pregnancy. However in her first pregnancy she developed anti D at 32 weeks where her level was 0.5Iu/ml then at end of her first pregnancy level was 1.0IU/ml. As per routine antenatal sample if booking blood is Rh negative we send sample for FDS for Rh D prediction. Could it be because lady had Allo antiD? When lady has Allo anti D do they use different techniques?

Not necessary, but thanks

Agree with Dr. Blumberg. The FDA guidance for CSPs states they can be used when "regular platelets are not available or not practical". This sounds like a more prophylactic use of platelets, which is also not practical. If you didn't have anything but CSPs on the shelf, and there is a request to transfuse, I guess it would be up to you as to how much you want to argue with cardiac surgeons for the sake of your inventory, given that these patients are not actively bleeding.

Main practical issue from a transfusion perspective is a positive IAT XM. If RBC given via electronic issue you would be unlikely to ever know the unit was DAT positive.

I have a little bit more info on my case. In July she had a T&S done and the ABID was neg. She came through our ER as an MVA patient. We use Capture R method (Echo) All panels show a perfect Jka. The throw off is the Complement is w+ after 5 min incubation. she antigen typed Jka+. Is this a true Jka or possible auto-Jka or varient. Patient was discharged same day. So no extra samples can be collected for send-off to reference lab. Our hospital does not handle OBGYN patients.

We are a large academic medical center / L1 adult and peds trauma center. We stock 4 helicopters, at least 4 county EMS units (with more onboarding) (all 2 Opos WB units each) We also have an Adult ED refrigerator where we try to keep a minimum of 8 WB along with a few RBC's and Liquid plasma units. We also stock 2 units O neg WB in our Peds ED refrigerator. Our Massive Transfusion protocols allow us to transfuse up to 10 O pos WB to anyone >/= 16 years of age. We have a standing order for WB with our supplier for 40 units per week.

why not just use grifols' cells?

Something one of my mentors said early in my career: "Don't worry about junk. If it's a real antibody and you transfuse against it, it'll be nice and strong by the next time you see the patient."

My motto was "when in doubt, shake it out". Seemed to work for me.

I've been a BB'er for 35 years (at the same hospital) my very first manager (who was a good, seasoned BB'er) used to tell us........., "if you have to hunt for it - it's not there". As you become more adept at reading tube reactions - your eyes will not fail you! Trust your gut. As for your technique - it all sounds good! Practice with a few techniques to find the one that works best for you I "tilt and giggle", button up, The tilt helps with seeing Mixed Field - which we tend to see a lot here - It also helps with seeing "how" cells are falling off the button - are they chipping off or are they "swirling" off.....or is there a little of both? (For some reason I always think of the "tail" of an old RPR test .....which probably dates me, LOL!)

I remember being really confused in school as I was trying to copy the swirling that the grad student did when reading his tubes. When I went to the hospital for my clinical rotations, the blood bank supervisor taught me to hold the tubes with the button up and just tip the tubes over the finger on my other hand and watch the button as it came off the tube. This has worked so well for me all of these years in the blood bank.

It sounds to me like you are doing everything that you should do, without either over-shaking the tube, or over-reading the contents. I am extremely glad that you are not using a microscope, as, if you did, you would almost certainly see the odd couple of red cells "kissing each other", even if they have been incubated in isotonic saline. The other thing is (and I speak with some 43 years of working in blood group serology) if the reactions in the tube are THAT weak, the chances of any atypical alloantibody that you might miss being clinically significant are absolutely minute. If you are still worried, however, get a more experienced worker to read your tests as well, until you feel confident. That is how I learned when I started. I wish you the best of luck in your future career.

If the model is discontinued and no parts are available for repairs, I'd say it has reached its 'end of life' - however I'll bet it will still work a long time after that before a part needs replaced (especially older, quality scopes). I can see 'end of life' for more complex or expensive equipment, but a microscope for blood bank is more of a minor equipment purchase. My 'new' scopes are student scopes that cost less than $500 and they work just fine for our purposes.

They are AO's, then I am sure that they are still working. Why is your upper management trying to mess with a good thing?

Do you have a company come in to service them? If so, they might be able to help you. It's possible that the company was bought out by a bigger one like Fisher Scientific. I am retired so I don't have contacts anymore.

Stop blaming the Canadian Smoke. We in Canada, do result as No Antibodies detected. If the patient had an antibody in the past, that is maybe below detectable limits, but was previously identified, those are also in report as historical and as such the patient would have a full crossmatch in gel as well as phenotypically matched for previously discovered antibodies.

Extended cross-match, UNLESS, the history of which other hospitals the patient has been treated is known. Of course, in the UK we have a national database of patient's antibodies, which makes life an awful lot easier, even if the data is just a "snap shop".

I agree with all the previous comments. You cannot manage a transfusion reaction in a patient who has died from lack of blood. One thing to add: In the time before time......emergency release units were always O negs. However, today's practice has evolved in a risk-based manner and it is now accepted that O pos units can fulfil this function. Perhaps ironically, if the old practice had been employed in this case (use O negs), it would have been very unlikely that this patient would get a E+ unit.

You did everything necessary as others have said. At our facility, physicians seem to be unphased by the use of emergency released blood - we issue a lot of it. It is not uncommon to discover that the patient has a historical antibody that may or may not be demonstrating. The physician and pathologist are notified when the history is discovered and the physician makes the medical decision to continue or stop the transfusion at that point. We perform antigen testing of the unit(s) and perform AHG compatibility testing of all units that are issued. Further laboratory testing is ordered by the physicians caring for the patient. The most immediate concern is an acute hemolytic reaction and that is rare. Shortened survival of incompatible transfused red cells is expected.

You did everything that was required in this situation. The patient was a trauma and needed emergency transfusion. The risk of death outweighed the risk of a hemolytic transfusion reaction in that scenario, according to the treating physician. I once had a trauma surgeon tell me "I can treat a transfusion reaction but I can't treat death!" That put things in perspective for me. That is why thy sign the consent. Next step would be to report this to your risk management department so that follow-up can be made, including monitoring the patient for the s/s of DTR.

My two pennies worth... I did measurement of uncertainty on KB - 47%. Shocking sensitivity... We changed our policy that any foetal cells required follow up by flowm while we were addressing the issue. We solved it by requiring all staff to take part in each EQA session and following up any discrepancy of >10%. We also introduced scoring for our controls and required all staff to do a count before moving onto the patient ones. Any discrepancies in the control scoring or EQA resulted in retraining. What actually happened was that because staff were required to do an actual count, rather than an eyeball, for every kleihauer, they organically became more proficient. We also were able to identify the staff member who was counting lymphocytes as foetal cells... For anyone who is interested - there is a modified KB that I have developed (sadly I never published before leaving the labs) that has a counter stain for the white cells - makes the foetal cells ping

Dear, You can find your answer in CLSI - QMS24 In this document, you only need to compare your result with at least 1 lab. 2 events/year; 2 samples/event

Agree. We don't issue type specific blood unless we have time to get a current type and perform an immediate spin crossmatch for ABO compatibility, and it's still issued as uncrossmatched until the antibody screen is done.

Over the years I came to realize that a lot of what we did was geared toward simply passing inspections and meeting requirement that, in reality, did little or nothing to aid the patients. Smoke and mirrors to confound the masses. I've said this multiple time on this site and still believe it strongly; "Complicating a process never made it better!" yet every time something happened everyone's first response was to add more layers to the process in a effort to make it fool proof until some new fool came along. Human error will occur as long as humans are involved. All we can hope for is minimizing the impact. This statement used to make our corporate transfusion QA folks lose their minds. I've kinda taken a tangent for a moment. Getting back on track, Cliff and Malcolm I agree with you completely.

Wastage with plates for solid phase depends on what platform you are going to use. With manual testing and the Echo you use antibody screen strips that test 2 patient samples per strip. When I last looked at the Galileo (5 years ago), you could run 4 patient per test plate. That may have changed - I don't know. I also don't know what the Neo uses. Early on with the Echo, you had to use 2 test strips (which would run 4 patients) per run, sacrificing 3 antibody screens if you ran 1 patient. Now if you have a run that is for 1 or 2 patients, you use a balance strip so that large waste factor is gone. With 1 patient runs, you will still lose 1 antibody screen. If you never, ever run more than one patient at a time, you will lose 50% of your total antibody screens. When cost per test is calculated, what you need to look at is how often you can 'batch' patient samples in runs of 2 (or 4 or whatever Neo uses) to determine waste. That percentage of waste is plugged into the reagent use formula and included in the cost per test figures. The Immucor sales people do that as part of your cost per test calculations (and very happily, too - naturally ;>). We calculated very conservatively and said we would have 40% waste and we still came out money ahead over gel for our contract with Immucor (3 years ago). Our actual useage pattern is better than 40% waste, as we are able to batch many of our runs with non-urgent tests like prenatal antibody screens, pre-surgical testing, next day transfusion patients and the like. So consider your work/patient order patterns when comparing automation methods. That should help make things clearer. We have been satisfied with our Echo's performance and the technical support we get for it. I was concerned with how far away our service person is - about a 5 hour drive. BUT...we are in a rural area and that is not uncommon for service with any of the companies we do business with for hematology, chemistry, etc. The plus with the Echo is that it has been extremely reliable and we've only needed 1 service call in 3 1/2 years. All the other problems (and there have not been that many of them) were fixed by me with telephone assistance from technical support and a little box of parts that come with the instrument. **Disclaimer: I am definitely not a mechanically adept person, but I get alone with the Echo tinkering just fine.** It was designed for parts replacement by users, very simple replacement. Their capability to 'dial in' to the instrument, just like the technical folks do for the big chem analyzers allows for long distance diagnostics and adjustments to camera and centrifuge operation. As of the first CAP automated survey of 2011, there were 407 Echos, 520 Provues, 130 Galileos, and 39 Tangos reporting. From the survey performance of each platform, I think you will see that they are all performing within acceptable limits. The switch from interpreting patient results in gel and interpreting patient results in solid phase is NOT difficult. None of my techs had a problem with that. (Note: we were manual gel users, not ProVue users.) We do have increased sensitivity, which is great for detecting alloantibodies in our patient population. We do see a few more warm autos that we did with gel, though that is a trade off I'm willing to make for the ability to catch a few more -Jk-a, Jk-b, Fy-a, Fy-b, and little c antibodies. We do not have an annoying number of non-specific reactions anymore (software upgrades, and a recent instrument adjustment, have helped that issue significantly). Would I switch from the Echo to an automated gel system? If the ProVue has some new features that improve it's function over the function of the Echo and the money difference is significant...it's a possibility - gel worked fine for us when we were manual users. Am I satisfied with what I have right now with the Echo, functions and $$s...definitely Yes.