gagpinks

Oh, I'm sorry, I wasn't criticizing; after all, I cannot either speak or write a word of German!
If you were cross-matching group A red cells, whilst your panel cells were group O, it sounds very likely that the patient has an auto-anti-H.  The reason I say this is because the H antigen is very strongly expressed on group O red cells, but very weakly expressed on group A red cells, and your reactions are exactly what I would expect to see in such a case.

I am unfamiliar with some of your terminology, but, as I understand what I do understand, what you have may well be an auto-anti-H (or an auto-anti-HI); I am fully appreciative that I may be wrong because of the unfamiliarity with your terminology.

I would thoroughly agree with you Beth.  UoM was only supposed to be used on quantitative assays, as I understood it.  Certainly, when the NHSBT RCI Laboratories were inspected the first time, UoM only reared its ugly head with quantification of anti-D and anti-c, measurement of FMH by flow, and a bit of a nod to the "art" of titrations.  They have recently been inspected for a second time, and passed with flying colours.  I would love to know where your particular inspector(s) got the idea about UoM  testing for DiaMed Gelstation/IH system.  I would suspect that he/she/they did not do blood transfusion as a primary discipline and, although UKAS seem to have taken over the mantle of "most arrogant organisation in UK Pathology" from the MHRA (and they were bad enough), I would still put the question formally to UKAS, if necessary via your Regional Transfusion Committee (so that they would be forced to answer).

Hi Jermin 
Your question regarding dilution,  you should follow manufacturer instruction because if you do anything outside manufacturer instructions you might have to validate process again. 
Second question regarding staining and storing sample 4 C  for 4 days.  
Why would store sample for 4 days. Because Rh neg lady should have her antiD dose within72 hours. 
Secondly I would suggest if you prepare slide and don't fix them then there might EDTA changes on your slide. If you fix your slide with different lot and when you stain patient slide it might be different batch no. You are not really controlling process. Control should be done the exactly the same way the way you run your patients sample or run parellal with patient. Otherwise check ISO 15189 manual 
I would suggest check with QMG staff.
 

I’m getting hung up on this item in regard to our KB qc:
 
TRM.40130 Alterative Control Procedures                                                                           Phase II

If the laboratory performs test procedures for which control materials are not commercially available, there are written procedures for an alternative mechanism to detect immediate errors and monitor test system performance over time.  The performance of alternative control procedures must be recorded. 

Note: “Performance” includes elements of accuracy, precision, and clinical discriminating power.  Examples of alternative procedures may include split sample testing with another method or with another laboratory, the testing of previously tested patient specimens in duplicate, testing of patient specimens in duplicate, or other defined processes approved by the laboratory director. 

Evidence of Compliance:

Written procedures for alternative quality control AND

Records of alternative control procedures

------------------------------------------------------------------------------------------------
Are most of you buying qc for Kleihauers?  We are still making our own positives by diluting a normal adult CBC tube with cord cells (high and low positive controls) and of course using the normal adult as the negative control. We count patients in duplicate and the two counts must be within 10% of each other.   Are we in compliance?  Control materials are commercially available, we jut don't use them (yet anyway!).  One other question, we have always said the number of fetal cells in the high positive control should be roughly twice the number in the low positive.  If still making your own controls, do you all define 'roughly'?
Thanks so much in advance!
Cathy
 
 
 
 
 
 
 

I am unable to answer your questions about the staining of Kleihauer slides, as this most definitely NOT my area of expertise, but I will have a crack at the bonus question (but with a comment about terminology thrown in!).
Yes, a transfusion certainly will have implications on the FMH screening/quantification, and it will lower the results, but only if the transfusion is given for an ante-partum haemorrhage very close to birth, or a post-partum haemorrhage soon after birth, but before the sample has been taken to estimate the FMH.
If you think about it, the only reason for the woman to have a transfusion at these times is if she, herself, has had a haemorrhage.  The ratio of "adult" red cells to foetal red cells she loses will be identical to the ration in her circulation, but as soon as she receives a transfusion, the ratio of "adult" red cells to foetal red cells in her circulation will rise.  The reason for this is that those red cells being transfused to her would contain no foetal red cells, and so, in effect, these transfused "adult" red cells will "dilute" the mixture of maternally-derived "adult" red cells and foetal red cells in her circulation.  Of course, and also in effect, this means that the amount of "adult" red cells will be concentrated (maternal red cells + transfused red cells), meaning that the ratio of foetal red cells to "adult" red cells in the circulation will be lower (if you like, it is a bit like the more saline you add to an antibody, the weaker will be the reaction, as is the case with an antibody titration).
Now, it may be argued that the ratio of foetal red cells to maternal red cells that are bled out during the haemorrhage will be the same as that of the original blood in the maternal circulation, which means that the actual volume of foetal red cells in the maternal circulation (as opposed to on the Labour Ward floor) is reduced, and I would find it difficult to gainsay this, so it may well be that the calculated amount of anti-D immunoglobulin required to prevent sensitisation to the D antigen, and so the dilution of the foetal red cells remaining in the maternal circulation, versus the actual volume of the foetal red cells in the circulation is irrelevant, and will still be adequate, but I would err on the side of caution, and give a slightly higher dose of anti-D immunoglobulin.
Now for my comment!
There is no such thing, and never has been such a thing as the Rhesus Blood Group System.  Rhesus with an upper case "R" was an ancient King of Thrace.  rhesus with a lower case "r" is a monkey.  As I have said many times, neither Rhesus, nor rhesus worked (directly) in blood transfusion.
The correct terminology for the Blood Group System is Rh.  However, the gene is RHD, the protein carrying the red cell antigen is RhD, but the antigen itself is just plain D (not Rhesus D, not rhesus D and not Rh D), and so the pregnant women of which you are talking are D Negative.
The wrong name has come about because Landsteiner and Wiener injected rhesus monkey red cells into various animals (rabbits and guinea pigs) in an effort to discover more antibodies against antigens expressed on human red cells.  They managed to do so, and the antibody they found was thought to be identical to the anti-D described in a human by Levine and Stetson, but in the early 1960's it was found that the antibody described by Landsteiner and Wiener, and that described by Levine and Stetson were far from identical (and, indeed, the genes encoding the antigens are found on different chromosomes).  As a result, the antibody described by Landsteiner and Wiener was designated as anti-LW, and this particular Blood Group System is now designated as LW.

So we have had 2 patient mysteries in the past week.  One of them probably has a simple solution....but is just not something I have ever seen in over 30 years.  The other one is more of a mystery.
1st case:  We received a Cord Specimen on the baby from an A NEG mom to evaluate for Rhogam.  The baby typed 4+ with Anti-A, but 1+ with Anti-B.  We did wash the cells many times.  We also obtained a heelstick but obtained the same results.  I am used to seeing weak A typing on newborns; but not used to seeing it with Anti-B (but then statistically, I have seen many more A's over the years than B's); especially when it was so strong with the Anti-A.  Have any of you seen that weak of typing with Anti-B on newborns, or are there any other thoughts on what is occurring here?
 
2nd case:  62 year old male with diagnosis of COPD, Dyspnea, GI Bleed, Chemo (as recently as yesterday).  So ongoing problems.  He has had MANY transfusions of RBCs and Platelets over the past year; including past 3 months.  The patient is A POS.  Yesterday, he was transfused with an O POS Platelet (we only keep 2-3 in-house at any given time so just have to give what we have, and do so by outdate).  Anyway, after receiving only 151 cc's of Platelets, he had Chest Pain, Respiratory Distress and Vomiting.  He was transferred by ambulance the 1 block to the Hospital ER.  All of our clerical check was fine.  Our Policy for giving Platelets is that we just have to have a historical type on the patient; it does not have to be a current type.  However, the Cancer Center had drawn a HOLD specimen that morning so as it turned out, we did have a pre-transfusion specimen (just had not been tested yet).  Upon testing both the pre- and post- specimens, the only issue we came across was that the pre-transfusion IgG DAT was Negative, but the post-transfusion IgG DAT was 3+.  When we spoke to the Medical Director of our Donor Facility, he said to report it as a hemolytic transfusion reaction.  Problems with that are:  After whatever treatment they gave patient in ER, he was sitting up and feeling just fine.  Also, no indications of it being TRALI.  So we became concerned that perhaps we had a platelet with a high-titer Anti-A,B.  We performed an Eluate on the post specimen and tested it against screening cells plus A1 and B cells.  All testing was NEG.  Now we were really stumped.  We had the patient re-drawn and now, several hours later, the IgG DAT had dropped to 1+.  Not a dramatic drop in Hgb.....from 7.4 before transfusion, to 7.1 after transfusion, to 6.9 this morning.  So my last "guess" was that perhaps he was just really unlucky and the donor of the platelets had an Antibody to a Low Incidence Antigen, and the patient just happened to be Positive for that Low Antigen??  So we are testing just the Lows that are on our panels (Cw, Kpa, Jsa and Lua).  Of course there are a lot more Low Incidence Antigens that it "could" be if that is what caused this.  But that decrease in strength of the DAT, in light of not really seeing evidence of hemolysis, is very confusing.  And if it is an Antibody to a Low Incidence, due to his many transfusions of RBCs, is the Antibody attaching to his own cells, or to donor cells he previously received which may have been Positive for a Low Incidence Antigen?  Any thoughts/ suggestions.
Also, as I am completing this, my Tech. just brought me a gel card with the results from 2 of the Low Incidence Antigens.  It looks like the card spun at an angle so I want it repeated, but it appears that the eluate is reacting with the Lua+ panel cell.  But I wouldn't expect an Anti-Lua to cause a severe reaction in a patient like that.
Anyway, will keep you posted on our serological results.....but if you have any other ideas/ thoughts, would love to hear them.
Thanks in advance for your input,
Brenda Hutson, MT(ASCP)SBB

We transfuse febrile patients regularly. The nurses look for an elevation in temperature (1.5 C) above the starting temp to call a febrile reaction. I don't feel that we are doing a large number of workups simply because the patient transfusion started with an elevated temp.

We are configured to save "Database and Column Images".  This will enable us to restore instrument configuration settings and images, as well as test/qc results.  The test results are in our LIS, but the images are not.  QC reports will be either saved electronically on a network drive or printed (multiple sites implemented-their choice).  We also document QC pass/fail on a daily log. We have enabled the Active automatic images synchronization, as this downloads images continuously to the backup folder/device, making the monthly backup time to process a bit shorter.

If you know she has anti-E, you can probably put together a custom screen of E negative cells.  That screen would only be positive if she developed another antibody.  Be careful that you cover all the antigens that the FDA requires.  That list used to be in the Technical Manual.  I think it is D, C, E, c, e, M, N, S, s, P1, Lea, Leb, K, k, Fya, Fyb, Jka, Jkb.  
 

Thank you  Scott
That makes sense for the alarm settings.
What is the the rationale behind the 1C tolerance limit between the chart and the displayed reading?
If both are calibrated +/- 0.5 C. I assume both could be out by 0.5 C  on the opposite end of the temperature scale, hence the 1C?
 

The thing is, an antibody specificity may not be clinically significant, but that does not mean that its titre or avidity is not affected by further stimulation.  As exlimey said earlier, the majority of anti-Yta antibodies are IgG4, and IgG4 antibodies never cause haemolytic transfusion reactions, but that does not mean that further stimulation by Yt(a+) red cells will not have an affect on the titre and avidity of this IgG4, or that the further stimulation will suddenly cause the antibody to switch IgG subgroup (although I also acknowledge that exlimey does talk about elements of IgG1 in the stronger examples of the specificity).  Are they ever naturally occurring examples of anti-Yta?  Again, to answer you honestly, I don't know.

1.  Without a doubt!  The thing is that not all antibody specificities will become detectable at exactly the same time (they are a pain, as they do not read the text books or, if they do, they do not take any notice of the bits they do not like)!  For example. if you detect an anti-D in the first sample, but nothing else, it does not mean that there is not some other "nasty" bubbling under the level of ability to detect,  The next time, there may be, for example, an anti-D and an anti-Jka.  It is always better to detect the anti-Jka in vitro, rather than in vivo!
2.  In contrast, no, we would not perform an elution every time on such a case, because, in the situation you describe (which, incidentally, working in a Reference Laboratory, we saw only a very regular basis) the patient's immune system is rarely, if ever, working at what may describe as "full capacity".  We match them for Rh and K to reduce the chances of "common" antibody production, but that is about all.  We would test an eluate about once a month, UNLESS there was clinical evidence of a transfusion reaction (which, given that they are haemolysing their own red cells, may be difficult to detect), or if the time between the need for transfusion becomes noticeably closer, in which case we will do elutions more frequently, but, it should be noted, as there will almost certainly be a panaggltutinin present, the eluate itself may have to undergo alloadsorption, which could weaken the reaction of any underlying atypical alloantibodies.

About half of our surgery patients are first timers to the blood bank.  Since we need two independent types, we use the pre admit type and screen as the first type and a heads up for any antibodies.  They always get redrawn the day of surgery for the type and screen we will crossmatch with.  That may be 28 days later or the next day.  We then have 2 independent types for our ABO/Rh confirmation.  We do not extend sample dates past 3 days without a really, really good reason and pathology approval.

Right now our facility will extend PreAdmit patient samples for 10 days.  This means the patient hasn't had any transfusions or been pregnant in the last 3 months.  Also the patient would be having surgery within 10 days of the specimen being collected.  Now some of our Dr.'s would like to have patients come in as early as 28 days before surgery to have their PreAdmit labs drawn.  Is anyone else doing this?  If so how do you handle your manufacture inserts and transfusion reactions?  Do you perform crossmatches on the day of surgery?  Did you validate anything before swapping to a longer date?  Any information would be greatly appreciated.

The very FIRST thing I would do is to sign a declaration that any patient who suffers either morbidity or mortality as a result of this change to your system is down to them (i.e. THEY take legal responsibility, and not you).  This will have one of two outcomes.  Firstly, they will sign such a document, and then you are free from accountability (as long as you record that you have explained to them the error of their ways), or secondly, they will withdraw to a private area to change their under-garments, and will abandon this plan.

In uk if quantification level is 0.4 IU/mL or above we consider as a immune anti-D and we do not issue RhIg.  However if lady comes in ED we perform Group and antibody screen before we issue RhIg.

After all these preparation patient delivered at home. Baby and Mum didn't need any blood.

Hi Cliff 
We count 4 hours from the time it's out of controlled temperature. If you pack your unit in controlled transport box than time start from it opened the box.
It's worth looking JPAC guidelines 
 

No problem at all gagpinks.  Anti-Inb is sensitive to proteolytic enzymes, and quantification uses enzyme-treated red cells, so the anti-Inb will not interfere with the anti-c levels.  Now take a deep breath and RELAX!!!!!!!!!!!!

They are too big (the Henry VIII one is not big - it is vast!) for me to upload on to here, and so I have sent them on a CD-ROM to Cliff to put them on here, but, as I said above, the CD-ROM has been sent by good old fashioned snail mail, so it should reach Cliff sometime towards the end of the year!!!!!!!!!!!!

OMG!  Well, at least we know the anti-Inb will not affect future pregnancies, but an anti-c could do so.  The good news is that, as far as I can remember, the UK units of In(b-) blood are R1R1; the bad news is that there are only a couple.
I suggest we start planning now!!!!!!!!!!!!!!!!!!!!!!!!

Well, in a way, yes.  They will not waste time on trying to perform alloadsorptions (as these don't work) and will probably perform genotyping from the word go, rather than trying to get a phenotype.
To be honest, the submitting hospital should give the Reference Laboratory as much information as they can about ANY patient, whether they be on ANTI-CD38 (gagpinks, they are on a monoclonal antibody - not a monoclonal antigen!!!!!!!!!!!) or not.

Yes it is same lady. Now this time she delivered at home☺