MinerJ

Hi Malcom, As always, thank you kindly for your detailed explanation. I feel like I am over-reliant on electronic issue, that sometimes I forget that there are antibodies (which have the potential to be clinically significant) that is missed by the screening cells. I will have a read of the article you have referred to, for an extra boost. Cheers!

Hey All, This is probably more to do with UK guidelines, but nonetheless I would like to hear everybody's thought on this. So the BSH guidelines on Pre-Transfusion Compatibility Procedures in Blood Transfusion Laboratories suggests that if a patient has known to have presented with alloantibodies, either current sample or historically, antigen-negative units should be provided on antibodies known to be clinically significant. The patient will no longer be eligible for electronic issue, and would require serological crossmatch to be performed if red cell component is required. My question is, if we are providing antigen-negative units, then what is the basis behind the need for crossmatching it serologically? If we do not perform serological crossmatching for patient known to have anti-A and anti-B antibodies (e.g. O patient), what of other antibodies? Is this simply the case of "That is what the guidelines says", or is there another element to this e.g. maybe the limitations of the LIMS being used?

Hey Malcom, Yes, you are absolutely right, meant to talk about the pH and not enzyme. And thank you again, that does clarify a lot of my queries

Thanks Malcolm I am going to diverge from my previous question. In regards to Anti-M, you mentioned that these antibodies tend to have an enhanced reaction in lower pH, which is present inside the column. In our laboratory, we perform Tube NISS strictly at 37'C to rule out the presence of anti-M reactive at 37'C (mainly for pregnant women). If there is no reaction, then its determined that anti-M is not reactive, and therefore not clinically significant. I was wondering why NISS? Would performing the test using CAT after pre-warming not sufficient? Or is it to do with the enhancement effect of the enzyme? And why NISS over LISS?

Hey All, I have always been told that the use of Tube Method, or conventional tube technique (CTT), is the 'gold standard' for blood grouping and allows a stronger reaction in the reverse group, compared to column agglutination technology (CAT). For a long time I just believed it, since the proof is in the pudding. I have managed to use tube method numerous times to confirm the blood group when it showed weaker expression in the reverse group in the automated CAT. However, I started to wonder why? I have looked into it as much as I could but I could not figure out the mechanism behind it, so I was wondering if anyone can shine some light on this?

In our hospital, it is the blood transfusion laboratory that handles Octaplas, since pharmacy does not have a plasma thawer. It is somewhat issued out similar to FFP, but our LIMS has been set-up to recognise Octopus as a "Batched Product", similar to Human Albumin Solution or Prophylactic Anti-D, but it recognises the need to be compatible with patient's blood group.

Hi All, We are about to move from using Bio-Rad IH-1000 to Immunocor NEO in our blood bank department. As most of you are already aware, the IH-1000 uses column agglutination technology (CAT), whereas the NEO uses Solid Phase Red Cell Adherence (SPRCA) assay. SPRCA is known to be more sensitive, which is great when picking up on elusive antibodies belonging to Kidd blood group system (I think ). My concern is about the techniques which employ the use of indicator cells that are coated with anti-IgG. It will only pick up on IgG antibodies and none of the IgM antibodies. How significant is this? Is there any way of picking up IgM antibodies using such technique? Or should we not worry since IgM antibody does not usually reaction at 37C? Regards, Jermin

We had both in our laboratory. Must say, although the user interface for Stago looks like was done by a 7-year-old, it's a stellar machine. Reagents last lot longer, and QC passes almost every time without issue. The Stago's calibration is also a dream for most reagents: just scan a barcode and you're all set. I can give more details if need being, so please feel free to ask.

Thanks for your replies and I believe I understand. So for this particular patient, we did send the sample to the reference laboratory which found the patient had autoantibodies, as well as alloantibodies (anti-Fya ). No. I will see if I can talk to my senior, but before that, I would like my colleagues to be able to understand why positive DAT or having autoantibodies may not be the end of the world, and that they could try and crossmatch the units in-house.

Hi All, I have a question, but firstly good old story time for some context. I came across a patient who had positive antibody screen on all three screening cells used (BioRad). I was concerned this may be an auto and pan-reactive, and required units. Performed a monospecific DAT, showing a positive reaction to IgG only. By this time antibody panel finished cooking and showed the patient may have anti-Fya , but couldn't do phenotype. By this time I was nearing my shift so handed it over to my colleague and asked for some units to be crossmatched. However, he refused as DAT was positive and said he rather send the sample to reference laboratory for them to crossmatch. The next day I crossmatched units to verify if it could have been done in our laboratory (just because I am sad that way), and turn out the unit I crossmatched was compatible (which I wasn't surprised about) Question Why does positive DAT (or the cause of positive DAT) sometimes interfere with IAT techniques (such as antibody panel and crossmatch) and sometimes it does not? If both use AHG, then wouldn't positive DAT with IgG cause antibody panels shows pan-reactive with red cells? But obviously it doesn't, but I'm trying to figure out why, and I'm sure the answer is quite obvious. My laboratory seems very hesitant whenever they see anything regarding autoantibodies or positive DAT, and thinks that sample cannot be crossmatched in-house and needs to be sent off without even trying to investigate. Hopefully, by me asking this question, I can explain it back to my colleagues (but obviously take all the credit). Cheers in advance, Jermin

Hi Malcolm, I agree with what you have to say. I have no problem relying on FDNA result, as accuracy is pretty damn high. The people who we are trying to convince/explain are the Midwives who don't understand why we are double checking something if you are meant to rely on it the initial result- and we kinda understand what they have to say. I will read the latest papers as you mentioned. I'm sure it would be helpful, Thanks, Jermin

I don't even know how to begin to question that. Thanks for your replies as it has really helped. Since we are on the topic of FDNA, our laboratory is still getting our head around the accuracy of the test. If the FDNA can give a false negative result, and the accuracy as stated on reports show there is a chance of discrepancy, should we take that risk? Shouldn't we either fully be behind FDNA result, or we are not. If FDNA initially showed D negative, but the baby turns out to be D positive, then wouldn't there have been a chance patient would have had a sensitising incident long before we figured out the true D status?

Hi All, Its been a while since I came back to this forum, but glad I feel like I have gained a lot more insight. I feel like I'm a bottomless cup. So I come with a question, for which there is not going to be a definitive answer (but with BB, is there ever one?), but hopefully, I would gain a bit of understanding. Background: So, our laboratory has started sending samples to reference laboratory for genotyping of the foetus by FDNA, which is great, since we would figure out the Rh(D) status of the baby (on most occasions) before they are born! So our laboratory has set up a flow chart which basically mentions that you do not need to send cord sample of Rh(D) negative mother if the baby is shown to be Rh(D) positive (or D positive, I am quite wary when trying to talk about Rh group), and only send cord if baby of Rh(D) negative mother if the FDNA shows the baby is Rh(D) negative, just to confirm the accuracy of FDNA. It sounds kinda counterintuitive, but we will soon be just not processing any cord sample for the ones we performed FDNA on. That means no cord Blood Group or DAT on a lot of post-delivery patients. Question: By missing out DAT, we would possibly be missing out on detecting ABO incompatible HDN. How significant do you think it is in the early stages? Is it OK to wait to see if the patient shows signs of jaundice and for them to send a DCT sample afterwards? Bonus Question: What does your Hospital/Laboratory do in the event of positive DAT on cord sample, and why do you do it? I had a read through one of the articles stating about the significant of DAT, but they called the Rh blood group as Rhesus, so I'm not going to take them too seriously Cheers, Jermin

Cheers. I have the Introduction to Transfusion Science Practice. Robina Qureshi, and I will seek others when I get the chance.

Hi Malcolm I have been using Rodak’s Haematology. Professionally speaking I am a Band 5 Biomedical Scientist still in course of doing his Specialist (which I may never finish) *sorry for late reply* Regards, Jermin