RichU

Ah ok. Makes sense.
Cheers

How do you know a positive screen isn't caused by an alloantibody underlying the prophylactic anti-D unless you do an ABID?

Jsbneg,
 
Am I missing something. You said the patient was truly a type O after receiving several type A RBC's. Maybe I'm missing something in the message

The same phenomenon is seen if you use a spun sample for DATs.
The cells at the top can be negative and the ones from the bottom positive if recently transfused.

The same phenomenon is seen if you use a spun sample for DATs.
The cells at the top can be negative and the ones from the bottom positive if recently transfused.

The same phenomenon is seen if you use a spun sample for DATs.
The cells at the top can be negative and the ones from the bottom positive if recently transfused.

The same phenomenon is seen if you use a spun sample for DATs.
The cells at the top can be negative and the ones from the bottom positive if recently transfused.

The same phenomenon is seen if you use a spun sample for DATs.
The cells at the top can be negative and the ones from the bottom positive if recently transfused.

The same phenomenon is seen if you use a spun sample for DATs.
The cells at the top can be negative and the ones from the bottom positive if recently transfused.

The same phenomenon is seen if you use a spun sample for DATs.
The cells at the top can be negative and the ones from the bottom positive if recently transfused.

I used this case study as part of my Higher Specialist Diploma in Blood Transfusion.
The IBMS have asked if I would like to give my PowerPoint presentation ('What the f?') at the 2023 Congress.
Thank you to all the contributors - I will certainly big up PathLabTalk if I do get to do it.
Rich

This statement is completely true, BUT the fact that NHSBT RCI Laboratories started to use these routine techniques followed a huge amount of work performed by Gordon Burgess when he was the Reference Service Manager at NHSBT-Cambridge Centre (before he became Head of RCI in NHSBT) to show that these were viable techniques that passed prolonged Quality Assessment.  To introduce such techniques without such work would not have allowed RCI to pass inspections by our various assessors.

I doubt if Clarest would be able to introduce such techniques into Canadian laboratories without similar work.

BCSH guideline for the use of anti-D immunoglobulin for the prevention of haemolytic disease of the fetus and newborn states 'Anomalous or indeterminate cord Rh D groups should be treated as D positive until confirmatory testing is completed.'
For neonate transfusions see Malcolm's answer.
 

I used this case study as part of my Higher Specialist Diploma in Blood Transfusion.
The IBMS have asked if I would like to give my PowerPoint presentation ('What the f?') at the 2023 Congress.
Thank you to all the contributors - I will certainly big up PathLabTalk if I do get to do it.
Rich

I used this case study as part of my Higher Specialist Diploma in Blood Transfusion.
The IBMS have asked if I would like to give my PowerPoint presentation ('What the f?') at the 2023 Congress.
Thank you to all the contributors - I will certainly big up PathLabTalk if I do get to do it.
Rich

I used this case study as part of my Higher Specialist Diploma in Blood Transfusion.
The IBMS have asked if I would like to give my PowerPoint presentation ('What the f?') at the 2023 Congress.
Thank you to all the contributors - I will certainly big up PathLabTalk if I do get to do it.
Rich

I used this case study as part of my Higher Specialist Diploma in Blood Transfusion.
The IBMS have asked if I would like to give my PowerPoint presentation ('What the f?') at the 2023 Congress.
Thank you to all the contributors - I will certainly big up PathLabTalk if I do get to do it.
Rich

I used this case study as part of my Higher Specialist Diploma in Blood Transfusion.
The IBMS have asked if I would like to give my PowerPoint presentation ('What the f?') at the 2023 Congress.
Thank you to all the contributors - I will certainly big up PathLabTalk if I do get to do it.
Rich

I used this case study as part of my Higher Specialist Diploma in Blood Transfusion.
The IBMS have asked if I would like to give my PowerPoint presentation ('What the f?') at the 2023 Congress.
Thank you to all the contributors - I will certainly big up PathLabTalk if I do get to do it.
Rich

I guess low titre anti-A and anti-B.
We don't have any whole blood. The usual major haemorrhage pack provided is 4 red cells and 4 FFP for transfusion in 1:1 ratio.
During the TT motorcycle road racing we keep a box of 2 O neg red cells and 2 group A FFP for immediate use. This hopefully gives us time to test a sample and issue group specific if further units are required.

We regularly used to run RT or even cold gel panels (LISS cells on Saline cards) to id M, P1, Le etc.
If suspected A2 patient with anti-A1, use A2 cells in the reverse grouping card.
We would test the grouping cells for the identified antibody.
WARNING! These may require a degree of skill as may have to perform manual testing.

No, there is a lot more to it than that.

Anti-A and anti-B are isoantibodies, rather than alloantibodies.  In other words, they are "naturally occurring" and do not have to be stimulated by either red cell transfusion or pregnancy.  They are usually stimulated by particles in the air (including human cells that have been shed into the air) that either express chemical compounds that mimic the A and/or B antigens or, in the case of shed human cells, actually do express these antigens (remember, the A, B and H antigens are histoantigens).
On the other hand, genuine alloantibodies (for example, let's say an anti-Jka) that are stimulated by transfusions and/or pregnancy, have, by definition, shown the individual to be a "responder".  It is by no means unusual for an individual who has produced a genuine alloantibody (such as the anti-Jka mentioned above) to produce an alloantibody of another specificity (or alloantibodies of other specificities).  Such other alloantibodies may not be easily detectable by routine serological techniques for various reasons.  Three of these are that the antibodies may not become serologically detectable at the same time (one may be detectable as early as the other, as not all antibodies "read the books"), that an antibody may be evanescent (or "disappears" from the circulation quite quickly - such as many Kidd antibodies - but these can remain clinically significant if re-stimulated), and thirdly, that the cognate antigen is not expressed on either the screening red cells or the red cells used in the antibody identification panel (for example, in the UK, to give two examples, the Jsa antigen and the Wra antigen, and both of these antibodies can be exceedingly clinically significant).

For this reason, it is very important that a serological cross-match is preformed (and found to be compatible), even if the blood provided is antigen negative for a known cognate antibody.

You may well ask, "Well, what about an anti-Wra (for example) that is present as a monospecific antibody?  Is that not clinically significant?", and the answer is "Yes"!  Indeed, there was a fatal case of an acute transfusion reaction caused by anti-Wra within the last decade in the UK, and the court decided that it was death by misadventure, because anti-Wra is known to be quite a common antibody, whereas the cognate antigen is sufficiently rare for the Law to recognise that it does not need to be expressed on screening cells (otherwise the Reference Laboratories would be overwhelmed with samples that have anti-Wra in their plasma/serum - and this is only one such specificity).  This may be one of the few times that our judiciary have used their brains (did I say that??????????!!!!!!!!!!!!!!!!!) and the decision may have been influenced by an editorial in Transfusion, written by the late, great Professor George Garratty (Garratty G.  How concerned should we be about missing antibodies to low incidence antigens?  Transfusion 2003; 43(7): 844-847.  DOI: 10.1046/j.1537-2995.2003.00492.x.).
SORRY THIS IS A BIT (VERY) LENGTHY!

Don't whoever makes your gelcards produce reagent cells too?
When I worked for NHSBT we used BioVue cells on BioVue cards and BioRad cells on BioRad cards.

No products/components since 2016 (see  my previous post) TO OUR KNOWLEDGE.
Being a small island nation, patients quite often get treatment in the UK which we don't know about and vice versa - very helpful. So he may have had D pos platelets. I think it unlikely he had D pos red cells for a planned procedure.
We did XM 4 units (O neg) in 2016 but none were required.
Thanks all

No products/components since 2016 (see  my previous post) TO OUR KNOWLEDGE.
Being a small island nation, patients quite often get treatment in the UK which we don't know about and vice versa - very helpful. So he may have had D pos platelets. I think it unlikely he had D pos red cells for a planned procedure.
We did XM 4 units (O neg) in 2016 but none were required.
Thanks all