RichU

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

In some plasma components, it would undoubtedly be residual D positive red cells, as long as the component has not been frozen, as the freezing and thawing process would disrupt the  structure of the membrane (although some people have theorised that the D antigen on disrupted red cell membranes may still cause sensitisation [I don't believe it]).  However, once anti-D has been produced by a person, it takes minute amounts of D positive red cells to cause a strong secondary production (see around and about slide 60 of the attached lecture - which I know is about HDFN, but the sensitisation is the same).
In Depth Lecture on Alloimmune Haemolytic Disease of the Foetus and Newborn HDFN.pptx

UK units are all K typed. We don't give K+ blood to females <50years, children, anti-CD38 patients, chronically transfused (eg Sickle) or anyone with anti-K. Anyone else is fair game.

The BioRad panel sheets only usually give + or 0 for P1 whereas NHSBT give numeric scores which is much more helpful when the antibody only reacts by IAT with strong examples.
A cold panel helps with any ambiguity too. (and P1 type on the patient, but who stocks anti-P1 at a hospital?)

Hi all,
Can I have your opinions/policies regarding the following please?
We currently have 15 members of the on call rota, 12 of these are not transfusion staff. Therefore we only get 2 sessions a month and sometimes wont be performing any serology for weeks.
Everyone does have to do 10 days in here per annum.
More people want to join the rota and the pathology manager thinks this is a great idea.
I am concerned that, especially the ones new to transfusion, won't be particularly competent with that level of experience.
Thanks,
Rich

Hi all,
Can I have your opinions/policies regarding the following please?
We currently have 15 members of the on call rota, 12 of these are not transfusion staff. Therefore we only get 2 sessions a month and sometimes wont be performing any serology for weeks.
Everyone does have to do 10 days in here per annum.
More people want to join the rota and the pathology manager thinks this is a great idea.
I am concerned that, especially the ones new to transfusion, won't be particularly competent with that level of experience.
Thanks,
Rich

I saw a discussion once that said draw it as soon as you can post delivery (ours is at 1 hour) - but that drawing it is more important than the time of the draw.  I think I remember that they discussed up to one week post delivery (sort of ridiculous to think about).  I have never really seen a maximum time for drawing.  
Make sure your procedures allow for double checking RH neg mom's with Rh pos babies - make sure L&D has some checkpoints and that your techs have some checkpoints to make sure tubes get drawn and tests get done.  Make sure the testing gets done and documented and the RHIG gets given - that is the most important part.
good luck

Thanks Malcolm, I was hoping you would reply.
I didn't fall asleep but had to reread a few times!
I left their employ 4 years ago. I don't recall selecting M- units if the anti-M was not detected by IAT. I did wonder if the policy had changed since I left, but from what you say it was already in place.
The unfortunate thing for us is that we produce our own red cells, which are compatible and (probably) safe for these patients, but we have to import M- units from the UK due to the RCI report. This means we have to pay for the units and the cost of air freight for blood which we are unlikely to use for the antenatal patient.(To cover delivery). (Rant over)
Having said (all of) that, we have a not insignificant number of residents of Thai stock who may fall into the category of been at risk of severe HDFN from a non-detectable anti-M! 
So maybe we will have to accept it.

 

I agree with you that it does sound daft, but I am in the position to tell you why this is the recommendation, despite it apparently being contrary to BSH Guidelines, as I was still working when the decision was made (albeit, I don't agree with it!).
The huge majority of hospital blood transfusion laboratories now use column agglutination technology (CAT) as their "first line of attack", and many of them use the CAT that uses gel in the column, rather than glass beads.  This form of CAT is particularly adept at detecting anti-M in plasma by IAT, even though the anti-M may not actually be reacting at strictly 37oC.  There are several reasons as to why this is so, but a couple of them are that "cold" reacting IgM anti-M can sensitise red cells particularly quickly (in a matter of seconds at room temperature), but can take quite a time, even at 37oC, to dissociate back off.  This means that the anti-M is often still sensitising the red cells at the end of the incubation time and, of course, centrifugation is, in itself, a potentiator of agglutination.  In addition, the gel in the column is at a slightly low pH, and many examples of anti-M "like" a slightly acid environment to sensitise the M antigen.  This all means that this particular kind of CAT is very good at detecting anti-M, but making it appear to react at 37oC, when, actually, it doesn't.
This left the RCI Laboratories with a dilemma.  Cross-matching blood by tube at strictly 37oC takes a long time, and the RCI Laboratories are not, shall we say, over staffed!  This meant that RCI Laboratories were being stretched to breaking point by having to cross-match for samples containing anti-M, as so few hospital laboratories could now perform IAT by tube technique (particularly with the need to demonstrate competence in the technique being used).  The alternative was to test many more units for the M antigen, and to provide M Negative units to the hospitals, whether they use CAT of that type or not, so that they could perform their own cross-matching, and actually end up with compatible units.  In theory, this was great, but it left the RCI Laboratories with fewer phenotyped units with which to select for, say Fy(a-b+) for a patient with anti-Fya, as the M Negative units that were also Fya Negative had been sent out to cover a cross-match in a patient who had an anti-M, who didn't actually need M Negative blood.
Having said all of that (and I KNOW I said it at length), anti-M can, rarely, cause severe haemolytic disease of the foetus and new-born (particularly in people from the Far East, even when the anti-M does NOT react overtly at 37oC), and so I have a certain amount of sympathy with giving M Negative units, even in the situation in which you find yourself with your patient, as M Positive units, albeit found to be compatible by IAT, could well stimulate the anti-M to become stronger during the pregnancy, "turn it" to an IgG production and increase its (at present, non-existent) IAT titre.
I hope that helps and that you haven't fallen asleep reading it!!!!!!!!

I just answered this question.

My Score PASS  

Wow this is a late post.   I just can't find the time to keep up sometimes.
I certainly was not implying that either Duffy antibody would not be able to cause HDN but rather theoretically speaking given the circumstances it didn't quite give the picture of HDN.   Again, even that is not a absolute.   Looking back at all the comments and possible causes, which all had merit,  I failed to see any reference to the possibility of an autoimmune issue and that there may be a possibility that the specificities are part of an newly development of autoantibody complex forming, i.e. mimicking specificities.   Although these are normally seen within the Rh-Hr specificities, other specificities are not unheard of.   Follow-up testing for cases like this rarely pan-out, if the infant clinically unaffected, the parents get their baby and disappear (sometimes and at least may not show up again until the next pregnancy).  Too bad, would make a good abstract....
"My" thoughts or opinions for this site are based on previous experiences or readings (actual book in hand journals) and etc.    Immunohematology Reference Laboratories see  a variety of cases sent for consultations and that is what makes it so intriguing and challenging for us to give the clinician the information he/she needs to take care of their patient and that we are right there with him to help.  We may not always have a specific answer but we can look for histories of similar cases and what the outcomes have been and give it our best educated interpretation of what might be happening and what transfusion recommendations we might propose.
I'm about to retire and my ramblings will decrease (Yea goes the crowd). 
As far a the gel system, again my own thoughts/experiences we had in our Immunohematology Reference Lab, starting back even  before Ortho commercially prepared system was as follows:   Basically it is a micro-LISS-system with an optimized serum to cell ratio.  Although we could not find a niche for using it on our investigations, we did start keeping it around to reproduce issues our hospitals were seeing with its use their routine transfusion service and to help provide educational information on what was happening and whether it had any clinical relevance.   There was a lot of weak reactivity of various strengths referred to us by a variety of hospitals.  Many these were related to the problems seen with  the LISS tube system.  Maybe even a little more since it much more sensitive based on how the method is set up commercially to work.   
Lastly, I believe that Malcolm Needs is truly an asset to this site and provides excellent information to all regarding such a variety of topics and also provides excellent references to support the information he provides.   Thank you Mr. Needs!   I hope you continue to provide your insight in this forum for many more years.
mic
 

All paediatric units produced by NHSBT in the UK are HbS negative.

Hear, hear Scott.
How can an algorithm tell the difference between an anti-D+C and either an anti-C+G or anti-G, anti-hrB, rather than anti-C+e or anti-hrS, rather than anti-ce (anti-f), to name but a few?  The answer is that it cannot, and these specificities are much more common than a lot of people think.

While I would agree with you that no antibodies within the Duffy Blood Group System are well known for causing clinically significant HDFN, and repeating what I said above, that I have grave doubts as to this being such a case, the fact that you have not seen one does not mean that such things do not occur.  I would cite Goodrick MJ, Hadley AG, Poole G.  Haemolytic disease of the fetus and newborn due to anti-Fya and the potential clinical value of Duffy genotyping in pregnancies at risk.  Transfusion Medicine 1997; 7: 301-304 (doi: 10.1046/j.1365-3148.1997.d01-38x), and indeed there has been a report of a "blocking" anti-Fya (which I should have remembered, not least because four of the six authors are personal friends!), namely Lee E, Cantwell C, Muyibi KO, Modasia R, Rowley M, New H.  Blocking phenomenon occurs with murine monoclonal antibodies (anti-Fya) in a neonate with a positive direct antiglobulin test due to maternal anti-Fya.  Blood Transfusion 2015; 13: 672-674 (doi: 10.2450/2015.0232-14).

I would query your choice of words with regard to, "Gel card methods do funny things sometimes."  I would rather like to know exactly what you mean.

I certainly agree with Mr. Blumberg and Mr. Needs as well as others, everyone brings up excellent points and explanations.   My only comment I could put forth for consideration would be from a BB Pathologist I once worked with many years ago having observed similar cases.  "Pregnancy is a disease".  

I've had another thought about the baby's Fy(a) type being 1+, even though the control was 4+.  It could be that the maternal anti-Fya was strong enough to be a blocking antibody.  I have grave doubts about this, as blocking is rare, and I have never heard of a blocking anti-Fya, but there is a first time for everything!

There's always a caveat with serology! Sometimes when things are so ingrained it's easy to take them as read.

Ah, there I totally agree (except for antibodies related to antigens within the Kell Blood Group System - again, see the Guidelines).

Sorry, it's not that I don't recognise the significance of a titre of 32, just that I wished to illustrate that a rising titre is significant during any pregnancy but if you don't do any titrations, due to detecting an antibody in a previous pregnancy, how would you pick it up?

We always require a second confirmatory sample before issuing group specific units if there is no historical group. We request this as soon as we know the patient has not been seen by us before.
This doesn't impact on the speed of providing cross matched blood due to the shorter test time for a forward group compared to a full group, antibody screen and cross match.
The units are selected based on a rapid tube spin group and set up with the first sample group and screen.
We do not do electronic issue for any patients.

Hi Rich,
I am not a clinician but as far as I know IVIG can be given to obstetrical patient in diff. conditions (autoimmune disorders, recurrent pregnancy loss, ...).
I thought about IVIG when I saw the DAT becoming positive plus additional reactions coming up over the time. Anti-A and Anti-B are indeed the most prevalent antibodies in plasma derived products but other specificities of low titre can be present sometimes such as anti-D, anti-K and a bunch of antibodies of undetermined specificity reacting with several to not say all RBCs. 
Just a thought that can be doublechecked with the clinician..?
Hereunder is a very great (not recent though) paper to be read and re-read again:
Problems Associated With Passively Transfused Blood Group Alloantibodies 
George Garratty, PhD, FRCPath American Journal of Clinical Pathology, Volume 109, Issue 6, 1 June 1998, Pages 769–777, https://doi.org/10.1093/ajcp/109.6.769

I have been thinking about this and I have come, more or less, to the same way of thinking as Neil Blumberg.
The first pregnancy almost certainly could not have caused sensitisation of most of the common antigens, as some would not be formed on the foetal red cells at 10 weeks of gestation, while, even with a huge foeto-maternal haemorrhage (FMH) (in terms of the ratio of the total foetal red cell mass), the actual volume of foetal red cells transferred to the maternal circulation would not be sufficient to cause sensitisation in anyone but a person who is a "super responder".
The second pregnancy could easily have caused a primary response, either at partum, or as a result of a chronic FMH throughout much of the pregnancy.  Unless the woman's antibody screen was performed at about six months post-partum, such antibodies may never have been detected at their peak, and then may have declined to levels where normal serological techniques would not detect them.  Of course, all of this is theoretical, but, given the fact that the mother is probably an R1R1 (from information given above), it is most unlikely that an FMH estimation, such as a Kleihauer test was performed, or that the mother would have been serologically "followed up".  You also do not give the woman's transfusion history.
It would be helpful to know the time between the second and third pregnancy, and also, of course, if the same male was the biological father in both pregnancies.  This latter piece of information may actually be very difficult indeed to ascertain, as the woman may not wish to disclose her sexual history.

It is not unknown for antibodies of a particular specificity (say, purely for example, an anti-Jka) to increase in strength (as measured by serial titres) during a pregnancy that is, in this example, Jk(a-).  This is more common in a pregnancy where there is at least one other specificity (let us say, again, just as an example, anti-K), where (again, just as an example) the foetal red cells do express the K antigen, but not the Jk(a) antigen.
Lastly, antibodies that are forming de novo, very often seem to cross-react with antigens to which they are not actually stimulated.  This is true, even in the case of some monoclonal antibodies (particularly those within the HLA system), but some antibodies (again, even monoclonal antibodies) maintain what I will call a pseudo-specificity even in the "mature state".  This includes monoclonal anti-D.  Thorpe et al have reported that monoclonal anti-D molecules possess a V4-34 moiety, that is also present in anti-I and  anti-i, which is why these reagents should never be used straight from the fridge (Thorpe SJ, Boult CE, Stevenson FK, Scott ML, Sutherland J, Spellerberg MB, Natvig JB, Thompson KM.  Cold agglutinin activity is common among human monoclonal IgM Rh system antibodies using the V4-34 heavy chain variable gene segment.  Transfusion 1997; 37: 1111-1116 and Thorpe SJ, Ball C, Fox B, Thompson KM, Thorpe R, Bristow A.  Anti-D and anti-i activities are inseparable in V4-34-encoded monoclonal  anti-D: the same framework 1 residues are required for both activities.  Transfusion 2008; 48: 930-940).
I hope this helps a little.

Probably the primary stimulation was not the fetus, but previous pregnancy, transfusion, tattooing, needle sharing, non-sterile tattooing, etc.  Pregnancy is a situation in which B cells are upregulated (type 2 immunity) and T cells down regulated (roughly speaking) and pregnancy may have increased B cell activity to the point where previously undetectable antibodies are now detectable.  Just a theory ;).

Again thank you.
The phenotype is probably R1R2 which is why I opted for anti-f and not anti-c.
No transfusion history.
The second pregnancy delivered in March 2018. We had no sample after her 28 week routine A/N in Dec '17.
The booking sample in which we found anti-f was in June '19 (approx 10 week gestation)
The woman's partner in the latest pregnancy is K- but we know how much store to set by that!
I will go with this.
Rich