YorkshireExile

I've had further thoughts upon this case (having told you not to worry about it - I live a sad life - NOT!).
It struck me that the patient has an Rh type of D+ C+ c+ E+ and e+, suggesting that the probability is that the patient has a genotype of DCe/DcE (R1R2), but this may not be the case.  She could have one of the rarer Rh genotypes, such as DCE/Dce (RzRo), DCE/dce (Rzr), Dce/dCE (Rory), etc, and this may be potentially important.
Some years ago, Joyce Poole explained to me that most grouping reagents labelled as anti-C are, in fact, a mixture of anti-c and anti-Ce, and this, she told me, included most monoclonal anti-C reagents (which surprised me, to be honest).  This is because the vast majority of the red cells transfused that stimulate an anti-C would have the haplotype of either DCe or dCe, or both, and will, therefore, also stimulate an anti-Ce.  As a result, these "hybrid" anti-C/anti-Ce reagents will react more strongly with red cells expressing the Ce compound Rh antigen (Rh7) and the C antigen (Rh2), than with red cells that only express the C (Rh2) antigen.
This would not, incidentally, explain the stronger than normal reaction with the e antigen.

However, if the patient does express one of the rarer Rh types mentioned above, say she is RzRo, she can actually produce an allo-anti-Ce, and most antibody panels only contain C+ red cells that are only Ce+ as well.  In other words, her antibody in the plasma MAY be identified as an anti-C, whereas it is actually a monospecific anti-Ce, which would neatly explain why she has an apparent anti-C.

Of course, she may also have an auto-anti-C, or a mimicking auto-anti-C (and, possibly, an allo-anti-Bg of some sort).  Sadly, for a nerd like me, I doubt if we will ever know!
I think it was John C Staley who once accused me of looking for zebras, when I hear horses hooves (I may be wrong, but I think it was John).  Anyway, this proves that he was absolutely correct about me!!!!!!!!!!!!!!!!!!!!!!!!

Our cell saver machines have an in-line optical Hct sensor. So we record that on our forms for documentation. There is a "line in" and "line out", so we get a good read on the low Hct coming in, and the high crit of the processed blood on the way out. If this is not recorded, or unable to be read, the perfusionists are supposed to collect a purple top for H/H determination in the lab. Once 10 units have been processed for the patient (this has never happened), they should be collecting a heparin level on the patient to ensure adequate washing of the processed blood. That is a manufacturer recommended QC step. 

Our blood supplier is shortly going to be introducing FFP Riboflavin treated, and Apheresis plasma Riboflavin treated. We have been told that the ISBT codes to use are EA435 and EA436. Does anyone know what the ISBT codes are these products when they are thawed or aliquoted? I do not have access to the ICCBBA website so I cannot check on there.

Our blood supplier is shortly going to be introducing FFP Riboflavin treated, and Apheresis plasma Riboflavin treated. We have been told that the ISBT codes to use are EA435 and EA436. Does anyone know what the ISBT codes are for these products when they are thawed or aliquoted? I do not have access to the ICCBBA website so I cannot check on there.

In our hospital, KBs are performed in the haematology department. If positive, the amount of mls bleed is calculated and documented. The RhIG is then given out by pharmacy based on the package insert information and after discussion with the doctor. Would an AABB inspector even look at this process in our hospital as Blood Bank is not involved at all?

Indefinitely 

In the UK, we keep these records indefinitely, as much as anything because the individual will have received something that is derived from human blood, and this may contain a de novo transfusion-transmitted viral infection, and so it is deemed that we need to know what batch and everything else about the injection (and the resulting antibody detected).

We are scanning all completed patient antigrams, worksheets, and reference reports into our BB LIS. That information is accessible (and printable) from the comment section of the patient profile.

We use MEDITECH MAGIC 5.6.7. Long ago, we started entering our Immucor Cell Panel lots into the QC function, along with the individual donor cell reactions. Over the years, our database has grown to where, every month, we only have to enter 1 or 2 new donor cell, out of the 16 on the panel, into the database when entering the new months donor panel. When we have a Passive D, we enter the cell reactions from the panel in the antibody ID field, which stores the reactions indefinitely in MEDITECH. That allows us to not have to keep the antigrams for passive D's. Everything is in the computer and easily accessible. BTW, doing it like this allows MEDITECH to calculate the antibody ID probability. It's a nice feature if you have the time to build and maintain it.
For all antibodies, we only keep the antigrams. Every other reaction is recorded and maintained indefinitely in MEDITECH and the ECHO backups.

Mrmic, are you saying that a prestigious an institution as the British Committee for Standards in Haematology is wrong in this recommendation? - Quote " Routine irradiation of red cells for transfusion to preterm or term infants (other than for EBT) is not required unless there has been a previous IUT". Even though they reviewed relevant publications over an eleven year period?  Note it is only a recommendation.

No bad outcomes at all.  So I suppose your next question would be " then why change anything?"  Which would be a good question!

Our neonatal intensive care transfusions are all irradiated because many severe immunodeficiency states are not evident until weeks to months after birth.  These are rare, and leukoreduced transfusions probably mitigate the risk of GVHD somewhat, but we are erring on the side of caution.  We irradiate just before transfusion so the storage based problems with irradiated red cells are less of a concern. We define fresh as <21 days of storage, because the data suggest very fresh blood is actually more dangerous to patients than blood stored 7-21 days or so.  Seat of the pants, to be sure, but somewhat data driven. No one knows for sure, but very fresh blood (<7 days storage) is totally unnecessary in terms of proven benefit and may actually be more dangerous, for reasons that are largely unknown.

Congratulations!!

I was immensely honoured to receive this through the post today (with a lapel badge).

I just saw this seminar being offered by Bio-Rad with our own, infamous, Malcolm Needs as the presenter. I registered and thought I'd pass the word to all of us here. Here is the link:https://info.bio-rad.com/ww-IHD-transfusion-w-registration-lp2.html?elq_mid=48765&elq_cid=10201434&elqCampaignId=30837&utm_campaign=30837&utm_source=eloquaEmail&utm_medium=email&utm_content=Email 13ER EM-R-CM-385201-FY21-TCHS-AWEN_BR-JRNL-TRF News 19 Nov&elqTrackId=6ecbbea5f2bb46849981687404578a8e&elq=7c5f74470efa434dbd4351e512f7ae7a&elqaid=48765&elqat=1&elqCampaignId=30837

Congratulations!!

Personally, I would give Rh and K-matched to all females from the age of 0 until the official age when they are "no longer of child-bearing potential" (this differs from country to country and, indeed, from individual to individual, but most countries "state an age"), unless there are extenuating circumstances, such as either an incredibly rare Rh phenotype or an incredibly rare Kell type, when "matched blood" may not be available, or may not be available in the time required.

There is a theory that if "unmatched blood" (Rh and K of course, NOT ABO!) in the first few days/weeks/months of life, then there can be lifetime tolerance of certain antigens (as there is with chimeras - a sort of "accommodation"), but I wouldn't like to be the one performing the experiments!!!!!!!

This scenario doesn't explain why the donor red cells react with the serum from most patients. For this to be a "low incidence antigen" issue, ALL of the patients would have to have an antibody to (probably) the same low incidence antigen. That is very unlikely. As Malcolm suggests, this sounds like an abnormality of the donor's red cells.
I believe Hemo bioscience have a lectin kit, but it may only be available in the USA.

I would suggest running a select panel of low-frequency antigens against your patient's plasma (V, Cw, Jsa, Kpa, LUa, Bga, Ch, etc). If the patient has one of those antibodies, the antibody screen would still be negative and, likely, so would your panel if there is no positive cell included. The unit may have the corresponding antigen. I have seen this several times. Since we don't routinely do serological crossmatches in the presence of a negative antibody screen, these antibodies are normally not found until a transfusion reaction investigation.

I think it more likely that the donor is expressing an antigen, such as T, Tn, Tk, Cad, etc, possibly as the result of a subclinical infection if this has not been seen before with his/her blood (which would rule out Cad).  Have you tried testing it with a lectin panel?

This is going back donkey's years, but when we used to adsorb raw AHG with human red cells to get rid of the xenoantibodies that reacted like anti-A and anti-B, we used the last supernatant to dilute an aliquot of a previous lot of AHG, and then saw if the AHG still worked.  If it did, then the red cells were washed sufficiently free of human protein, which, otherwise, would have inhibited the AHG.

We use COBE 2991s, and use protein dipsticks to test the supernatant. The positive control is diluted plasma and we dilute it to get a level of 30, the negative control is saline, and the samples are collected from the wasteline after the washing is done. The washed sample should test for negative or trace protein, following Standard 5.7.4.6, which lists that washed cells should be prepared in a way that removes almost all of the plasma. We don't look at the crit for these.
There are some other threads on here that also discuss washed QC -- I would also search for those!
 

You have NEVER seen a baby who is Weak D Positive.
There is no such thing as anti-Weak D!  May I suggest that you read Stratton F.  A new Rh allelomorph.  Nature 1946; 158: 25-26, followed closely by Race RR, Sanger R, Lawler SD.  The Rh antigen Du. Ann Eugen (Camb) 1948; 14: 171-184, which will explain why there is no such thing as anti-Weak D.

I appreciate that CAP seem to be incapable of using correct terminology, but that does not mean that we should all descend to their levels of incompetence.
Sorry for the "vent", but this wrong terminology has gone on now for 72 years; six years more (embarrassingly) than I have been alive!
I'm sorry if this sounds like a personal RANT against you. YorkshireExile; it is certainly not meant as such.  It is just a general rant against people who use poor nomenclature because they don't learn even the basic history of their own specialist subject - and that includes the people who SUPPOSEDLY make sure the rest of us "follow the rules"!

Hope this is okay to post administrators, but I have been asked to publicise the MHRA Discussion Forum, especially for members of PathLabTalk who are either UK citizens, or who are working in a laboratory inspected by the MHRA.  The address is forums.mhra.gov.uk/forumdisplay.php?60-Blood-Forum.
You can go on there anonymously and ask virtually any questions you like concerning their inspections, quality, haemovigilance and SABRE, and a whole lot of other subjects.
This will also help the UK TLC group (of which I am currently a member) formulate their standards.
Lastly, you have to remember that despite both the MHRA and UK TLC being rather regarded as "sticks" with which to "beat" Biomedical Scientists, both are actually there to help.

My argument would be that blood bank testing is qualitative and not quantitative.  We have run into this a little bit in the US as well, they re-organized the federal regulations and starting using chemistry and hematology requirements for blood banking.  Our method comparison requirement in particular has never made sense to me.  Of course LISS, PEG, solid phase, and gel methods give different results, they are designed to!