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The actual place where there is a feto-maternal haemorrhage probably will heal (although some of these are chronic), but by then the damage has been done. If the mother is going to make an allo-anti-D, she will have been stimulated so to do. However, it is not through the "fistula" between the foetus's and the mother's circulation that the anti-D gets to the foetal circulation, but by passing through the placenta. Indeed, not only does the maternal IgG pass through the placenta, but it is actively transported across the placenta, so that the concentration of the anti-D is often higher in the circulation of the foetus, than it is in the circulation of the mother. The reason so many foetuses survive HDFN even if there is Rh incompatibility is mostly down to the skill and dedication of the staff who work in Foetal Medicine Units, all of whom deserve utter admiration.

Personally I never liked the term CMV safe! We always referred to this as "reduced risk" which, as pointed out many time above, is all you can possibly hope for.

The father John. He may not be the father!

I am an idiot! I will try to edit my original post. Thanks for pointing out my error BankerGirl.

There remains controversy about this, but we have been using leukoreduction as our only method of CMV risk reduction for close to 30 years, with no reported cases of CMV transmission. We have a 70 bed newborn intensive care unit, do about 180 stem cell transplants (about 40% allogeneic), and do the occasional intrauterine exchange transfusion. CMV serotesting is never necessary for donor blood in my opinion. The existing literature isn't entirely definitive but studies have not shown that combining leukoreduction and CMV serotesting has much, if any clinical benefit. Both observational series and randomized trials demonstrate that CMV transmission after leukoreduction is not any more common than after CMV serotesting. Indeed, most CMV transmissions are likely due to seronegative donors who have recently acquired virus, but are still seronegative, or at least that's one theory. Bottom line, if you are 100% leukoreduced there is no need for CMV serotesting.

It should be noted that IgG crossing the placenta is, over all, a good thing in that this is the mechanism by which the mother is able to confer active immunity to many diseases to the fetus which lasts for some time after birth.

As the baby's DAT is negative, it could be that the anaemia is being caused by another underlying pathology, such as Parvovirus B19.

If you are seeing a lot of weak results in your anti-D well that subsequently turn out to be negative, I suspect the reason to be one of manipulation rather than anything serological. I would guess that NONE of these babies are group O. I am guessing that you are seeing carryover from your anti-AB. It can happen that if cards are stored somewhere where condensation can take place then drops of antiserum can condense into the reaction chamber and 'jump' into the next well or even next 2 wells when you remove the aluminium. This can cause false positive results. I suggest you check the cards before pipetting in them and see if there are any signs of these drops. Don't use the cards if there are and look for another place to store them

As far as I know, there is no reason why not.

One unit of hemoglobin AS blood will contribute perhaps 5% to the S level in a patient with hemoglobin SS whose overall post-apheresis hemoglobin level is 10 g/dl. Not enough to make a real difference. A lot of work for pretty much nothing in my view. But we do it anyway. Probably would be less work to test donor units if the %S doesn't drop quite as far as expected. Hemoglobin S in AS red cells does not behave the way it does in SS red cells, so this has absolutely no clinical implications. The hemoglobin S goal for most treatment is 30% or less. 5% is not going to make any difference in treatment plans. Just an alternative view from the usual :).

yan xia, are you ABSOLUTELY certain that it is IgG anti-A, and not IgG anti-A1?

Just found this from the BBTS; https://www.bbts.org.uk/downloads/bbts2016/presentations/15.00_wed_qs_3_kate_aplin_bbts_2016.pdf/

The problem is not just that the unit is or is not within particular temperature range before being put back into use, but rather the unit has not been monitored while not in the care of the blood bank. A unit sent to, say. OR in a cooler, may have been "checked" when it got into the theater -- and left for a time on the counter (maybe next to an incubator!) -- returned in the cooler on ice you will never know if it was kept at a proper temp all that time. And how do you really "validate" a unit's potential for a "detrimental" effect? Transfuse various units left on a counter for different times and see which patients have a bad outcome? Scott

That is definitely what we do here. We do not have what we would need for an autoabsorption, and our ARC Reference Lab folks serve us well.

All the blood in our hospital is leucoreduced, and we have classified this as "CMV safe". But is this actually the case? Is leucoreduced blood the equivalent of CMV negative blood? For the following patients would you just give leucoreduced blood, or leucoreduced blood that is also CMV negative? Intra-Uterine Transfusion Exchange transfusion for a baby Top-up transfusion for a premature baby Top-up transfusion for a full term baby

There is no such thing as never in science and medicine. But while leukoreduced transfusions may on rare occasions be associated with a CMV seroconversion, the same is true of CMV seronegative, since it is possible to have a donor who is viremic but not yet seropositive. There are those who believe CMV is almost never transmitted by transfusion, but that these seroconversions are by the usual route of individual to individual environmental transmission. I am close to that point of view. We have not used CMV seronegative, as pointed out above, for the last 20 years plus. We have a 70 bed+ neonatal intensive care unit, do about 80-100 allogeneic transplants of stem cells, heart transplants, etc. CMV seronegative is totally unnecessary and provides little or no benefit to patients. Leukoreduction is much more important overall and provides enough CMV safety on its own, in my view, to beat a dead horse here :).

what the heck does that mean?

This is something that only works when there is expert physician to physician communication. Your medical director needs to undertake this project. There are substantial data from randomized trials and observational cohort studies that leukoreduction abrogates CMV seroconversion. These are the studies we used twenty plus years ago to convince our practitioners that leukoreduction was not only good enough, but almost certainly superior in overall clinical outcomes to CMV seronegative non-leukoreduced transfusions. Of course no patient should be receiving non-leukoreduced transfusions at this late date, but in the USA not all transfusion medicine physicians are convinced of this, in my opinion, strongly justified clinical practice.

I take it that there was more than one example of R2R2 used, as you say "one R2R2 that was negative", which is a pity, otherwise I would have been thinking in terms of an anti-e (or, possibly, anti-hrB, depending upon the lady's ethnicity. It still could be, but perhaps there is another specificity there too. The real problem here is the transfusion three weeks ago. This could lead to alloimmunisation, but, according to Petz and Garratty (and I certainly wouldn't argue with them!), it could easily be exacerbating a low-grade, almost undetectable auto-antibody, and anti-e is a very common specificity found as an auto-antibody, although often as a mimicking specificity. This, together with the lady's underlying pathology, suggests to me that it is an auto-anti-e, BUT I HAVE TO STRESS THAT THIS IS A GUESS. In a case like this,a sample really should be sent to a Reference Laboratory.

Malcolm, I'm just curious but what may not be reliable, the father or the phenotye??

As I am on the "wrong side of the pond", I'm not sure I should answer this, but I'll have a go! We say a titre of 32 for anti-Fya and any Rh antibodies (but we perform concentrations on anti-D and anti-c, rather than titres, and for them we begin to worry if the anti-D levels go above 4IUmL-1 and anti-c lvels go above 7.5IUmL-1), however, I cannot recall seeing any real problems with anti-Fya below a titre of 128. Anti-K (and other Kell-related antibodies) are a different kettle of fish. After battling for years with poor correlation between anti-K titres and the severity of HDFN, and thinking it was poor titration technique, and then finding it wasn't, and finding out that it was more to do with how the antibody attacks the precursor red cells, we sort of gave up, and now we refer any pregnant women with anti-K to a foetal medicine unit for screening, just to be sure (unless cell free foetal DNA shows that the foetus lacks the KE L1 gene). This is all based on British Committee for Standards in Haematology (BCSH): White J, Qureshi H, Massey E, Needs M, Byrne G, Daniels G, Allard S. Guidelines for blood grouping and red cell antibody testing in pregnancy. Transfusion Medicine 2016; 26: 246-263 (doi: 10:1111/tme.12299) and Royal College of Obstetricians and Gynaecologists (RCOG). The management of women with red cell antibodies during pregnancy. Green-top Guidelines No.65; May 2014. https://www.rcog.org.uk/globalassets/documents/guidelines/rbc_gtg65.pdf.

I would classify my wife in the super responders category. To attempt to answer the first question, it depends on a number of variables. To start with, assuming she has the same father for all her children, what is his genotype? R1R2 or R1r. It makes a difference. On another note, FMH during the pregnancy will only be a factor if the baby is D positive and mom's titer needs a boost. If mom starts with a high enough titer FMH during the pregnancy is not required for sever HDN. My daughter was born with sever HDN and there was no known FMH during the pregnancy and all of the antibody studies suggested that she should not have been as affected as she was. Bottom line, there is no cut and dried answer to your question and honestly, there never is in the wonderful world of blood banking. I suggest you get used to gray because black and white rarely if ever exists.

There are three types of people. About 10 - 15% are non-responders, and never produce an antibody, however many times their immune system is challenged. About another 70 - 80% are normal responders and, given sufficient stimulus, will produce antibodies. The other 10 - 15% are super responders, and produce antibodies with the slightest insult to their immune system. I once heard the wonderful Dr Ed Synder describe these people as being able to produce an anti-D after being given a "virtual transfusion". When questioned as to what was a "virtual transfusion", he said that you showed a photograph of a D Positive red cell to such a person, and they produce an anti-D!!!! I would suggest, Kathyang, that your mother was an extreme member of the first group.

Based on an observational study of ABO grouping in Gel I reported at the 1997 AABB Annual Meeting, ABO Plasma Grouping discrepancies occurred in 0.8% (26/3183) adult ABO grouping tests in Gel. Anti-B was not detected in 24/26 patients, anti-A was not detected in 2/26 patients, and anti-A1 was not detected in 3183 patients. In comparison, anti-A and anti-B was detected in 19/26 patients by the immediate-spin tube test, and was detected in 7/26 patients after 10 minute incubation room temperature incubation and centrifugation. Based on this study and 20 years of gel testing since that time have shown me the anti-A1 is rarely detected in Gel and that 70-80% of ABO plasma grouping discrepancies are resolved using the immediate-spin tube test. Centrifugation is used quite differently in gel versus tube testing. Centrifugation is used to separate agglutinated cells from un-agglutinated cells within the gel column, but is used to enhance agglutination in standard tube tests by forcing cells together at the bottom of the tube. This may contribute to the increased sensitivity of tube testing in ABO Plasma grouping tests.

Incubating patient plasma with patient red blood cells and then applying the antiglobulin test is no longer a Direct Antiglobulin Test but an Autocontrol test which is an Indirect Antiglobulin Test. Some may think an Autocontrol test gives the same results as a Direct Antiglobulin Test, but that is not always true.

https://www.nacblood.ca/resources/guidelines/CMV.html These are the Canadian National Advisory Committee Guidelines for use of CMV Negative Blood Products.

Most CMV infections are acquired through environmental exposure, including breastfeeding from and close contact with a CMV infected mother. The likely source of the infection in question was exposure to family members, not transfusion. That's why close to 80% of adults in some populations are CMV seropositive. The virus is ubiquitous and highly infectious, but rarely causes any serious clinical effects except in utero and in severely immunocompromised patients.

There are one or two comments I would make, which you may find pedantic, but, that notwithstanding, they are true. There is, and never has been, a blood group system named Rhesus. Rhesus was an ancient king of Thrace. The correct name for the blood group system is Rh. So, it is the Rh Blood Group System, the two genes involved are RHD and RHCE, the carrier proteins are RhD and RHCcEe, but the antigen of which you are talking is just plain D, and not Rh D. There is a very good reason why the instructions that come with the anti-D state that the tests should be read macroscopically. Thorpe et al, in two papers, reported that monoclonal anti-D molecules possess a V4-34 moiety, that is also present in anti-I and anti-i. As a result, if papain-treated D- red cells are tested with such antisera, or untreated D- red cells are tested with such antisera that have not been brought to room temperature, they may agglutinate. This could result in D- red cells being mistyped as D+ - a particular danger in females of child-bearing potential, and babies (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). In addition, if you do not follow the manufacturer's instruction, and something goes wrong, under UK (and EU) Law, you could well be liable, as described by Bob Doughty some 30 years ago now (Doughty RW. Product liability in the medical laboratory. Medical Laboratory Sciences 1989; 46: 68-71. In the case that you describe, do you know the Weak D type of the baby (it may well be Weak D Type 2, which can be particularly weak) and, at any time, did you test the mother's red cells to see if she was also a Weak D of the same type? If she was, then it is highly likely that anti-D immunoglobulin would not have been required anyway, although I am aware that this is not part of the BSH Guideline (White J, Qureshi H, Massey E, Needs M, Byrne G, Daniels G, Allard S and British Committee for Standards in Haematology. Guidelines for blood grouping and red cell antibody testing in pregnancy. Transfusion Medicine 2016; 26: 246-263. doi: 10.1111/tme.12299). My honest advice is that you do not read the tests under a microscope. If you have ANY doubt, give the mother anti-D immunoglobulin anyway - it is not that expensive, and has a good safety record in terms of TTI. .

Some good materials here as well => https://www.bbguy.org/2016/06/17/want-g-wiz/

You could use it on your automated device but you would have to validate that it works. If you offered the test then you would have serum because you would indicate that serum is the only specimen which can be used. Personally, I think that the reactions you see are mostly HTLA's (at least that's what I think I am seeing in gel - most (~80%) are ficin sensitive). They usually react 2+ or weaker, so I never can see them in tubes.

A number of years ago the President made a visit to our area. His advance team visited our hospital and the blood bank. They asked if we were AABB accredited which we regrettably answered no. We are accredited by the Joint Commission Consequently our blood bank was told we could not provide blood product in the event of a medical emergency!