I remember there is a rule says for futus younger than 4 months we will transfuse them with type O red cells instead of the same type as the baby's, because there is antibodies comes from mom will destroy the transfused cells in the baby's circulation.

As to the weak A antigen, I have noticed some futus's A and /or B antigen is weaker than normal , in gel it looks like A3 or B3, but no reverse antibodies. In this condition ,I will suggest them go back to retype when they 1 year old.

For A subgroup , if they have not 37 degree reactive anti-A, I will transfuse them with type A red cells.

Edited April 6, 201312 yr by shily
spelling error

I don't think we will be karyotyping the babies, and being male-female, they are most definitely not identical twins. I am in a pediatric hospital, and very familiar dealing with maternal antibodies in babies. We usually give O to babies because they require such small volume transfusions and this way we can use one unit for a few different babies, regardless of their blood type. If we are going to give non-group O blood to a baby, we do the reverse Coomb's to detect maternal IgG antibody against A or B cells. If negative, we give the non-O blood but if Mom has the IgG anti-A or anti-B, we will stick with O blood.

This situation was a challenge for us. It seemed that it would be safe to give the type A1 blood because the baby's plasma lacked maternal anti-A1 and we even went so far as to crossmatch the dad's blood to the baby at the AHG phase. Everything was fine, and we won't expect the baby to start making ABO antibodies for a while. I read more on chimerism in twins and I think that makes perfect sense. This baby could very well really be type O with some of her twin's blood in her circulation. I most definitely do not want to be giving type A to a patient who may be group O, regardless of the lack of circulating ABO antibodies.

This baby is a preemie. I would be very interested to see what her typing looks like 1 year from now, but with any luck, she will not have any reason to come back for more transfusions at that age.

Thanks for the update Kathy.

Just a thought:

How are you testing these babies? If you are using cord samples or if there were some maternal-fetal bleeding (how was the birth?), the child you are tagging as an A3 because of the 'mixed field' reactions may actually be a normal Group A ... the mixed reaction due to maternal red cells in the cord sample/baby.

If you are using MTS, this is obvious and I know there is some literature out there illustrating this warning because it is a change from what we were taught 'way back when', i.e. that cord samples/babies may have weaker reactions with Anti-A and/or Anti-B ... but that was the days of tube testing. Today, we know better.

Which parent is Group A1? What is the mother's blood type?

I'm with the group suggesting to use Group O to circumvent this question ... but then, you have this directed donor to deal with ... a more psychological than a practical problem.

On this same line of thought, I assume that you would also give type A1 blood in the following scenario: Twins <1 month old at our hospital. One is type A (positive with A1 lectin), and the other is possible type A3 (mixed field reactions with anti-A, has not been transfused, negative with A1 lectin). Neither has anti-A1 in their serum at immediate spin or IgG. We have a directed donor type A1 unit from one of the parents. Unit is fully compatible with the A subgroup twin. Do we give the directed donor unit to the A subgroup twin? If so, should we get specimens every 3 days to ensure that the baby doesn't start making anti-A1? I know that babies don't normally make anti-A until 3-6 months, but I'm not sure I want to take any chances.

If you are using MTS, this is obvious and I know there is some literature out there illustrating this warning because it is a change from what we were taught 'way back when', i.e. that cord samples/babies may have weaker reactions with Anti-A and/or Anti-B ... but that was the days of tube testing. Today, we know better.

I'm afraid I can't agree there JPCroke. Although the monoclonal ABO antibodies we use are extremely potent, cord blood will still often give weaker reactions than adult blood, because it is a function of the ABO transferase enzymes not working to their full potential at birth (thus the antigens are weaker), rather than a function of the potency of the ABO antibodies. This is one of the reasons why clinically significant ABO HDFN is comparatively rare.

True ... agreed.

My point was that we shouldn't 'jump' to the conclusion that a baby is an A3 just because mixed field reactivity is present without considering the testing platform/sample and the possibility of maternal-fetal bleed/contamination.

True ... agreed.

My point was that we shouldn't 'jump' to the conclusion that a baby is an A3 just because mixed field reactivity is present without considering the testing platform/sample and the possibility of maternal-fetal bleed/contamination.

Yes, I agree 100% with that.

" If you are using cord samples or if there were some maternal-fetal bleeding (how was the birth?)"

 

I just want to point out that the only Rh neg mom I ever found that needed more than one dose of RhIG (in the absence of trauma) totally shocked the nurse because it was a perfectly normal birth that gave them no idea that she might have had an excessive bleed. Not disagreeing that a difficult delivery might have more FMH but you can't be sure that a normal one didn't.  Sorry.  This is sort of a side comment.