Few days ago we had the following patient:

 

5 day old baby due for cardiac surgery. Mother was group B Positive with antibody screen negative. Baby is group O Positive with DAT positive - IgG 3+, (IgG1 1+), C3d 2+, three cell Biorad antibody screen all positive, and eluate showed pan-agglutination.

 

Reverse grouping on the baby 2+ using liss/coombs cards with A1 and B-cells, and at room temp A1-cells: weak positive, B-cells: Negative.

 

We crossmatched a few units and all were 2+ incompatible. A transfusion actually took place with one of the units, with no transfusion reactions reported.

 

So what caused the positive results for the baby?  Our head of department wants to send the sample to a reference lab to investigate if there is an antibody to a high incidence antigen. Is that worthwhile? Could that be a possibility?

 

If this was an adult I would just say it was a warm autoantibody, but for a baby.....?

 

We actually found a paper that describes a rare case of apparent in utero RBC autoantibody development. Is that what is happening in this case?

 

Any insights greatfully received!

My first thought was Wharton's jelly - but the baby is 5 days old so this can't be the case obviously. I'm tagging along with interest...

Strange case.  the first thing I would do is an eluate.  There is a little bit of me saying that baby is really group A but all the A-sites are blocked with anti-A (DAT pos...)  On the other hand that would not explain why the antibody screen was positive, nor why the XM was positive, given that mum's antibody screen was negative.  OK - so has this baby been transfused in utero?  Is there any possiblity that this was a twin and that one of the twins has died in utero?  Is the mother the biological mother?  Is the baby septic? (I'm thinking maybe PCH).  Has baby already received meds+++ If so what?  Could be drug-induced....

Interesting, thanks for posting. I saw a couple other articles about this on PubMed but those cases didn't require transfusion. How's the baby?

Thanks to Anna for her suggested reasons. Baby is actually doing fine at the moment. Will get back with more details as soon as possible.

Okay, now have further information about the baby:

 

The baby has not been transfused before and as far as we know the mother had no transfuson during the pregnancy.  Baby transferred from another hospital to us on day 5 and underwent aortic arch repair and VSD on day 8. The surgery was postponed 3 days for IVIG.  One aliquot of incompatible blood was transfused prior to surgery, one whole unit during the surgery and one aliquot post surgery  - all 2+ incompatible.

-          Baby is recovering fine from the surgeries, second  one was to close the chest.

-          Both parents are Bpos.

-          Baby is not septic

 

We also did a 16 cell panel screen, all 2+. Rh phenotype mother and baby both R2R2.

Bilirubin on day 5  was 215,  today  it is 52.9. 

Baby also received plasma, platelets and cryo at the time of surgery. Probably enough blood and plasma for the equivalent of a full exchange.

 

Any further ideas?

Are you saying the baby received the IVIG prior to all of this testing?

My question too.  And - what medication is the baby on?

To clarify, the baby received IVIG after the initial samples were drawn. So all the positive results were pre-IVIG administration

I was thinking drug induced also.

Only medicine we could find out that the baby had was Prostin.

I suspect it was the mother who received this, not the baby. 

Well, if the baby really had no drugs at all, it is still possible that there was something in the IvIg that was responsible for these reactions.  Many batches of IvIg have quite considerable levels of blood group antibodies in them.  If you can get a dose of the same batch, you can try putting up a panel on it and seeing how it reacts.

Could it be anti-i?

I doubt it cthherbal, as anti-i tends to be IgM, and so would not pass through the placenta, but there have been rare cases of IgG anti-i that have caused mild HDFN.

Although I doubt it, it may just be worthwhile making an eluate from the baby's red cells and reacting that against other cord cells and some adult cells - and, if they are available, adult ii cells.

That bilirubin is rather shocking.  Considering the baby's cardiac anomalies, might there also be some congenital liver issue (biliary atresia comes to mind).  There are, of course, babies whose bili's elevate due to mother's milk or other physiologic causes.  This is really puzzling.  What is the baby's Hct?

Removed

Edited June 3, 201510 yr by RollSlow10