Has anyone ever seen a case of delayed HDN? We have a 6 week old with a 2+ DAT, 2+ anti-E in baby plasma, 4+ anti-E in Mom's plasma drawn 9/2 and a bili that started at 17 on 8/31 but dropped to 13 by 9/2. LDH was high 8/31. Hct is within normal range for age although at low end. Retic is normal. Both are A pos so no testing was done at birth and we assume the baby had no jaundice then that would have triggered a bili.

All opinions, experience and speculation appreciated.

Obviously you have ruled out ABO HDN (this is often delayed), but antibodies to the Gerbich Blood Group SYstem can also cause delayed haemolytic anaemia.

I realise that your case involves neither of these.

Was the baby term? I just wonder if the maternal anti-E, the DAT, the bilirubin levels and the LDH levels are coincidental to these, as the baby's will naturally fall after a while, giving a raised bilirubin level and raised LDH? I'm not saying it isn't a case of delayed HDN, but other things would also have to be ruled out.

Has anyone ever seen a case of delayed HDN? We have a 6 week old with a 2+ DAT, 2+ anti-E in baby plasma, 4+ anti-E in Mom's plasma drawn 9/2 and a bili that started at 17 on 8/31 but dropped to 13 by 9/2. LDH was high 8/31. Hct is within normal range for age although at low end. Retic is normal. Both are A pos so no testing was done at birth and we assume the baby had no jaundice then that would have triggered a bili.

All opinions, experience and speculation appreciated.

A question maybe a little not fit, what about the baby's E antigen expression? If it is not anti-E caused DAT pos, And what about the baby's transfusion history? Maybe the anti-E is transfused.

The baby is E positive and was not transfused.

If it was anti-E delayed HDFN, why the delay? I have a theory but nothing to back it up. I suspect that the anti-E coating the baby's cells since birth just wasn't really causing those cells to be removed from circulation in any large degree until now. Maybe the speen and rest of RE system has matured enough to finally start removing those cells. Throw in dehydration due to poor feeding secondary to a increasing bili and it may have made the bili even higher--especially in our very dry climate in August--leading to a vicious cycle. Does this make any sense?

Thinking back, I have seen one case of delayed HDN due to anti-E with a titre of 128 to 256 (the mum also had an anti-c, but this was extremely weak), but it was not as delayed as this case (about a week). We could find no other explanation for the drop in Hb and the rise in bilirubin, and the baby did require multiple transfusions (although not an exchange).

This may be another such case, but I still say that every other avenue must be explored, as a positive DAT and the ability to elute a specific red cell antibody from the baby's red cells points to, but does not prove, HDN. As I say, this could be coincidental.

We had a case where the mum had an anti-Era, and the baby required an IUT and further transfusion after birth, but after extensive investigation (and boy, do I mean extensive), it turned out that the baby had a viral infection in utero, and that the anti-Era was a coincidental element (anti-Era still has not, therefore, ever been shown to cause HDN - otherwise I would have published quick as a flash to get my name associated with the first case!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!).

Edited September 6, 201113 yr by Malcolm Needs

If it was anti-E delayed HDFN, why the delay? I have a theory but nothing to back it up. I suspect that the anti-E coating the baby's cells since birth just wasn't really causing those cells to be removed from circulation in any large degree until now. Maybe the speen and rest of RE system has matured enough to finally start removing those cells. Throw in dehydration due to poor feeding secondary to a increasing bili and it may have made the bili even higher--especially in our very dry climate in August--leading to a vicious cycle. Does this make any sense?

The fetus uses the mother's RES to clean up and once the baby is born, because of the immature immune system and RES that is when the bili etc shows. I am still wondering why the delay..

As a scientist, rather than a clinician, I could be talking a complete load of rubbish here Liz, but could it possibly be that there is an apparent delay, rather than an actual delay, because the baby's red cells are being removed comparatively slowly by the RES, and that the rise in the post-natal bilirubin is, therefore, also slow, and so we are just not noticing the fall in the Hb and the rise in the bilirubin as early as we would with a more aggressive antibody?

Just a thought and probably wrong!

well, well well, lookie what I found: of the Dombrock blood group sysytem, Dob; and of the Rh blood group anti-e can cause delayed HDN. Why and how are to follow....

Oh I am not ignoring you Malcolm, sorry about that. I just need to analyse what you said.

Nothing like going in after the weekend and getting a clearer picture of the story. It isn't so delayed as I was led to believe. The baby was born at 39 1/7 wks gestation on 7/18 after a scheduled induction so I am pretty sure he was born afternoon or evening. On the morning of the 20th his bili was 6.3. Then he went home and ended up being readmitted a week later 7/25 with a bili of about 25. They kept him under the lights and got it down to 13.9 by 7/27. Then we saw nothing of him until a month later on Aug 31st when his bili was 17.0. Note that his D bili's done 7/25 & 8/31 were both 0.4, near the top but not above the normal range. That's not very high considering his T bili. His liver really wasn't conjugating very well. So, if this is HDFN at all, he may have been tested a bit early (< 36 hrs old) for his first bili to be able to detect it and then sent home. Then, he might as you have suggested, had sort of a "slow blow" course of HDFN, possibly peaking at a week old although maybe sooner since no testing was done. The persistence for another month could maybe be due to just the low-grade aspect of it which will finally end when all the anti-E in his circulation is gone. Or he could have a liver problem that may have nothing to do with the +DAT but his abnormal bili's may have been exacerbated by it. His two older siblings were slightly jaundiced at birth but did not require treatment. Mom's Ab screen was neg last Dec. I hope they will do another bili and maybe other testing soon.

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birth 7/18

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7/20

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7/25

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7/25

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7/25

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7/26

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7/27

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Aug

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8/31

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9/2

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9/5

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T. Bili

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6.3

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24.2

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25.2

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19.9

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16.9

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13.9

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17.0

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13.7

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7.4

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As a scientist, rather than a clinician, I could be talking a complete load of rubbish here Liz, but could it possibly be that there is an apparent delay, rather than an actual delay, because the baby's red cells are being removed comparatively slowly by the RES, and that the rise in the post-natal bilirubin is, therefore, also slow, and so we are just not noticing the fall in the Hb and the rise in the bilirubin as early as we would with a more aggressive antibody?

Just a thought and probably wrong!

It is possible. I like the way you think!

It is possible. I like the way you think!

VERY few people ever say that - particularly my line manager or my wife!!!!!!!!!!!!!!!

:lonely::lonely::lonely::lonely::lonely:

Nooooooooooooooo!! I can't believe it!!!! What!!??!!!!!

Do you know if the mother is breast feeding? If so, the infant would be receiving a regular infusion of anti-E which would then be contributing to the on-going process.

The mother is breast feeding. But wouldn't that be IgA anti-E which should not be detectable in our tests, right?

Right.

She's back! We just got a prenatal workup on this same mom and her anti-E (saline/IgG) titer is 1 at this time. The previous baby has had some labwork since. For most of the first 5 mo. of his life he had low to low normal levels of absolute neutrophils. A CBC done last month when he was about a year old showed a very low end of normal absolute neutrophil count and a slightly low absolute lymphocyte count. Percantages of both were in the normal range. Any advice for this pregnancy?