ABO Incompatibility
Friday, October 10, 2008
Kenneth F. Trofatter, Jr., MD, PhD
• At Tue Sep 30, 09:21:00 PM 2008, Zoe said…
Dear Dr,
Blood tests taken at the time of the birth of my first baby showed an ABO incompatibility - our pediatrician informed us that my body had released antibodies that had attacked our baby's immune system. As a result he had jaundice for almost 12 weeks and many many tests. I am O+ and my son is A+.
I am currently pregnant with our second child and am concerned after reading articles that state the severity of the condition is greater with subsequent pregnancies, and can result in serious conditions or even fetal death.
Should we be concerned? Are there tests that can be done during the pregnancy to determine if the baby is at risk?
Many many thanks for your help.
• At Wed Oct 08, 10:37:00 AM 2008, Kenneth F. Trofatter, Jr., MD, PhD said…
To Zoe:
All people who have O blood types make antibodies against both the A and the B blood group antigens. These antibodies develop very early in life, usually during the first year after birth, probably as the results of similar antigens carried on certain foods and bacteria that normally colonize the gut. Usually these antibodies are of the class of IgM antibodies that are too large to cross the placenta, so that even if you have a baby with A or B blood, the antibodies won't be able to get on the baby's side of the placenta and cause destruction of the baby's red blood cells. You are someone who has antibodies against these blood groups of the IgG class. IgG antibodies readily cross the placenta to the baby, are actively concentrated from your blood to the baby’s side and, indeed, are a major source of protection against many of the things in the environment that could hurt the baby during the first 3-6 months of life before its own immune system has matured.
Unfortunately, the placenta cannot differentiate which IgG antibodies are there to protect the baby and which might hurt, as is also the case in Rh-disease. Your IgG anti-A antibodies can cross the placenta, attach to the baby’s red blood cells, and then mediate destruction of the baby's red blood cells by the baby's own immune system. Not only can that cause fetal anemia (more common in Rh-isoimmunization than with ABO incompatibility) but it can also release large quantities of hemoglobin from the baby’s blood cells. One of the breakdown products of hemoglobin is bilirubin. Bilirubin is metabolized by the liver, but the fetal liver is not efficient at that until after the baby is born. Indeed, high levels of bilirubin can accumulate in the baby before or, more commonly, after birth and if these are not quickly reduced by phototherapy, exchange transfusion, and simple maturation of the liver’s metabolic pathways, this can accumulate in the baby’s brain and cause brain damage (kernicterus).
ABO incompatibility occurs in approximately 15% of all pregnancies. Indeed, since we implemented prophylactic therapy for Rh-disease, ABO incompatibility has become the major cause of hemolytic disease of the newborn (HDN). Fortunately, less than 5% of ABO incompatibility pregnancies result in babies that develop HDN (less than 1% of all pregnancies) and usually the primary manifestation is hyperbilirubinemia rather than anemia. ABO incompatibity can occur in first pregnancies but severity is not necessarily worse in subsequent pregnancies (unlike the situation with Rh-isoimmunization). Black babies are more likely to have severe complications than Caucasians.
The hyperbilirubinemia can often be recognized by a yellow-orange appearance of the baby’s skin and eyes (jaundice). Usually simple phototherapy (bili lights) during the first few days after delivery is sufficient to manage increased bilirubin levels until the baby’s liver adjusts to life outside the womb. Some babies can have a more severe and prolonged course because of the concentration of the antibodies throughout their bodies. However, exchange transfusion is necessary in only about 0.1% of HMD pregnancies related to ABO incompatibility.
If you have another baby with an A blood type, this could happen again, but the recurrence rate is much lower and the outcome much less predictable with ABO incompatibity than with Rh-isoimmunization. You did not tell me whether your baby’s complications were from severe anemia or from hyperbilirubinemia (or both). However, tests that you could consider having done before and during another pregnancy are the following:
1) Check your husband’s blood type to see if he has one (heterozygote) or two (homozygote) doses of the A gene. If he has two, then all your babies with him MUST end up having the A blood type. If he has only one, then half your babies could have O blood types just like you and not be affected by the antibodies at all
2) If your husband is homozygous, then there would be no sense in testing another baby to find out what its blood type is during the pregnancy since it would have to have an A blood type and would therefore be ‘at risk’. But, if he is heterozygous, that testing could be done (by amniocentesis or direct testing of the baby’s blood by percutaneous umbilical cord blood sampling – PUBS) and if the baby has O blood, then you could rest assured and relax the rest of the pregnancy
3) If fetal anemia is a concern, the degree of fetal anemia caused by the antibodies can be monitored by a noninvasive ultrasound procedure called Doppler flow velocimetry (DFV). Using DFV we can measure the velocity of blood (peak systolic velocity – PSV) in a vessel called the middle cerebral artery in the baby's brain. If that blood flow velocity is higher than expected at a given gestational age, this might indicate the baby is developing severe anemia. PUBS could then be done, the degree of anemia determined precisely (as well as the bilirubin levels), and the baby could be transfused with O blood directly by injection in the umbilical vein
4) For your next pregnancy, if you choose to have one, you should get a consultation with a specialist in Maternal-Fetal Medicine. In fact, you might even want to do that BEFORE you think seriously about getting pregnant again.
Hope this helps. Best wishes! Dr T
Labels: ABO incompatibility, Rh-isoimmunization
9 Comments:
At Tue Oct 14, 05:36:00 PM 2008,
gloryrevealed said…
I have a question that is unrelated to your most recent post, but I'm not sure where else to post.
I have seen some research about the connection between IGUR and hypertension. Is there a similar connection between hypotension in pregnancy and IGUR or low-birthweight? It seems to me that prolonged low-blood pressure might restrict blood flow to the placenta, thereby limiting the baby's supply of oxygen and nutrients.
I am 26 weeks pregnant and have been taking nifedepine for 6 weeks to deal with preterm labor contractions. Baby has fallen off the growth curve in that same window. My blood pressure on the med has been as low as 68 over 45 with a pulse of 130+. Any thoughts?
At Fri Oct 17, 07:48:00 PM 2008,
Kenneth F. Trofatter, Jr., MD, PhD said…
To gloryrevealed: My thoughts are yes, it could be causing a problem. However, the reason for your preterm uterine contractions might also be contributing. Placental abnormalities that begin early in pregnancy and lead to growth restriction later in pregnancy, are often accompanied by preterm contractions,labor, and delivery. In normal pregnancies, blood pressure actually does drop in midtrimester before it begins to rise again toward prepregnancy baseline levels at term. But if the blood pressure is too low, the placenta will not be well-perfused (the uterus and even the placenta can be looked at as 'nonessential organs' from your own body's standpoint), and the baby may not receive sufficient nutrients to continue to do well. Your blood pressure may be so low at times that this is contibuting to your baby's growth delay and your doctors may need to give you a break from the nifedipine and, if necessary, come up with an alternative tocolytic agent. Best wishes and thanks for writing.
Dr T
At Fri Nov 07, 07:17:00 AM 2008,
Jeff said…
Dr. T,
My wife and I are preganant with twins (fraternal) through ICSI (male infertility). At our 12 week ultrasound, it appeared that one of the twins had a septated cystic hygroma of 8mm. The Doc told us the results were not generally posisitve and things look grim. Needless to say things are very difficult now. He also said he suspected Turners syndrome or possibly Downs syndrome if the baby makes it at all, but more likely Turners.
Two questions, why would he suspect Turners over Downs? And secondly, if the baby does not make it, but succumbs later in the pregnancy (week 22 or so) will this put the other twin in more danger?
At Fri Jan 23, 01:19:00 PM 2009,
Anonymous said…
My 18 yr old son was ABO incompatible at birth and received a complete blood transfusion. He is now A-
Recently he has been ill and has possibly developed celiac disease. He is also experiencing problems with his liver.
Could this be caused from being ABO incompatible and possibly waiting too long before the transfusion was done? (he was 3 days old when he received the transfusion)
At Thu Jul 09, 11:34:00 AM 2009,
mala said…
I have a question related to ABO incompatibility. I recently delivered a boy (about a week old now) through normal delivery. On the very second day of his birth he was diagnosed with jaundice and has been since kept in NICU with fluctuating levels of billirubin. Recently (just couple of days back), they discovered that his haemoglobin level is dropping drastically and felt that this could be an ABO incompatibility issue (though the initial DCT report showed negative results) and as a result has to go for top-up transfusion of o+ blood after a cross match between my blood (which is O+) and my son's blood group (which is A+). His current billirubin level is between 11 and 12 (which they feel is safe). They feel this transfusion should maintain his rbc count for sometime while his system matures gradually and the antibodies in his system are flushed out. However, I am not sure and have not got a clarity on how long does it take for those antibodies to get completely out of the fetal system, so that the baby does not have any further issues with his rbc count or the billirubin produced as a result of excessive breakdown of rbcs. Any clarification you can provide on this would be helpful. As of now, it seems to be some vague point in future.
At Sat Aug 22, 06:18:00 AM 2009,
Anonymous said…
Hello Doctor,
I have a question. I recently underwent an amniocentesis after which i had an injection to prevent me developing antibodies against my babies blood - I'm A-.
Every month I have a blood test and the Coombs tests had always been negative. However the bloodtest that I had one week after the amnio (and the injection)came back positive. I've read that this is normal so I didn't worry about it until the lab sent me a second identical letter warning me that the test indicated the presence of anti-D at a level superieur to 6ng/ml.
My doctor is on holidays and I'm worried that something is wrong. Can you tell me if this is normal please?
Thanks,
Lolo
At Mon Aug 24, 05:56:00 PM 2009,
Lily said…
Dear Dr. T,
I am blood type A- and have two children. My husband is O+. The first pregnancy was uneventful, the baby was A+, and I received Rhogam within 24 hours of the birth as recommended. Upon birth we found my first child had an abnormal placenta (extra lobe and velementous insertion) and a minor congenital heart defect (VSD, resolved itself before age one). The cardiologists and other doctors said it was probably just a random fluke, unlikely to happen again.
Sometime during my second pregnancy I became Rh sensitized, before the usual third trimester Rhogam shot could be given. My titres stayed low (last measured as 1:4 at 36 weeks) and the baby was born healthy and hearty. She is also A+ but the Coombs test was negative and she experienced no elevated bilirubin or other problems, no heart problems, no NICU, came home with me from the hospital.
Because this first sensitized pregnancy was so uneventful my perinatologist encouraged me to have a third child if I wish. I am worried because we never determined what caused the sensitization in the first place, nor the cardiovascular anomalies in my first child. In your experience, are there any maternal conditions that tend to go along with this? I had normal blood pressure, normal blood glucose, average weight gain, no red flags. Could there be some other condition that we overlooked which caused this? I admit I am a worrier and I am trying to understand what the realistic risks would be with another pregnancy, both to myself and the baby.
Thanks for letting me pick your brain!
At Tue Sep 08, 05:43:00 PM 2009,
Kenneth F. Trofatter, Jr., MD, PhD said…
To Lolo Aug 22: The anti-D found one week after you had the procedure is probably from the Rh-immune globulin (anti-D containing) you were given following the amniocentesis. It is very unlikely that you became 'sensitized' and developed a significant anti-D titer of your own from that procedure. However, if you had been previously sensitized (and from what you have told me there is no evidence you had been), then exposure at the time of the amniocentesis could lead to an anamnestic (booster-like) immune response. The best thing to do at this point is to simply have your antibody titer followed over time. Another option is to test the anti-D that was found to see if it came from the Rh-immune globulin you received. Best wishes.
Dr T
At Tue Sep 08, 06:07:00 PM 2009,
Kenneth F. Trofatter, Jr., MD, PhD said…
To Lily Aug 24: The abnormal placentation of your last pregnancy most likely led to the Rh-isoimmunization. This is nothing you could have done anything about, but the point is, you are now sensitized. The course of a pregnancy in which you become first sensitized is often a good outcome such as you experienced, usually because the sensitization occurs later in the pregnancy and the woman does not develop a significant antibody titer. However, now that you are sensitized, the outcome of the next pregnancy depends on the Rh-status of the baby, how soon and to what extent your antibodies increase in response to another Rh-positive baby and the subclass and avidity of the IgG anti-Rh antibodies you produce - so the course of the pregnancy is much less predictable.
With regard to your previous child's VSD, we typically tell patients that such abnormalities are multifactorial in origin. Typically, such abnormalities have a 5% or less chance of recurrence. Certain medical conditions such as diabetes, chromosomal abnormalities and genetic polymorphisms, and environmental exposures (often medications) are associated with greater risk for cardiac defects. Cardiac malformations are THE most common fetal malformations and the minor ones are often not diagnosed until after delivery. You might be able to reduce your risk for certain heart abnormalities by taking supplemental folic acid prior to conception and throughout first trimester. These are very good questions so thank you for writing.
Dr T
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