Rh Disease – Sweet, Sweet Blood Cells – Part 2

Welcome back!  Click here for Part 1.  Last time we left off with mom’s body sending anti-RhD antibodies through the placenta to her second baby.

What happens to baby? 

In all cases of Rh disease, baby loses some RBCs – in fact, baby’s own immune system destroys the RBCs because they were marked with maternal antibodies.   What happens next depends on how many antibodies baby was exposed to.

In mild cases, baby has slight anemia – too few oxygen-carrying RBCs.  Baby might show no symptoms at all.

Baby might develop jaundice ((the yellow-colored skin for which babies are placed under blue lights)) after he’s born.  When RBCs are destroyed, they release their hemoglobin. ((the red, oxygen-carrying protein))  Baby starts to break down the hemoglobin so he can recycle the iron, and one of the breakdown products is a yellow substance called bilirubin.  In large amounts, it can damage baby’s brain.  While he’s still in the womb, baby passes the bilirubin back to mom’s liver for disposal.  However, right after birth, mom is no longer taking care of the bilirubin and baby’s liver doesn’t know what to do yet, so the yellow-colored substance accumulates in baby’s skin.  Blue lights break down the bilirubin into small enough pieces that baby’s liver can handle it. ((The superficial cause of jaundice is always the same – excess bilirubin in the blood. However, all sorts of things besides blood type differences can cause an excess of bilirubin, some of which may be covered in another post.))

Blue light breaks up the bilirubin into small enough pieces that baby's liver can digest them.
Blue light breaks up the bilirubin into small enough pieces that baby’s liver can digest them.

In severe cases, baby loses a lot of RBCs.  Baby’s heart is pumping harder and harder to get the remaining RBCs around his body to deliver oxygen.  Sometimes, this effort is too much for the heart and baby dies.

How it’s treated

Many babies died of Rh disease until the discovery of a treatment in the late 1960s.

Strangely, the solution and the problem are one and the same.  If a pregnant mother is Rh-  and has not yet been sensitized, doctors give her a shot of anti-RhD antibodies (known as RhoGAM in the United States).  These “special forces” antibodies attack and destroy any fetal RBCs in mom’s blood before mom can recognize them and make antibodies of her own.

The antibodies in RhoGAM cover up the RhD sugars on baby's blood cells so that mom's WBCs never see them.
The antibodies in RhoGAM cover up the RhD sugars on baby’s blood cells so that mom’s WBCs never see them.

Why don’t these “special forces” cause problems for baby?  Doctors carefully monitor the amount of antibodies they give mom so that there aren’t enough antibodies left over to cross the placenta and attack baby.

If mom never gets the chance to be sensitized to RhD, she will never make antibodies that attack an Rh+ baby.  She’ll have to get a shot with each new pregnancy that has a chance to be Rh+.

Sometimes, doctors will meet a pregnant Rh- woman who is already sensitized to the D antigen, meaning she’s already producing anti-RhD antibodies.  They’ll then do tests on dad to see if the baby is likely to be Rh+.  If baby is, they will monitor mom very closely.  Doctors can even give baby a blood transfusion in the womb if he needs it!

Because of these advances, Rh disease is largely nonexistent in developed countries, though low-income countries still need access to this life-saving care.

In summary:

Blood Types - Overview

But what about ABO?

Wondering why babies who have a different ABO blood type than their mother seem to have no problems?

One reason is that it takes time for baby’s A or B sugars to develop on the blood cells, longer than the RhD sugars do.  If mom is type B, her anti-A antibodies simply don’t see baby’s A sugars until very late in the pregnancy, when they have little time to cause any harm.

Another reason is that while Rh sugars are basically only on baby’s RBCs, A or B sugars appear on many different types of cells in baby’s body.  If mom’s antibodies do look for things to destroy, they might bind to a hundred different tissues.  Thus, the destructive effect is diluted compared to when the same number of antibodies are all attacking RBCs, and baby doesn’t show symptoms.

Mom's anti-A antibodies could bind to almost any tissue.
Mom’s anti-A antibodies could bind to almost any tissue.

Hemolytic disease of the newborn due to ABO incompatibility is possible, but it tends to be much less severe than with Rh disease.

Thanks for reading! It would make my blood pump if you’d like my Facebook page.

Sources and Further Reading

If you’ve made it this far, I’m sure you need your own plush red blood cell. I have one on my desk! (affiliate link)

Why do we have blood types? Should you eat according to your blood type? Are you more prone to certain diseases?

Fun Blood Typing Game: test your understanding of blood types, donors, and receivers.

The article that started it all: where do those “special forces” antibodies come from?  Very special donors.

A person whose blood type switched from A to B during infection.

A particularly severe case of Rh disease with a happy ending.

Blood Groups and Red Cell Antigens by Laura Dean.

How RhoGAM works.

Does RhoGAM cause HDN?

More on RhoGAM.

How common is Rh disease? 

Antibody half-life.

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