Rh Incompatibility in Pregnancy

Rh Incompatibility in Pregnancy


The most common type of Rh incompatibility occurs when an Rh-negative pregnant mother is exposed to Rh-positive fetal red blood cells secondary to fetomaternal hemorrhage during the course of pregnancy from spontaneous or induced abortion, trauma, invasive obstetric procedures, or normal delivery .

Rh incompatibility can also occur when an Rh-negative female receives an Rh-positive blood transfusion.

An Rh-negative woman become alloimmunized to the D antigen present on fetal red blood cells (RBCs) during the first Rh-incompatible pregnancy. The first pregnancy is rarely affected because the number of Rh antibodies produced by the mother during primary immunization is low and the antibodies are usually IgM in nature . IgM can’t cross placental barrier.

When the mother is exposed to D-positive fetal RBCs during a subsequent Rh-incompatible pregnancy, the mother mounts an anamnestic, or secondary, immune response to the fetus’ RBCs. A large number of IgG-class Rh antibodies are produced. The IgG antibodies cross the placenta and make fetal red cells susceptible to destruction. The fetal RBCs are then destroyed by the fetal immune system. Anemia develops in the fetus with a concomitant increase in unconjugated bilirubin. The anemia and unconjugated bilirubin levels can lead to a number of conditions.

Treatment with Rh IgG (RhoGAM)

The current recommendation is that every Rh-negative nonimmunized woman who presents to the ED with antepartum bleeding or potential fetomaternal hemorrhage should receive 300 mcg of Rh IgG IM. For every 30 mL of fetal whole blood exposed to maternal circulation, 300 mcg of Rh IgG should be administered . A lower 50-mcg dose preparation of Rh IgG is available and recommended for Rh-negative females who have termination of pregnancy in the first trimester when fetomaternal hemorrhage is believed to be minimal.

Because of its short half-life, Rh IgG routinely is administered once at 28-32 weeks’ gestation and again within 72 hours after birth to all Rh-negative pregnant females as a part of routine prenatal care.

Other important points:

Determination of Rh blood type is required in every pregnant female.
Overall, 16% of Rh-negative women will become sensitized after their first pregnancy if not given Rhogam.
In a pregnant woman with Rh-negative blood type, the Rosette screening test often is the first test performed. The Rosette test can detect alloimmunization caused by very small amounts of fetomaternal hemorrhage.
Amniotic bilirubin scan (also known as ΔOD450) is a prenatal testing procedure . Results interpreted using a Liley or Queenan chart (Queenan chart is reported to have higher diagnostic accuracy for identifying severe anemia).

The Liley curve is divided into three zones.
 
A result in Zone I indicates mild or no disease. Fetuses in zone I are usually followed with amniocentesis every 3 weeks.
A result in zone II indicates intermediate disease. Fetuses in low Zone II are usually followed by amniocentesis every 1-2 weeks.
A result above the middle of Zone II may require transfusion or delivery.
Obtaining maternal Rh antibody titers can be helpful for future follow-up care of pregnant females who are known to be Rh negative. Maternal serum antibody Rh titer >15 IU/mL indicates high risk of severe fetal anemia.
Immediately after the birth of any infant with an Rh-negative mother examine blood from the umbilical cord of the infant for ABO blood group and Rh type, measure hematocrit and hemoglobin levels, perform a serum bilirubin analysis, obtain a blood smear, and perform a direct Coombs test.
A positive direct Coombs test result confirms the diagnosis of antibody-induced hemolytic anemia, which suggests the presence of ABO or Rh incompatibility.

Blood Types

Normally we might ask others what is your blood type and refer to A, B, AB, or O, and Rh positive or negative system. But do you know we have other blood types system? There are actually 30 other ways to types blood, including two just identified by French scientists. The latest are based on proteins called Langereis and Junior. According to Biologist Lionel Arnaud of the French Institute of Blood Transfusion they're almost universal.

For the first time, Arnaud’s team discovered that some people can be negative – for instance, over fifty thousand Japanese people lack the Junior protein.  These rare variations could explain why some blood transfusions go awry, even when the standard blood types match.  And pregnant women who lack these proteins may also be at risk for miscarriages, if the fetus is positive.  I’m Bob Hirshon for AAAS, the Science Society.

Making Sense of the Research

A common school science experiment is to try and determine your own blood type.  (Note: Don't assume your conclusion is accurate!)  You may also know your blood type from a doctors' visit or filling out medical forms.  The blood types we usually hear about are A, B, AB, and O, with a positive or negative attached.
These types indicate what kind of antigens, or proteins, are on the surface of your red blood cells.  Type A has an antigen we call A, type B has antigen B, type AB has both, and type O has neither.  The positive or negative refers to a type of Rhesus protein, specifically Rh-D, and it may be present (positive) or absent (negative).
Blood typing is important because if you receive another kind of blood or tissue – for example, a transfusion or an organ transplant – it must be compatible with your blood type.  Giving type B blood to a type A person, for example, would trigger what's essentially an allergic reaction to the blood.  That's because the type A person's body would recognize the B protein as a foreign invader, just like a bacteria or virus.  It would attack the B-type blood with immune cells called antibodies, creating a serious and potentially life-threatening allergic reaction.
The A/B/O and Rh-D systems create eight different blood types, which represent most of the variation in blood proteins in the human population.  However, as you heard, there are actually a total of 30 surface proteins that can vary from person to person.  Their names include M and N, Kell, Lewis, and others, often named after the patient in which they were first identified.
The other blood types aren't as well known for one of two reasons: either the vast majority of people have one of the types (therefore making incompatibility rare), or incompatibility doesn't usually cause significant medical problems.  In the case of the new blood types, Langereis and Junior, the first is true: until now, it was assumed that virtually everyone carried the proteins.  But Arnaud's team found that there are small but significant populations that have Langereis or Junior-negative people – enough to classify the presence or absence of these proteins as a new blood type.
As you heard, the negative blood types are found mainly in certain populations.  Therefore, for example, it may only be important to check the Junior type in people of Japanese descent.  But knowing about these minor blood types could help explain some otherwise mysterious cases – for instance, women who have unexplained miscarriages.  An Rh-negative mother carrying an Rh-positive baby can develop antibodies that harm the fetus, but this is widely recognized and can be prevented with certain drugs.  When there's no Rh incompatibility, it's possible that a conflict in one of the lesser-known blood types could be causing the reaction.
Now try and answer these questions:

1. What are the best-known blood type systems?
2. Why are other blood type systems less well known?
3. What does it take for a protein on a red blood cell's surface to be part of a blood type system – positive or negative?
4. Why is it important to understand other blood type systems?

References:
http://sciencenetlinks.com/science-news/science-updates/other-blood-types/#.T3ytYeP7fwg.facebook