Rh – incompatibility
What is Treatment
Rh?
Patho - Prevention
Physiology
Supervisor Prepare
Ruda Bashar
Prof. Dr. Rabiaa Ali
Alia Saleem
Aya Jassim
Objectives:
• Describe the clinical significance of Rh incompatibility.
• Describe the pathophysiology of Rh incompatibility and
alloimmunization.
• Identify indications for Rh D immunoglobulin (RhIg)
treatment.
• Explain the importance of improving care coordination
amongst the interprofessional team to enhance the delivery of
care for patients at risk for Rh incompatibility.
Definition
The Rh blood group is present on the surface of erythrocytes of
most of the population. When it is present a person is said to be
Rh positive. Those without the factor are Rh negative. If an Rh-
negative person is exposed to Rh-positive blood, an antigen-
antibody response occurs, antibodies are formed, and the person
is said to be sensitized. Subsequent exposure to Rh- positive
blood can then cause a serious reaction that results in
agglutination and hemolysis of red blood cells
Cont...
when an Rh-positive fetus begins to grow inside an Rh-negative
mother who is sensitized, it is as though her body is being in-
vaded by a foreign agent. Her body reacts in the same manner it
would if the invading factor were a substance such as a virus:
she forms antibodies against the invading substance. The Rh
factor exists as a portion of the red blood cell, so these mater-
nal antibodies cross the placenta and cause red blood cell de-
struction (hemolysis) of fetal red blood cells (Fig. 21.10). A fetus
can become so deficient in red blood cells that sufficient oxygen
transport to body cells cannot be maintained. This condition is
termed hemolytic disease of the newborn or erythroblastosis
fetalis.
Patho - Physiology
During a normal pregnancy, small amounts of fetal blood may
cross the placenta. An Rh-negative mother whose fetus is Rh
positive may develop anti-D antibodies in response to this ex-
posure. During delivery of the placenta or as a result of trauma.
even larger quantities of fetal blood can enter maternal circula-
tion. After exposure to the Rh-positive antigen, the primary im-
mune response is development of immunoglobulin M (IgM)
antibodies. This primary response develops slowly over
severalweeks or months with a detectable titer developing 5 to
16 weeks after the sensitizing event. IgM antibodies are large
and do not cross the placenta.
Fetal-Neonatal Risks
The hemolysis caused by the maternal IgG antibodies in the fe-
tus creates fetal anemia. The fetus responds by increasing RBC
production. The presence of nucleated RBCs (erythroblasts) is
why the term erythroblastosis fetalis was coined for this se- vere
hemolytic disease of the fetus and newborn. If treatment is not
initiated, this anemia can also cause marked fetal edema, called
hydrops fetalis. Congestive heart failure may result. Al- though
maternal sensitization can now be prevented by appro- priate
administration of Rh immune globulin, infants still die of
hemolytic disease secondary to Rh incompatibility
. RBC destruction also leads to hyperbilirubinemia and jaun-
dice (called icterus gravis), which can lead to neurologic dam-
age (kernicterus)
Antenatal investigation protocol of
Rh-negative mothers
• Investigation of blood for Rh and ABO grouping become
almost a routine during the first antenatal visit in first trimester.
• If the women is found Rh-negative, Rh grouping of the
husband is to be done to find out whether the pregnancy is a
result of incompatible or compatible mating.
• If the husband found to be Rh-positive, further investigation
are to be carried out:
investigation for newborn baby
Higher-than-normal levels of bilirubin in infant's blood is a sign
of Rh incompatibility. In a full-term baby who is less than 24
hours old, the levels of bilirubin should be less than 6.0
milligrams per deciliter.
• Signs of red blood cell destruction in infant's blood are signs of
Rh incompatibility.
Therapeutic Management
To reduce the number of maternal Rh (D) antibodies being formed, Rh (D)
immune globulin (RhIG), a commercial preparation of passive Rh (D)
antibodies against the Rh fac- tor, is administered to women who are Rh-
negative at 28 weeks of pregnancy. These cannot cross the placenta and de-
stroy fetal red blood cells. RhIG is given again by injection to the mother in
the first 72 hours after birth of an Rh-positive child to further prevent the
woman from forming natural antibodies.
Intrauterine transfusion
The fetus can die in utero from severe anaemia and hydrops before he can be
delivered.
• An intrauterine transfusion can prolong the life in utero
of a fetus to a gestation where the risks of prematurity
are estimated as being less than those of the Rh disease.
This can be done by an:
1. Intraperitoneal transfusion guided by ultrasound.
2. Umbilical vein transfusion guided by ultrasound.
Rh-negative blood is either transfused under ultrasound control. Repeat as
necessary, according to amniotic optical density, or fetal haematocrit. The
intravenous route is becoming increasingly the preferred method.
Nursing care during pregnancy
As part of the initial prenatal history, the nurse asks the mother
if she knows her blood type and Rh factor. Many women realize
that they are Rh negative and that this condition has
implications for pregnancy. If a woman knows that her Rhesus
factor is negative, we take the following procedures
1-Determine blood group & Rh factor and indirect coombs test
for antibody screening for all pregnant mother
2-RhIG immunoglobulin is given. In the 28th week of
pregnancy.
3- RhIG is given again by injection to the mother in the first 72
hours after the birth of an Rh-positive baby to prevent the
woman from developing natural antibodies.
postpartum care for mother
The goals of postpartum care are to prevent sensitization in the as-
yet-unsensitized pregnant woman and to treat the isoim- mune
hemolytic disease in the newborn.
The Rh-negative mother who has no titer (indirect Coombs' negative,
nonsensitized) and who has given birth to an Rh-positive fetus (direct
Coombs' negative) is given an intramuscular injection of 300 mcg Rh
immune globulin within 72 hours . This protocol reduces the
incidence of antenatal sensitization dramatically. Rh immune globulin
works to destroy the fetal cells in the maternal circulation be- fore
sensitization occurs, thereby blocking maternal anti- body production.
This provides temporary passive immunity for the mother, which
prevents the development of perma- nent active immunity (antibody
formation).
If a larger fetomaternal bleed might have occurred, a Kleihauer-Betke
test can be performed to obtain an estimate of the extent of the bleed
and the dose of Rh immune globulin can be increased as necessary.
postpartum care for newborn
• Measurement of antibody levels in titers at regular intervals,
• Amniocentesis for bilirubin levels
• Serial ultrasound for detection of hydrops and management of
neonatal anemia and hyperbilirubinemia.
Prevention
Anti-D immunoglobulin 300 micro gram of D Antibody is
given to D-negative , non sensitized mothers to prevent the
hazards f sensitization.
Anti-D globulin is provided to D-negative mothers after
miscarriage, evacuation of molar pregnancy or ectopic
pregnancy.
It is also administered when there is heavy feto maternal
bleeding such as placental abruption, intrauterine manipulation.
Dose of 300 micro gram D-antibody will neutralize about
15ml of red cells.
Rosette test is done to all such mothers to know the accurate
amount of Anti-D required.
Suggestion
all pregnant women should have blood typing and Rh
testing on their first visit to their doctor for pregnancy
care. recommend retesting between the 24th and 28th
weeks of pregnancy.
It may also be done after a miscarriage, an abortion, or
an amniocentesis (a gene screening test done during
pregnancy).
References
ESSENTIALS of Maternity, Newborn, & Women's Health Nursing/Rh
incompatibility/isoimmunization, 637-638 847-850,
Maternal- NewbornNURSING &Women's Health
Rh alloimmunization/ p.n476-480
Maternal & Child Health Nursing: Care of the Childbearing & Childrearing
Family
Rh incompatibility /P.N. 586-588