I.

INTRODUCTION

Rh incompatibility, also known as Rh disease, is a condition that occurs when a woman with Rh-
negative blood type is exposed to Rh-positive blood cells, leading to the development of Rh
antibodies. The most common cause of Rh incompatibility is exposure from an Rh-negative mother
by Rh-positive fetal blood during pregnancy or delivery. As a consequence, blood from the fetal
circulation may leak into the maternal circulation, and, after a significant exposure, sensitization
occurs leading to maternal antibody production against the foreign Rh antigen. Rh incompatibility
can also occur when an Rh-negative female receives an Rh-positive blood transfusion.

II. OBJECTIVES
III. ANATOMY AND PHYSIOLOGY
IV. TEXTBOOK DISCUSSION

Approximately 15% of Caucasians and 10% of African Americans in the United States are missing the
Rh (D) factor in their blood or have an Rh-negative blood type. Rh incompatibility occurs when an
Rh-negative mother (one negative for a D antigen or one with a dd genotype) carries a fetus with an
Rh-positive blood type (DD or Dd genotype). For such a situation to occur, the father of the child
must either be homozygous (DD) or heterozygous (Dd) Rh positive. If the father of the child is
homozygous (DD) for the factor, 100% of the couple’s children will be Rh positive (Dd). If the father
is heterozygous for the trait, 50% of their children can be expected to be Rh positive (Dd). Although
blood incompatibility is basically a problem that affects the fetus, it can cause such concern and
apprehension in a woman during pregnancy that it becomes a maternal problem as well. Because
people who have Rh-positive blood have a protein factor (the D antigen) that Rh-negative people do
not, when an Rh-positive fetus begins to grow inside an Rh-negative mother who is sensitized, 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 maternal antibodies cross the placenta and cause destruction (i.e., hemolysis) of
fetal red blood cells. A fetus can become so defi cient in red blood cells from this that a sufficient
oxygen transport to body cells cannot be maintained. This condition is termed hemolytic disease of
the newborn or erythroblastosis fetalis. Theoretically, there is no connection between fetal blood
and maternal blood during pregnancy, so the mother should not be exposed to fetal blood. In
reality, a small amount of fetal blood does enter maternal circulation (Kim & Makar, 2012).
Procedures such as amniocentesis or percutaneous umbilical blood sampling can allow this to occur.
During a first pregnancy, this effect is small. As the placenta separates after birth of the fi rst child,
however, there is an active exchange of fetal and maternal blood from damaged villi. This causes
most of the maternal antibodies formed against the Rh positive blood to be formed in the first 72
hours after birth. These become a threat in a second pregnancy.

V. PATHOPHYSIOLOGY
VI. VITAL INFORMATION
VII. CLINICAL ASSESSMENT
VIII. LABORATORY AND DIAGNOSTIC TEST
a. Prenatal
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. When a high clinical suspicion of large
fetomaternal hemorrhage is present (>30 mL blood), the Kleihauer-Betke acid elution
test can be performed. The Kleihauer-Betke test is a quantitative measurement of fetal
red blood cells in maternal blood, and it can be valuable for determining if additional
amounts of Rh IgG should be administered. The amount of Rh IgG required for
treatment after sensitization is at least 20 mcg/mL of fetal RBCs.
IX. MEDICAL MANAGEMENT
X. NURSING MANAGEMENT
XI. DISCHARGE PLANNING
XII.