Running Head: RH INCOMPATIBILITY Rh Incompatibility Abstract Rh is an abbreviation for Rhesus. Everyone is born with a certain blood type that is either Rh positive or Rh negative. Rh incompatibility occurs when the mother’s blood type is Rh negative and her fetus’s blood type is Rh positive. The possible mixing of fetal and maternal blood can stimulate the mother’s immune system to produce anti-Rh antibodies. The anti-Rh antibodies are not produced in significant amounts until after delivery, therefore, a woman’s first infant is not affected.
During the following pregnancies, when fetal and maternal circulatory systems are closely intertwined, the mother’s antibodies may cross the placenta. Hemolytic anemia can form when the mother’s antibodies enter the fetal circulatory system. Rh incompatibility is almost completely preventable. Rh-negative mothers should be followed closely by their obstetricians during pregnancy. If the father of the infant is Rh-positive, the mother is given a mid-term injection of RhoGAM and a second injection within a few days of delivery. These injections prevent the development of antibodies against Rh-positive blood.
This effectively prevents the condition. Introduction Rh incompatibility occurs when the mother’s blood type is Rh negative and her fetus’s blood type is Rh positive. Rh is an abbreviation for Rhesus. Everyone is born with a certain blood type that is either Rh positive or Rh negative. Rh-positive blood is more common than Rh-negative blood. If the mother is Rh positive, or if both parents are Rh negative, there is no reason to worry about Rh incompatibility. However, if the mother is Rh negative and the baby’s father is Rh positive, then the baby may inherit the father’s blood type, creating incompatibility between the mother and the fetus.
Description of Condition The Rhesus factor (Rh factor) is a red blood cell surface antigen that was named after the monkey’s in which it was first discovered. Rh incompatibility 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. Once produced, maternal Rh immunoglobulin antibodies may cross freely from the placenta into the fetal circulation. It is in the fetal circulation where they form antigen-antibody complexes with Rh-positive fetal erythrocytes which eventually are destroyed, resulting in a fetal alloimmune-induced hemolytic anemia. Pathophysiology Antigens are substances that can trigger an immune response.
Cell membranes contain surface antigens that a person’s immune system recognizes as normal. Blood type is a classification determined by the presence or absence of specific surface antigens in red blood cell membranes. The surface antigens involved are integral membrane glycoproteins or glycolipids whose characteristics are genetically determined (Martini, 2006). The term Rh-positive indicates the presence of the Rh surface antigen. The absence of this antigen is indicated as Rh-negative. The Rh system consists of at least eight different kinds of Rh antigens, each referred to as an Rh factor.
The most important of these factors is antigen D. About 85% of United States residents who are of western European descent are Rh-positive (Berg, Martin, & Soloman, 1999). This means that they have the antigen D on the surfaces of their red blood cells. Those of the population who are Rh-negative have no antigen D. Rh-negative persons do not naturally produce antibodies against antigen D (anti-D). These Rh-negative people will produce anti-D antibodies if they are exposed to Rh-positive blood. The allele coding for antigen D is dominant to the allele for the absence of antigen D.
Rh-negative people are homozygous recessive, and Rh-positive people are heterozygous or homozygous dominant (Martini, 2006). Although several kinds of maternal-fetal blood type incompatibilities are known, Rh incompatibility is probably the most important. If a woman is Rh-negative and the father of the fetus she is carrying is Rh-positive, the fetus may also be Rh-positive, having inherited the D allele from the father. Ordinarily no mixing of the maternal and fetal blood occurs but late in pregnancy and during the birth process a small quantity of blood from the etus may pass through some defect in the placenta. The fetus’s red blood cells, which bear antigen D, activate the mother’s white blood cells, inducing them to form antibodies to antigen D. If the woman becomes pregnant again, her sensitized white blood cells produce anti-D antibodies that can cross an intact placenta and enter the fetal blood. There they combine with the antigen D molecules on the surface of the fetal red blood cells, causing the cells to rupture. Breakdown products of the hemoglobin released into the circulation damage many organs, including the brain (Berg et al. , 1999).
In extreme cases of this disease so many fetal red blood cells are destroyed that the fetus may die. During pregnancy, when fetal and maternal circulatory systems are closely intertwined, the mother’s antibodies may cross the placenta. The resulting condition is called hemolytic disease of the newborn. This disease has many forms from mild and undetected to dangerous. Those involving the Rh surface antigen are dangerous because of the anti-Rh antibodies ability to cross the placenta and enter the fetal blood stream. An Rh-positive mother can carry an Rh-negative fetus without difficulty.
It is because of the ability of maternal antibodies to cross the placenta that problems may appear when an Rh-negative mother carries an Rh-positive fetus. Sensitization usually occurs at delivery when bleeding takes place at the placenta and uterus. This mixing of fetal and maternal blood can stimulate the mother’s immune system to produce anti-Rh antibodies. The anti-Rh antibodies are not produced in significant amounts until after delivery, therefore, a woman’s first infant is not affected. The problem occurs later in another pregnancy if the fetus is Rh-positive.
It is in this situation that maternal anti-Rh antibodies produced after the first delivery cross the placenta and enter the fetal bloodstream. These antibodies destroy fetal red blood cells and produce a dangerous anemia (Martini, 2006). The fetal demand for red blood cells increases, and they begin leaving the bone marrow and entering the bloodstream before completing their development. According to Salem and Singer (2008) the amount of fetal blood necessary to produce Rh incompatibility varies. In one study, less than 1 milliliter of Rh-positive blood was shown to sensitize volunteers with Rh-negative blood.
Conversely, other studies have suggested that 30% of persons with Rh-negative blood never develop Rh incompatibility, even when challenged with large volumes of Rh-positive blood. Once sensitized, it takes approximately one month for Rh antibodies in the maternal circulation to equilibrate in the fetal circulation. In 90% of cases, sensitization occurs during delivery. Therefore, most firstborn infants with Rh-positive blood type are not affected because the short period from first exposure of Rh-positive fetal erythrocytes to the birth of the infant is insufficient to produce a significant maternal IgG antibody response.
The risk and severity of the sensitization response increases with each pregnancy involving a fetus with Rh-positive blood. In women who are prone to Rh incompatibility, the second pregnancy with an Rh-positive fetus often produces a mildly anemic infant, whereas succeeding pregnancies produce more seriously affected infants who ultimately may die in utero from massive antibody-induced hemolytic anemia (Salem & Singer, 2008). Treatment The early detection of Rh-negative blood type in the pregnant woman is of substantial benefit if the patient is not isoimmunized and the father is not known to be Rh-negative.
Since Rh incompatibility is almost completely preventable with the use of RhoGAM, prevention remains the best treatment. The goals of treating Rh incompatibility are to ensure that the infant is healthy and to lower the risk for the condition in future pregnancies. The diagnoses of Rh incompatibility can be done during the prenatal or postnatal time of pregnancy. Determination of Rh blood type is required in every pregnant female. 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 [Screening for D(Rh) incompatibility, 1989]. Obtaining maternal Rh antibody titers can be helpful for future follow-up care of pregnant females who are known to be Rh negative. High levels of maternal Rh antibodies suggest that Rh sensitization has occurred, and further studies, such as amniocentesis, may be necessary to evaluate the health of the fetus (Salem & Singer, 2008). Postnatal diagnosis can be made immediately after the birth of any infant with an Rh-negative mother in the hospital setting.
This is done by examining blood from the umbilical cord of the infant for ABO blood group and Rh type. In addition, a measure of the hematocrit and hemoglobin levels is obtained, and a serum bilirubin analysis. A direct Coombs test is also performed with a blood smear. A positive direct Coombs test result confirms the diagnosis of antibody-induced hemolytic anemia, which suggests the presence of ABO or Rh incompatibility (Salem & Singer, 2008). If Rh incompatibility is diagnosed during pregnancy the mother will receive Rh immune globulin in the seventh month of pregnancy and again within 72 hours of delivery.
This is a preparation of anti-D antibodies known as RhoGAM. RhoGAM works by coating and destroying fetal cells in the maternal circulation. These antibodies clear the Rh-positive fetal red blood cells from the mother’s blood quickly minimizing the chance for her own white blood cells to be sensitized (Berg et al. , 1999). When this happens, the body does not react to the baby’s Rh-positive cells as a foreign substance (Kumpel, 2006). As a result, if she becomes pregnant again, her blood does not contain the anti-D that could harm her baby.
Once the Rh antibodies have formed, the RhoGAM will no longer help. That’s why a woman who has Rh-negative blood must be treated with the Rh immune globulin with each pregnancy or any other event that allows her blood to mix with Rh-positive blood. After the administration of RhoGAM, a Kleihauer-Betke blood test is performed to ensure that the proper amount of RhoGAM was given. The Kleihauer-Betke test estimates the number of fetal red blood cells in the mother’s circulation. Several options are available for treating hemolytic anemia in an infant. In mild cases, no treatment may be needed.
If hemolytic anemia is severe and the baby is almost full-term, the doctor may induce labor early. This allows the baby’s doctor to begin treatment right away. Newborns also may be treated with special lights to reduce the amount of bilirubin in their blood. The use of lights to reduce bilirubin levels is called phototherapy. The newborns skin and blood absorb the light waves which change the bilirubin into products which can pass through the neonates system. Reducing the blood’s bilirubin level is important because high levels of this compound can cause brain damage.
In severe cases of hemolytic disease affecting a fetus at an earlier stage, transfusions can be given while the fetus continues to develop in the uterus (Martini, 2006). Washed maternal red blood cells are a potential source of blood with little risk that the donations would be harmful to the mother or fetus. Serial maternal blood donation for intrauterine transfusion is now common practice among major regional referral centers that treat these high risk pregnancies (Denomme, Fernandes, Kelly, Ryan, & Seaward, 2004). Nursing Diagnoses
An important nursing diagnosis involving a first time Rh-negative mother with a possible Rh-positive fetus is deficient knowledge of sensitization regarding Rh incompatibility related to lack of exposure to resources as evidenced by a request for information. Desired outcomes for the patient would include verbalizing an understanding of the disease process and appropriate treatment plans. In addition, the patient should participate in the treatment regimen. These outcomes are important because the patient needs to have an understanding of Rh incompatibility.
By understanding what is going on in her body, she can follow through with an appropriate treatment plan to avoid sensitization and complications during possible future pregnancies. The priority intervention in this case would be to assess the patient’s knowledge of Rh incompatibility. The nurse can then provide information about the pathophysiology of sensitization, the implications for the mother and fetus, and rational for interventions, procedures and tests. This provides information about areas in which learning is needed.
Receiving information can promote understanding, reduce fear, and help to facilitate the treatment plan for the client (Doenges, Moorhouse, & Murr, 2007). Another possible nursing diagnosis involving a sensitized mother is maternal anxiety related to a threat of harm to her fetus as evidenced by feelings of helplessness from an Rh incompatibility diagnoses. Desired outcomes for the patient would include identifying healthy ways to deal with the anxiety. In addition, the patient should appear relaxed and report that the anxiety is reduced to a manageable level.
The priority intervention would be to assess the level of anxiety and assist the patient in identifying feelings and how to cope with the feelings. By understanding how a patient copes with anxiety one can determine the effectiveness of the coping strategies. It may also be beneficial to list helpful resources that provide information and support about Rh incompatibility. Educating the patient and providing support can help reduce the amount of anxiety (Doenges, Moorhouse, & Murr, 2007). Conclusion During pregnancy, red blood cells from the fetus can get into the mother’s loodstream as she nourishes her child through the placenta. If the mother is Rh-negative, her system cannot tolerate the presence of Rh-positive red blood cells. In such cases, the mother’s immune system treats the Rh-positive fetal cells as if they were a foreign substance and makes antibodies against the fetal blood cells. These anti-Rh antibodies may cross the placenta into the fetus, where they can destroy the fetus’s circulating red blood cells. Special immune globulins, called RhoGAM, are now used to prevent this sensitization.
The early detection of Rh-negative blood type in the pregnant woman is of substantial benefit if the patient is not isoimmunized and the father is not known to be Rh-negative. Rh incompatibility is almost completely preventable with the use of RhoGAM and prevention remains the best treatment. The goals of treating Rh incompatibility are to ensure that the infant is healthy and to lower the risk for the condition in future pregnancies. References Berg, L. R. , Martin, D. W. , & Soloman, E. P. (1999). Biology (5th ed. ). Orlando: Harcourt.
Denomme, G. A. , Fernandes, B. J. , Kelly, E. N. , Ryan, G. , & Seaward, P. G. R. (2004). Maternal ABO-mismatched blood for intrauterine transfusion of severe hemolytic disease of the newborn due to anti-RH17. Transfusion Practice, 44, 1357-1360. Retrieved August 1, 2009, from Ebsco Database. Doenges, M. E. , Moorhouse, M. F. , & Murr, A. C. (2007). Nurses pocket guide, diagnoses, _ interventions, and rationales (11th ed. ). Philadelphia: F. A. Davis. _ Kumpel, B. (2006). On the immunologic basis of RH immune globulin (anti-D) prophylaxis.
Transfusion, 46, 1271-1275. Retrieved August 1, 2009, from Ebsco Database. Martini, F. H. (2006). Fundamentals of anatomy and physiology (7th ed. ). San Francisco: Pearson Benjamin Cummings. Salem, L. , & Singer, K. (July 29, 2008). Rh incompatibility. Retrieved August 1, 2009, from http://emedicine. medscape. com. Screening for D(Rh) incompatibility, (1989). U. S. Preventative Services Task Force Office of _ Disease Prevention and Health Promotion, _2. Retrieved August 4, 2009, from Ebsco Database.