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A Study of Erythroblastosis Fetalis: a silent killer

 

A Research Project Submitted to:

                                                  

Ms. Reneliza Sta. Ana

 

College of Nursing

 

Manila Central University

 

 

 

In Partial Fulfillment of the Course Requirements

 

In English 5

 

 

By:

Cabello, Glaiza J.

Latag, Alexander G.

Lopez III, Severino D.

BSN 2-12

 

March 2005

 

 

Table of contents

                                                                                            Page

Acknowledgement …………………………………………………....3

Chapter 1: Introduction

General consideration ………………………………………………... 4

Statement of the Problem……………………………………………,.. 5

Objective of the study/

Significance of the study…………………………………………………... 6

 

Definition of terms……………………………………………………….…7

Chapter II

Review of Related Literature……………………………………………....9

 

Chapter III

The Body……………………………………………………………………13

 

Chapter IV

Summary/Conclusion

Recommendation…………………………………………………………...20

 

Appendix A………………………………………………………………...21

 

Appendix B………………………………………………………………...22

 

Bibliography…………………………………………………………….....25

 

 

 

 

 

 

 

 

 

 

 

Acknowledgement

 

            Human is blessed by the gift of life he have. Blessed by a unique body structure, skillful mind, and a soul.

            We are very grateful that we’re alive, very blessed to give an opportunity to share the gifts God has given us. To share the blessings and the knowledge we gain for almost 18 years of our lives. We want to thank those people who became our inspirations in fulfilling the gifts we have shared, in believing that we can.

            First and foremost, we want to thank God for the talents we have. He, who became our center in everything that we considered in making this project, thank you.

            To our instructor, Ms. Reneliza Sta. Ana, thank you for this challenging project that test us the aspects of friendships, unity, hope and trust. She, who enhanced our knowledge and our skills in making this research paper.

To our family, who supported us in everything we do. This project is not possible without your financial and emotional support.

And to our dearest friends namely, Jaycee, Grace, Kath, Yves, Zhette, Rezie and Aldin. Without you guys, this project is not possible. Without your moral support and advices, maybe we cannot make this on time.

            To all the people who became our inspiration and serves as the mentor in building and enhancing our knowledge and skills. Thank you and we love you so much!

 

   Glaiza, Alex, Severino

 

CHAPTER I

INTRODUCTION

 

A. GENERAL CONSIDERATION:

 

            Blood is vital to our life, it is essential in transporting many substances through the body. When blood loss occurs, the bone marrow can produce blood cell formation to keep the circulation going. However our body can compensate for a loss of blood volume only up to certain limit. Losses of over 30%, cause severe shock, which can be fatal. Whole blood transfusion is given to replace blood loss.

 

            Although blood transfusion can save lives, people have different blood groups. It can be type, A, B, AB or O. Transfusing incompatible blood can be fatal, and by this, Erythroblastosis Fetalis occurs.

 

            Erythroblastosis Fetalis is the hemolytic disease of the unborn baby. A disease caused by Rh factor incompatibility & blood type incompatibility. Due to the difference of agglutinogen & agglutinins of the mother & the fetus inside her womb, there is big tendency of death of the unborn baby.

 

            Erythroblastosis Fetalis is much more prone to women who have Rh positive that is opposite to her husband that is Rh negative. There is a big tendency that the baby might be Rh negative. And this may cause severe anemia, brain damage and worst death.

 

B. STATEMENT OF THE PROBLEM:

           

This study envelops about the hemolytic disease of the unborn baby, due to the incompatibility of Rh factor and the blood type of the mother and her baby.

 

            Specifically this study aims to answer the following questions:

 

1.      What is Erythroblastosis Fetalis?

2.      What are the causes and symptoms of Erythroblastosis Fetalis

3.      Are there any particular ways of preventing this kind of disease?

4.      What is the main concern of blood transfusion to the occurrence of Erythroblastosis Fetalis?

5.       Is there any particular way of predicting whether the mother and the baby have incompatible Rh factor and blood type?

6.      What is the role of agglutinogen and agglutinins in this disease?

7.      What is the relation of Hydrops Fetalis in this blood type incompatibility?

 

 

 

 

 

 

 

 

 

C. OBJECTIVES OF THE STUDY:

 

            Erythroblastosis Fetalis is considered one of an unknown disease. Most people don’t have sufficient knowledge regarding this issue. We may find difficult to understand the concept of this disease. So after reading this study, the readers are expected:

 

1.      To know more about Erythroblastosis Fetalis.

2.      To be aware of the Rh factor & blood type incompatibility to every individual.

3.      To define the truth behind the old concepts of this issue.

4.      To minimize the malpractice performing blood transfusion.

5.      To be careful enough in choosing their partners in life to avoid blood type and Rh factor incompatibility.

 

 

D. Significance of the study:

 

            This study is designed for individuals, especially mothers in the prevention of baby’s miscarriage. It aims to protect the unborn baby inside the mother’s womb, other than that it is essential for the nurses or medical students in conducting blood transfusion, to avoid malpractice. This is also vital for the treatment of this disease. Lastly, this study will serve as a reference for future studies.

 

 

 

 

E. Definition of Terms:

Amniocentesis – a procedure in which a needle is inserted through a pregnant woman’s abdomen and into her uterus to withdraw a small sample of amniotic   fluid. The amniotic fluid can be examined for signs of disease and other problems affecting the fetus.

Amniotic fluid - a fluid that surrounds a fetus in the uterus.

Anemia – a condition in which there is an abnormally low number of red blood cells in the bloodstream. Major symptoms are paleness, shortness of breath, usually fast or strong heartbeats, and tiredness.

Antibody – a protein molecule produced by the immune system in response to a protein that is not recognized as belonging to the body.

Antigen – a protein that can elicit an immune response in the form of antibody formation. With regard to red blood cells, the major antigens are A, B, O, and the Rh factor.

Bilirubin – a yellow colored end-product of hemoglobin degradation. It is normally present at very low in the bloodstream; at high levels, it produces jaundice.

Cordocentesis – a procedure for delivering a blood transfusion to a fetus. It involves a fine needle being threaded through a pregnant woman’s abdomen and into the umbilical cord with the aid of ultrasound imaging.

Hemoglobin – a molecule in red blood cells that transports oxygen and give the cells their characteristic color.

Hydrops Fetalis – a condition in which a fetus or a new born baby accumulates fluids, causing swollen arms and legs, and impaired breathing.

Hyperbilirubinemia – a condition in which bilirubin accumulates to abnormally high levels in the bloodstream.

Placenta – a protective membrane that surrounds and protects the fetus during pregnancy.

Platelet – a blood factor that is important in forming blood clots.

Rh factor – an antigen that is found on the red blood cells of most people. If it is present, the blood type is referred to as Rh-positive; if absent, the blood type is Rh-negative.

RHOGAM - It is an immune serum that prevents this sensitization and her subsequent immune response.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Chapter II

REVIEW OF RELATED LITERATURE

 

            Erythroblastosis Fetalis have different points of view by some authors. Some of them don’t emphasize it too much about the topic. They mainly give the definition and just tackle some important points.

 

            Manuel Sy in his Merriam’s Nurses Dictionary in 1987, stated that Erythroblastosis Fetalis as the hemolytic disease of the newborn in which the antibodies of a mother will cross through placenta and destroy red blood cells. Simply just stated the definition of some facts and theories, he didn’t emphasize a bigger vision regarding this disease.[1]

            Both books (Textbook of Medical Physiology 8th edition and Human Physiology and Mechanisms of Disease 5th edition) that Arthur C. Guyton wrote in 1991, have just merely stated the same definition regarding Erythroblastosis Fetalis. He defined it as a disease of the fetus and newborn infant characterized by progressive agglutination and subsequent phagocytosis of the red blood cells.[2]

 

            In 1992, “Essentials of Human Anatomy and Physiology 4th edition” by John W. Hole Jr. widened the idea about the disease. He defined Erythroblastosis Fetalis as the fetus develops in a condition which when the mother, who has already developed anti-Rh agglutinins can pass slowly through the placental membrane and react with fetal red cells, causing them to agglutinate.[3]

 

            The definition and the knowledge regarding Erythroblastosis Fetalis have become wider and specific. And by 1995, Sylvia S. Mader have simply defined Erythroblastosis Fetalis on her book entitled “Human Biology” as the destruction of the child’s red blood cells due to crossing of Rh antibodies into the placenta, mostly with the mother who becomes pregnant with another positive baby.[4]

 

            In 2002, the theory made by Alice M. Stein and Judith C. Miller (NCLEX-RN Review 4th edition) have also added the ABO incompatibility in their definition of the disease. They defined it as characterized by RBC destruction in the newborn,  a disease possibly caused by Rh or ABO incompatibility the mother and the fetus.[5]

 

            And by 2004, Elaine Marieb (Essentials of Human Anatomy and Physiology) have her own definition  and views about this disease  by just simply emphasizing that if the mother is not treated and becomes pregnant again with an Rh-positive baby, her antibodies will cross through the placenta and destroy the baby’s RBC.[6]

 

            The site www.chorus.rad.mew published a view of Erythroblastosis Fetalis in 1992 and retrieved in 2004 some points about agglutinogen and agglutinin in accordance with their disease. And in their recent study envelops the used of Rhogam, It is an immune serum that prevents this sensitization and her subsequent immune response.[7]

 

            The same goes in the site of www.nlm.nih.gov in 2004, added the ABO incompatibility and emphasize the transfusion and Rh factor incompatibility. . These serious complications are life threatening, but with good medical treatment, the fatality rate is very low. According to the U.S. Centers for Disease Control and Prevention, there were 21 infant deaths in the United States during 1996 that were attributable to hemolytic disease (erythroblastosis fetalis) and jaundice.[8]

 

            The website www.erythroblastosis_fetalis.com gave the definition of this disease as the hemolytic disease of a newborn infant caused by blood group incompatibility between mother and child. Emphasizing the technique on how to determine whether the mother and her child have incompatible Rh factor through an unknown kind of test. And by this year, they discovered a therapy called photherapy in which the baby is placed under a special light. [9]

 

            And the site www.rhfactor.com described Erythroblastosis Fetalis as the hemolytic disease of the newborn or in a condition develops in a fetus when antibodies produced by the mother attack the fetus red blood cells. Stating some informations regarding another kind of treatment called exchange transfusion, in which the bilirubin concentration reduces in the infants tissues in the addition of the removal of agglutinating red blood cells, anti-Rh agglutinins, free hemoglobins and other product of erythrocyte destruction. [10]

 

            The search continuous on how to prevent much more about Erythroblastosis Fetalis and to gain more about this disease.

 

 

 

 

 

 

 

 

 

 

 

Chapter III

The Body

 

            We are truly a God’s greatest creation. We are very blessed for being here, alive, smiling. We are privileged to be brought inside our mother’s womb for nine months, because some are not that lucky to live in this world.

 

            For some reasons, we may encounter mother’s who unfortunately loses their baby before or after birth. Mostly this happens on the second, third, and even fourth pregnancies. Until the mother will found out that he baby has a hemolytic disease caused by blood type or Rh factor incompatibility called Erythroblastosis Fetalis.

 

            This disease maybe produced by any other blood group antigens, such as those of ABO system. An Rh-negative mother and a Rh-positive father, there is a tendency that the fetus will be Rh-positive. But before we move closely, let us discuss some points that is related in the occurrence of this disease.

 

            There are different blood type which eventually have also called ABO blood group. This is based upon the presence (or absence) of two major agglutinogens in red cell membrane, agglutinogen A and agglutinogen B which are present at birth as a result in inheritance. The erythrocytes of each person contain one of the four following combinations of agglutinogens; only A, only B, both A and B, or neither A nor B.

 

 

            All humans have one of four possible blood type- A,B, AB or O. A person with agglutinogen A is said to have type A blood, a person with an agglutinogen B is said to have type B blood. One with both agglutinogen A and B has said to have type AB blood, and those who have neither agglutinogen A or B has type O.

 

            Agglutinins develop spontaneously in the plasma for about two to eight months after birth. Whenever agglutinogen A is absent in the red blood cells, an agglutinin called anti-A develops, and whenever agglutinogen B is absent, an agglutinin called Anti-B develops. IN figure 1.1 in appendix A summarizes the agglutinogens and agglutinins of the ABO blood group.

 

            Therefore, persons with type A blood have agglutinin of Anti-B in their plasma. Those persons with type b blood have anti-A agglutinin, and those with type O blood have both agglutinin anti-A and anti-B.

 

            Although ABO incompatibility is not more severe, still there is a tendency of occurring Erythroblastosis Fetalis. Blood transfusion occurs here. In blood transfusion, the transfused blood must not be given or agglutinated by the agglutinins in the recipient plasma . a person with type A (anti-B) blood must not be given blood type B or AB because the red cells of both types would agglutinated by the anti-B in the recipient’s type A blood. And so the other blood type, but for AB individuals, it is always best to use donor blood of the will cause agglutination of the red blood cells before administering a transfusion to  a patient. Figure 1.2 in appendix A shows the preferred and permissible blood type for transfusions an in figure 1.1A in appendix A.

 

            There is another red blood cells antigen, called the Rh factor, also plays a role in describing a person’s in describing a person’s blood type. This was named after a rhesus monkey in which it was first studied. a person with at least one copy of the gene for the Rh factor has Rh-positive blood; if no copies are inherited, the person’s blood type is Rh-negative. In blood typing, the presence of A, B, and O antigens, plus the presence or absence of the Rh factor, determine a person’s specific blood type, such as A-positive, B-negative and so on.

 

            In blood transfusion, if a person with Rh-negative blood receives a transfusion of Rh-positive blood, the recipient’s antibody producing cells are stimulated by the presence of the Rh agglutinogen, and they begin producing an anti-Rh agglutinin. Generally, no serious consequences result from this initial transfusion, but if the Rh-negative person now sensitized to Rh-positive blood receives another transfusion of the Rh-positive blood some months later, the donor’s red cells are likely to agglutinate.

 

            When a mother whose Rh negative blood is pregnant with an Rh-positive father fetus for the first time, some pregnancy may be uneventful; however at this time of this infant’s birth (or if miscarriage occurs), the placental membrane which separates the maternal blood from the fetal blood, maybe broken, and some of the infant’s Rh-positive blood cells may get into the maternal circulation. These Rh-positive cells may then stimulate the maternal tissues to begin producing anti-Rh agglutinins. Only 15% of the white population is Rh-negative, compared to 5-7% of the black population and virtually none of Asian populations but nowadays, the population of Asians who have cases of this disease grew as the marriage of two people in different countries.

 

            Usually this incompatibility is not a factor in a first pregnancy, because few fetal blood cells reach the mother’s bloodstream until delivery. The antibodies that form after delivery cannot affect the first child. In later pregnancies fetuses and babies may be in a grave danger. The danger arises from the possibility that the mother’s antibodies will attack the fetal red blood cells. If this happens, the fetus or baby can suffer severe health effects and may die. The fetus then develops a condition called Erythroblastosis Fetalis.

 

            As said earlier, Erythroblastosis Fetalis is said to be the hemolytic disease of the newborn infant caused by blood group and Rh factor incompatibility, caused when a mother’s immune system produces antibodies against the red blood cells of her unborn child to be destroyed and the baby develops anemia. The baby’s body tries to compensate for anemia by releasing immature red blood cells called erythroblasts from the bone marrow. See appendix B, figure 2.1 for more illustrations.

 

            Erythroblasts overproduction can cause the liver and spleen to become enlarged, potentially causing liver damage or a ruptured spleen. The destroyed red blood cells release the blood’s red pigment (hemoglobin) which degrades into a yellow substance called bilirubin. Bilirubin is normally produced as red blood cells die, but the body is only equipped to handle a certain low level of bilirubin in the bloodstream at one time. Bilirubin accumulates, causing hyperbilirubinemia, a condition in which the baby becomes jaundiced. The jaundiced is apparent from the yellowish tone of the baby’s eyes and skin. If hyperbilirubinemia cannot be controlled, the baby develops kernicterus, this possibly causing permanent damage. See Appendix B fig. 2.5.

 

            Presence of the other symptoms such as Hydrops Fetalis is also included. It is characterized by an accumulation of fluids or within the baby’s body, giving it a swollen appearance. It inhibits normal breathing, the lung cannot expand fully and may contain fluid. The condition may interfere with lung growth if it will continue for an extended period. Hydrops Fetalis often results in the death of the infant shortly before or after delivery.

 

            In Kernicterus, it is extremely develops jaundiced infants, especially those with severe Rh incompatibility. Kernicterus is a neurological syndrome caused by deposition of bilirubin into the brain (CNS) tissues. Other symptoms are hypotonia, motor mental retardation and polyhydraminios. 

 

            Erythroblastosis Fetalis can be predicted before birth by determining the mother’s blood type. if the mother is Rh-negative and the father’s blood type is tested to determine whether he is Rh-positive. If the father is Rh-positive, the mother will be checked if her blood has antibodies against  Rh factor. There is a certain test to know whether the father have incompatible Rh factor, if the test demonstrate no antibodies, it will be repeated at week 26 or 27 of the pregnancy.  If the antibodies are present, treatment is begun. The disease can be also be treated through the use of the phototherapy, the use of fluorescent light. The infant will be exposed to a blue or white light . by this there is a high tendency to decrease the bilirubin concentration. Bilirubin is sensitive to white light when exposed.

 

            There is also another way to replace the Rh-positive blood with Rh-negative. There is a procedure called exchange transfusion in which the bilirubin concentration reduces in the infants tissues in the addition of the removal of agglutinating red blood cells, anti-Rh agglutinins, free hemoglobins and other product of erythrocyte destruction. There are such transfusions that not easily replace the agglutinate red cells by any remaining anti-Rh agglutinins. But in time, the baby’s blood cells forming tissues will be replaced by the donor’s blood cells with the Rh-positive cells, but by then the maternal agglutinin will be disappeared. For exchange transfusion, see appendix B, figure 2.3 and fig. 2.4.

 

            There are two techniques that are used to deliver a blood transfusion to a baby before birth. In the first, a needle is inserted through the mother’s abdomen and uterus, and into the baby’s abdomen. The red blood cells injected into the baby’s abdominal cavity are absorbed into its bloodstream.

 

            There are certain times that the baby’s bilirubin levels are gravely high; in this case cordocentisis is performed.  By this procedure, it involves sliding a very fine needle through the mother’s abdomen and guided by ultrasound, into a vein in the umbilical cord to inject red blood cells directly into the baby’s bloodstream.

 

            Even the pregnancy results in alive births, miscarriage, still birth abortion, blood typing is a universal precaution against blood incompatibility disease. Blood types cannot be changed, but adequate forewarning allows precautions and treatment that limit the danger to unborn babies.

 

            If an Rh-negative woman gives birth to an Rh-positive baby, she is given an injection of immunoglobulin G, a type of antibody protein, within 72 hours of the birth. The immunoglobulin immune system can react to them. In cases where this precaution is not taken, antibodies are created and future pregnancies may be complicated.

 

Another way in treating in anti Rh-positive antigen, it is called RHOGAM. It is an immune serum that prevents this sensitization and her subsequent immune response.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Chapter IV

 

SUMMARY/CONCLUSION:

           

Erythroblastosis Fetalis is not just due to difference in blood incompatibility but much initiated by the Rh factor incompatibility. As we go along to our research, we’ve discovered the treatment and how to identify whether the mother and the baby have blood type/Rh factor incompatibility.  The wrong theories regarding baby’s miscarriage have found out not true. We’ve learned the treatment such as through exchange transfusion or either phototherapy.

 

 

 

RECOMMENDATION:

 

            For further reading, the authors recommend the use of other resources like medicine, OB-Gyne, biology books to enhance your knowledge about hemolytic disease of the newborn baby. It will help you a lot to analyze and understand regarding this disease. We also recommend those people who would like to continue our research to focus more in the treatment of Erythroblastosis Fetalis.  For your own benefits see also www.erythroblastosis_fetalis.com.

 

 

 

 

 

 

 

 

 

APPENDIX A

 

Blood type

Agglutinogen

Agglutinin

A

A

anti B

B

B

anti A

AB

A & B

Neither anti A nor anti B

O

Neither A nor B

Both anti A & anti B

 

Fig. 1.1 (Agglutinogen and Agglutinins of the ABO blood group)

 

 

 

Blood Type

Preferred Transfusions

Permissible Transfusion (in extreme energy)

A

A

A,O

B

B

B,O

AB

AB

AB,A,B,O

O

O

O

 

Fig. 1.2 Preferred and Permissible Blood type for transfusions

 

 

 

 

APPENDIX B

 

 

Fig. 2.1 Agglutinogen and Agglutinins of the ABO blood group

 

 

Fig.2.2 The action of Rh agglutinogen and agglutinins in mother and the baby

 

 

 

fig. 2.3 hemolytic disease of newborn, second pregnancy

 

 

 

Fig. 2.4 an intrauterine transfusion, also known as exchange transfusion

 

 

 

 

 

 

 

 

 

Fig. 2.5 a microscopic view of Bilirubin

 

 

Fig. 2.6  a microscopic view showing the difference of ABO and Rh factor incompatibility

 

 

Fig. 2.7 a microscopic view of Erythroblastosis Fetalis

 

Bibliography

 

 

A. Books

 

Guyton, Arthur C. Human Physiology and Mechanisms of Disease 5th

         edition. W.B. Saunders Company, pp. 270-271.

 

Guyton, Arthur C. Textbook of Medical Physiology 8th edition. W.B.

         Saunders Company, Harcourt Brace Jovanovich Inc. 1991. pp. 387-388

 

Hole, John Jr. W. Essentials of Human Anatomy and Physiology 4th

         edition. WM.C. Brown Publisher, 1992. pp. 381-385.

 

Mader, Sylvia S. Human Biology. WM.C. Brown Publisher, pp. 136-137.

 

Marieb, Elaine N. Essentials of Human Anatomy and Physiology, San

         Francisco, California: Pearson Education Inc.

 

Lisowski, Strauss. Biology, The Web of Life 2nd Edition. San Francisco,

         California: Pearson Education Inc.

 

Stein, Judith Miller. NCLEX-RN Review 4th Edition. Singapore: Delmar

          Publishers, 2000.

 

Sy, Manuel C. Merriam’s Nurses Dictionary. Manila: Merriam and

         Webster Bookstore Inc., 1987.

 

 

B. Internet

 

Blood Incompatibility (1992) .Blood Incompatibility and Rh Factor

          Incompatibility Retrieved, January 15, 2004 from

          http://www.chorus.rad.mew.edu

 

Erythroblastosis Fetalis (1990),.Erythroblastosis Fetalis

          Retrieved, January 15, 2004 from

          http://nlm.nih.gov

 

 

Erythroblastosis Fetalis (1997), Erythroblastosis Fetalis

           Retrieved, January 14, 2004 from

           http://www.erythroblastosis_fetalis.com

 

Erythroblastosis Fetalis (2000), Rh factor incompatibility

           Retrieved, January 14, 2004 from

           http://www.rhfactor.com

 



[1]Manuel Sy, Merriam’s  Nurses Dictionary ( Manila: Merriam and Webster Bookstore Inc.,1985)

 

[2]Arthur C. Gayton, Textbook of Medical Physiology 8th edition (W.B. Saundres Company, Hardcourt Brace Jovanovich Inc., 1991) pp. 387-388.

[3]John W. Hole Jr., Essentials of Human Anatomy and Physiology 4th edition (Wm.C. Brown Publisher, 1992) pp. 381-385.

[4]Sylvia S. Mader, Human Biology (WM.C Brown Publisher, 1995) pp. 136-137.

[5]Alice M. Stein and Judith C. Miller, NCLEX-RN Review 4th edition (Singapore: Delmar Publisher, 2000).

[6] Elaine N. Marieb, Essentials of Human Anatomy and Physiology (San Francisco, California: Pearson Education Inc., 2004).

[7]Blood Incompatibility (1992), Blood Incompatibility and Rh Factor Incompatibilyty

Retrieved, January 15, 2004 from

http://www.chorus.rad.mew.edu.

[8]Erythroblastosis Fetalis (1990),. Erythroblastosis Fetalis

                Retrived, January 15, 2004 from

                http://nlm.nih.gov. 

[9]Erythroblastosis Fetalis (1997),. Erythroblastosis Fetalis

                Retrived, January 14, 2004 from

                http://www.erythroblasosis_fetalis.com.

[10]Erythroblastosis Fetalis ( 2000), Rh factor incompatibility

                Retrieved, January 14, 2004 from

                http://www.rhfactor.com.



 


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