Last year according to Dr. D.

Buenafe (personal communication, March 19, 2011) a pediatric doctor in Labasa Hospital the number of hemolytic incompatibility in Fiji is unknown. However, two cases of neonates were diagnosed with hemolytic disease. Sadly, the neonates died within their first week of life. This hemolytic disease of neonates is caused by hemolytic incompatibility in pregnancy. This is when maternal and fetal blood type that does not match is mixed and thus causing a reaction called hemolysis. According to Mosby dictionary for medical, nursing and allied health (1990) hemolysis is defined as The breakdown of red blood cells and the release of hemoglobin. In the world according to Cooper and Fraser (2003) 15% of the population of Caucasians is affected compared to the 8% of Africans and 1% of Asian populations. In this report I will be talking about what is hemolytic incompatibility, how it is caused, its mechanism in the human body and the management for mothers who undergo this incompatibility. There are two types of hemolytic incompatibility in pregnancy which are ABO incompatibility and Rh incompatibility. ABO incompatibility is much milder and doesnt have severe side effects to the fetus compared to Rh incompatibility. This is because A and B antibodies are class immunoglobin M, which have five antibodies attached together as its structure thus are too big to cross the placenta. However, Rhesus incompatibility occurs when a mother, of rhesus negative blood type, defense system gets sensitized by a rhesus-positive red blood cell from her fetus during her first pregnancy. Although sensitization occurs during the first pregnancy the massive

breakdown of fetal red blood cells will occur during her next pregnancy if her baby is a rhesus positive blood type. For such events to occur fetal blood must enter the maternal circulation either during or before delivery for example, during a miscarriage, heavy vaginal bleeding during pregnancy as a result of a fall or any physical impact on the mother or even during placenta abruption. Mixing of fetal and maternal blood during delivery is possible because of the exposed broken villi of the placenta when the placenta itself is being separated from the mothers uterus (Pillitteri,1995) (Callahan, Caughey & Heffner, 2004). Inorder to understand the mechanism of Rh incompatibility we need to know about blood types and how the transportation across the placenta occurs. Firstly, a fetus blood type is inherited from its parents. One gene from its mother and the other gene from its father, these two genes will combine and produce the fetus blood type. These two genes determine the blood type by forming proteins or antigens called agglutionogens that will be present on the red blood cell membrane. There are three types of alleles that produces these proteins that is type A, B and O, each having their own distinctive property. As for the O allele this allele will not code for any protein on the membrane of the red blood cell. The O allele does not show any characteristic effect if pair up with either A or B, thus it is said that O allele is recessive whereas A and B are considered to be codominant alleles. Codominant meaning A and B if paired together will show A and B characteristic. Therefore ABO blood group system arises, this system uses these agglutinogens to put blood into four groups that is A, B, AB or O. Blood group A arise

from genotype AA or AO, blood group B from genotype of BB or BO, blood type AB for genotype AB and blood type O from genotype OO. Furthermore, antibodies that are against the antigen on the RBC will not be found in the same plasma the RBC is in (Thibodeau & Patton, 2007). Another way blood can be divided is using the Rhesus factor. Rhesus factor can be present or not present on an individuals red blood cell regardless of what ABO blood system they are in. It is said that the Rhesus factor also known as antigen D is located on the short arm of chromosome one. Thus an individuals genes will determine if they are rhesus negative or rhesus positive. This genes are also retrieved from the fetus parents either they can be both recessive (dd) or dominant (DD) thus regarded has homozygous genes or one dominant and one recessive thus regarded as heterozygous genes (DD). If a mother is a Rh negative is it said that her genes are both recessive as recessive genes do not express their characteristics. If a father is said to be a Rh positive then his genes can either be both dominant or a heterozygous gene. Secondly, the placenta consist of four layers of tissue that prevents maternal blood to mix with the fetal blood. The external layer of the villus consist of the syncitiotrophoblast and cytotrophoblast then comes the villi connective tissues and endothelium of the fetal capillaries. These layers only let certain substances or

molecules to enter the fetal circulation. The size of the molecules is one factor that will determine the rate of diffusion between the layers. It is said that a molecular weight of less than 500 can readily diffusion from the maternal to the fetal circulation. Thus the

smaller the molecules the faster the diffusion some examples of molecules are oxgygen, carbondioxide, water and most electrolytes. However, substances that are very big in size find it hard to travel across these layers with the exception of immunegamma globulin G (IgG) antibodies. IgG antibodies are structured with two antibodies attached together and with the help of a receptor mediated mechanism it is able to pass through the layers (Cunningham et al, 2001), The pathophysiology of Rh incompatibility first occurs by the sensitizing of a Rh negative mother by a Rh positive red blood cell from her fetus due to fetomaternal hemorrhage or even during normal delivery. Since the fetal red bood cell is a foreign antigen to the mothers body, the B-lymphocytes of the mother recognizes this and produces antibodies against this foreign antigen. If this mother by chance gets an Rh positive fetus in her second pregnancy her body automatically rapidly produces antibodies against this antigen. These antibodies known as anti-D antibodies are said to be class IgG antibodies and thus can cross the placental into the fetal circulation and attaches itself to the Rh positive RBC of the fetus. (Cunningham et al, 2001).An antibody-antigen complex arises and a type II hypersensivity reaction occurs where fetal RBC are destroyed (Mrs Darshan, FNK notes, 2010). The fetal RBC are then broken down into two components Heme and globin. The Heme component is than broken down into iron and bilirubin. Due to less fetal RBC this leads fetal to have low levels of hemoglobin thus oxygen distribution in the fetal are disrupted. According to Cunningham et al (2001) this event causes excessive reproduction of immature RBC in

the bone marrow and areas of the extramedullary hematopoiesis usually located in the liver and spleen to replace RBC lost. Since not enough oxygen is reaching the fetal cells this cause the heart to pump harder and harder. Thus causes pheripheral blood redistribution to aid the heart as a result fluid buildup in places such as the thorax, abdomen and skin (Dr D. Buenafe, personal communication, March 19, 2011). Fluid in the abdomen is referred to as fetal ascites. In addition fetal bilirubin levels are also increased that can cause neurological damage as high levels of bilirubin can settle in the fetal brain (Cooper and Fracer, 2003). Knowing the pathophysiology we can now detect the signs and symptoms of a pregnant mother undergoing hemolytic incompatibility. During her antenatal visit the mother can voice out that she is feeling decrease fetal activity compared to previous days. Her ultrasound could show fetal ascites, fetal growth retardation, polyhydrominous and congestive heart failure. Fetus hemoglobin level would be low however there will be an increase in fetal bilirubin levels. Maternal side is not really affected during this incompatibility. However because of sensitization she would have produced anti-D antibodies. She may feel stress due to uncertainty of her fetal outcome. On the other hand the fetus will undergo many effects. These include fetal ascites, enlargement of the liver and spleen, fluid in the thorax where fetal lung development maybe affected and also hypoxia which can cause fetal growth retardation. Inaddition neonates can have neonatal jaundice where neonate will

look yellowish in color. Furthermore, neonatal anemia where the neonate will appear pale and swollen at birth (Cunningham et al, 2001). Inorder to identify hemolytic incompatibility in pregnant mothers they undergo several test. Firstly, antibody screening should be done on antenatal clinic appointments for Rh negative mothers. Maternal blood is taken to test for the presence of Rh antibodies by using indirect Coombs test. An antibody titre of less than 1:16 is said to be manageable however if it exceeds this it is said that the fetus is going through a condition called fetal hydrops. Secondly, amniocentesis is done by taking amniotic fluid and testing it for bilirubin levels. The measurements are placed on Liley chart which is divided into three zones. Zone one being less complicated to zone 3 where fetus is diagnosis with anaemia. Thirdly, middle cerebral artery Doppler ultrasound is done to assess the velocity of systolic blood flow in the middle cerebral artery. It is said that anemic fetus will have a faster systolic blood flow than a normal fetus. Thus this test will help diagnosis the severity of anemia in the fetus. Fourthly, using Klehaver-Betke test will assess the severity of fetal bleeding by calculating the percentage of fetal cells in the maternal circulation. In addition cordiocentesis is done by obtaining fetal blood through the umbilical cord. Cordiocentesis will determine the fetus hemoglobin levels and the percentage of the total blood volume fetal red blood cells take up (Bader, 2005). These test results will determine the severity of the disease by correlating with the results to see which organs are affected.

A mother who is diagnosed with this incompatibility will need to undergo frequent antenatal monitoring and treatment of RHD isoimmunization if she has not been sensitized yet. She will receive a treatment of anti-D antibodies at 28 weeks and 34weeks of gestation. If isoimmunization has occurred the aim is to reduce any more complications until the fetus is ready to be delivered thus maternal blood is tested every four weeks to see any increase in antibody titre (Cooper & Fraser, 2003). Furthermore, in cases where the life of the fetus is being compromised labor has to be induced. The management for these cases during labor is to aid comfort during delivery. If the fetus is already suffering from severe anemia the doctor may order intrauterine blood transfusions. In cases where the baby is too big to come through the vaginal passage, due to fetal ascites, caesarian section has to occur (Cunningham et al, 2001). In postpartum management Rh negative mother will received an Anti-D IgG injections within 72 hours after delivery. In order to reduce the number of anti-D antibodies the mothers body has produced. Counseling is done to mothers to explain about the condition of their newborn and the outcome. For the neonates they will have blood transfusions done to increase their hemoglobin level due to severe anemia. In addition, if lungs are not fully matured they will be put under oxygen therapy or helped to breathe using machines. To prevent a nonsensitized Rh negative mother to undergo this hemolytic incompatibility 300ug of anti-D IgG injections is given intramuscularly on the upper arm after she have had any kind of blood transfusion or after her first pregnancy. Any

events such as ectopic pregnancy, a miscarriage or any other events where fetal and maternal blood can mix, anti-D IgG injection should be given. It is important to note that this injection is not effective on sensitized Rh negative mothers. However is still given to atleast reduce the amount of anti-D antibodies present in her body. If this incompatibility is prevented complications such as dystocia and intrauterine fetal death can be prevented. Before the mother is sent home after her delivery is it important to educate her on the complications of hemolytic incompatibility and what she can do to prevent her from undergoing this complications again. Educate her that during her subsequent pregnancy she should come in for antenatal checkup as early as possible to prevent any complications. If she is satisfied with the number of children she has we can advise her on using family planning methods that she can use. To conclude, people neglect the importance of antenatal checkups. If all pregnant mothers come during their early weeks of gestation and are compliance to their clinic dates these complications such as hemolytic incompatibility will not occur. Thus the number of neonatal deaths due to complication can be reduced and prevented. (approx of 1998 words).

Reference list Bader, T. J. (2005). OB/GYN (3rd ed.). Philadelphia: Mosby.

Callahan, T. L., Caughey, A. B., & Heffner, L. J. (2004). Fetal complications of pregnancy. In Obstetrics and Gynaecology (3rd ed.). (pp. 77-79). Massachusetts: Blackwell.

Cunningham, F. G., Gant, N. F., Leveno, K. J., Gilstrap, L. C., Hauth, J. C., & Westrom, K. D. (2001). Diseases and injuries of the fetus and newborn. In Williams Obsterics (21st ed.). (pp. 1058-1071). New York: McGraw-Hill.

Fracer, D. M., & Cooper, M. A. (2003). Myles textbook for midwives (14th ed.). New York: Churchill-Livingstone. Glanze, W. D., Anderson, K. N., & Anderson, E. L. (1990). Mosbys Dictionary: Medical, Nursing and allied Health (3rd ed.). (pp. 558). St Louise: Mosby.

Pilliteri, A. (1995). High Risk Pregnancy: The women who develops a complication of pregnancy. In Maternal and child health nursing care of the childbearing and childbearing family (2nd ed.). (pp. 415-417). Philadelphia: Lippincott.

Thibodeau, G. A., & Patton, K. T. (2007). Anatomy and Physiology (6th ed.). St Louise: Mosby.