Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper

Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper Hemolytic disease of the newborn (HDN) is a blood disorder in a fetus or newborn infant. In some infants, it can be life threatening. What is hemolytic disease of the newborn? Hemolytic disease of the newborn (HDN) is a blood problem in newborn babies. It occurs when your baby’s red blood cells break down at a fast rate. It’s also called erythroblastosis fetalis. Hemolytic means breaking down of red blood cells. Erythroblastosis means making immature red blood cells. Fetalis means fetus. What causes HDN in a newborn? All people have a blood type (A, B, AB, or O). Everyone also has an Rh factor (positive or negative). There can be a problem if a mother and baby have a different blood type and Rh factor. HDN happens most often when an Rh negative mother has a baby with an Rh positive father. If the baby’s Rh factor is positive, like his or her father’s, this can be an issue if the baby’s red blood cells cross to the Rh negative mother. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper Pregnancies potentially affected by HDFN should be cared for by specialist teams with facilities for early diagnosis, intrauterine transfusion and support of high-dependency neonates. Permalink: https://nursingpaperessays.com/ hemolytic-diseas…ions-essay-paper / HDFN occurs when the mother has IgG red cell alloantibodies in her plasma that cross the placenta and bind to fetal red cells possessing the corresponding antigen. Immune haemolysis may then cause variable degrees of fetal anaemia; in the most severe cases the fetus may die of heart failure in utero (hydrops fetalis). After delivery, affected babies may develop jaundice due to high unconjugated bilirubin levels and are at risk of neurological damage. The three most important red cell alloantibodies in clinical practice are to RhD (anti-D), Rhc (anti-c) and Kell (anti-K). The major effect of anti-K is suppression of red cell production in the fetus, rather than haemolysis. Hemolytic disease of the fetus and newborn (HDFN) is rare condition that occurs when maternal red blood cell (RBC) or blood group antibodies cross the placenta during pregnancy and cause fetal red cell destruction. The fetal physiological consequences of severe anemia in the fetus can also lead to edema, ascites, hydrops, heart failure, and death. In less severe cases, the in utero red cell incompatibility can persist postnatally with neonatal anemia due to hemolysis, along with hyperbilirubinemia and erythropoietic suppression. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper Previous Section Next Section Epidemiology and pathophysiology There are an estimated 3/100 000 to 80/100 000 cases of HDFN per year in the United States.1 The maternal blood group antibodies that cause HDFN can be naturally occurring ABO antibodies (isohemagglutinins), or develop after exposure to foreign RBC; the latter are called blood group alloantibodies. For HDFN to occur, the fetus must be antigen positive (paternally inherited) and the mother must be antigen negative. Several studies have investigated the prevalence of red cell sensitization. In a large series of 22 102 females in the US, 254 (1.15%) of the women were found to have a red cell alloantibodies, of whom 18% had more than one alloantibody.2 In the Netherlands, the prevalence of red cell alloantibodies detected in the first trimester was 1.2%.3 The most common cause of blood group incompatibility results from the ABO blood group system, with incompatibility present in up to 20% of infants.4 However, because anti-ABO antibodies are predominantly IgM class, most are not effectively transported across the placenta. In addition, the A and B antigens are not well developed on fetal red blood cells. Together, this results in a low rate of clinically severe HDFN due to ABO compatibility, although the incidence of more mild disease varies from 1:150 to 1:3000, depending on the parameters used for the case definition, such as bilirubin levels or neonatal anemia.1 Because maternal ABO antibodies are present without previous sensitization, HDFN due to ABO antibodies can occur in the first pregnancy and has a recurrence rate up to 87%.1 It is most commonly seen in group O mothers with group A infants (European ancestry) or group B infants (African ancestry). Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper The most clinically significant forms of HDFN are caused by maternal blood group alloantibodies are of IgG1 and IgG subclasses, which cause hemolysis more effectively than other IgG subclasses. IgG1 and IgG3 are transported across the placenta by the Fc receptor from the second trimester onward.5 Once in the fetal circulation, the antibody binds antigen-positive fetal red cells that are then cleared by the fetal spleen. Free hemoglobin is metabolized into bilirubin that is conjugated by the maternal liver. As anemia worsens, fetal hematopoiesis increases, termed “erythroblastosis fetalis” and organs involved in red blood cell synthesis (liver, spleen) may enlarge. In the most severe cases, portal hypertension and reduced hepatic synthesis of albumin leads to low plasma oncotic pressure, edema and ascites. “Hydrops fetalis” refers to the state of widespread effusions and associated high-output cardiac failure and death.6 A large population-based study in Sweden found that the presence of maternal red cell antibodies was significantly associated with adverse outcomes, with a 1.4-2.4 relative risk of preterm delivery and a 1.5-2.6 relative risk of stillbirth in mothers with red cell allosensitization as compared to those without Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper Antibodies are produced when the body is exposed to an antigen foreign to the make-up of the body. If a mother is exposed to a foreign antigen and produces IgG (as opposed to IgM which does not cross the placenta), the IgG will target the antigen, if present in the fetus, and may affect it in utero and persist after delivery. The three most common models in which a woman becomes sensitized toward (i.e., produces IgG antibodies against) a particular antigen are hemorrhage, blood transfusion, and ABO incompatibility. Fetal-maternal hemorrhage, which is the movement of fetal blood cells across the placenta, can occur during abortion, ectopic pregnancy, childbirth, ruptures in the placenta during pregnancy (often caused by trauma), or medical procedures carried out during pregnancy that breach the uterine wall. In subsequent pregnancies, if there is a similar incompatibility in the fetus, these antibodies are then able to cross the placenta into the fetal bloodstream to attach to the red blood cells and cause their destruction (hemolysis). This is a major cause of HDN, because 75% of pregnancies result in some contact between fetal and maternal blood, and 15-50% of pregnancies have hemorrhages with the potential for immune sensitization. The amount of fetal blood needed to cause maternal sensitization depends on the individual’s immune system and ranges from 0.1 mL to 30 mL Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper The woman may have received a therapeutic blood transfusion. ABO blood group system and the D antigen of the Rhesus (Rh) blood group system typing are routine prior to transfusion. Suggestions have been made that women of child-bearing age or young girls should not be given a transfusion with Rhc-positive blood or Kell1-positive blood to avoid possible sensitization, but this would strain the resources of blood transfusion services, and it is currently considered uneconomical to screen for these blood groups. HDFN can also be caused by antibodies to a variety of other blood group system antigens, but Kell and Rh are the most frequently encountered. The third sensitization model can occur in women of blood type O. The immune response to A and B antigens, that are widespread in the environment, usually leads to the production of IgM or IgG anti-A and anti-B antibodies early in life. Women of blood type O are more prone than women of types A and B to making IgG anti-A and anti-B antibodies, and these IgG antibodies are able to cross the placenta. For unknown reasons, the incidence of maternal antibodies against type A and B antigens of the IgG type that could potentially cause hemolytic disease of the newborn is greater than the observed incidence of “ABO disease.” About 15% of pregnancies involve a type O mother and a type A or type B child; only 3% of these pregnancies result in hemolytic disease due to A/B/O incompatibility. In contrast to antibodies to A and B antigens, Rhesus antibodies are generally not produced from exposure to environmental antigens.[citation needed] In cases where there is ABO incompatibility and Rh incompatibility, the risk of alloimmunization is decreased because fetal red blood cells are removed from maternal circulation due to anti-ABO antibodies before they can trigger an anti-Rh response. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper Hemolytic disease of the fetus and newborn (HDFN) is a condition in which transplacental passage of maternal antibodies results in immune hemolysis of fetal / neonatal red cells. The implicated antibodies could be naturally occurring (anti A, anti B) or immune antibodies which develop following a sensitizing event like transfusion or pregnancy. The hemolytic process may result in anemia or hyperbilirubinemia or both; thereby affecting fetal / neonatal morbidity and mortality. Before the discovery of the Rhesus immunoglobulin (Rh IG), HDFN due to anti D was a significant cause of perinatal mortality. Administration of Rh IG to Rh (D) negative women during pregnancy and shortly after the birth of D positive infants has reduced the incidence of Rh D hemolytic disease.[1] ABO incompatibility is now the single largest cause of HDFN in the western world.[2] Consequent to the introduction of routine Rh IG immunoprophylaxis; alloantibodies other than anti D have emerged as an important cause of HDFN and are now responsible for greater proportion of these cases.[3] Timely detection and close follow up of this condition is necessary to reduce harmful effects on the newborn. Transfusion services play a vital role in the antenatal detection, monitoring and providing transfusion support to such cases. Hemolytic disease of the newborn may result in high levels of bilirubin in the blood (hyperbilirubinemia), a low red blood cell count (anemia), and, very rarely, in the most severe forms, death. Bilirubin is a yellow pigment produced during the normal breakdown of red blood cells. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper Rh incompatibility The Rh factor is a molecule on the surface of red blood cells in some people. Blood is Rh-positive if a person’s red blood cells have the Rh factor. Blood is Rh-negative if a person’s red blood cells do not have the Rh factor. Most people are Rh-positive. When a baby has Rh-positive blood and the mother has Rh-negative blood, the two have Rh incompatibility. As a result, the immune system of an Rh-negative mother may recognize the Rh-positive fetus’s red blood cells as “foreign” and produce antibodies against the Rh factor on the fetus’s red blood cells (this process is called Rh sensitization). The mother’s antibodies can pass from her blood through the placenta into the fetus’s blood before delivery. The mother’s antibodies attach to and destroy (hemolyze) the fetus’s red blood cells. The rapid breakdown of red blood cells begins while the fetus is still in the womb and continues after delivery. A mother who is Rh-negative can produce the Rh antibodies if she is exposed to Rh-positive red blood cells. The most common way women are exposed to Rh-positive blood is when they have a fetus who is Rh-positive. Mothers are exposed to the most blood from the fetus during delivery, so that is when most Rh sensitization occurs. However, mothers also can be exposed earlier in pregnancy, for example, during a miscarriage or elective abortion, during a diagnostic test on the fetus (such as amniocentesis or chorionic villus sampling), if they have an injury to their abdomen, or if the placenta separates too early (placental abruption). Thus, most hemolytic disease happens to a fetus whose mother was sensitized during an earlier pregnancy. However, rarely, a mother may produce antibodies early in a pregnancy and then these antibodies affect the same fetus later during that pregnancy. Exposure may also occur outside of pregnancy, for example if the mother was transfused with Rh-positive blood at any time earlier in her life. Once the mother has been exposed and developed antibodies, problems are more likely with each subsequent pregnancy in which the fetus is Rh-positive. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper ABO incompatibility Sometimes other blood group incompatibilities may lead to a similar (but milder) hemolytic disease. For example, if the mother has blood type O and the fetus has blood type A or B, then the mother’s body produces anti-A or anti-B antibodies that can cross the placenta, attach to fetal red blood cells, and cause their breakdown (hemolysis), leading to mild anemia and hyperbilirubinemia. This type of incompatibility is called ABO incompatibility. ABO incompatibility usually leads to less severe anemia than Rh incompatibility and, unlike Rh incompatibility, it usually gets less severe with each subsequent pregnancy. Symptoms After delivery, newborns who have hemolytic disease may be swollen, pale, or yellow (a condition called jaundice) or may have a large liver or spleen, anemia, or accumulations of fluid in their body. Diagnosis Blood tests of the mother during pregnancy and sometimes the father At the first prenatal visit during a pregnancy, the mother gets a blood test to determine whether she has Rh-negative or Rh-positive blood. If the mother has Rh-negative blood and tests positive for anti-Rh antibodies or if she tests positive for another antibody that can cause hemolytic disease of the newborn, the father’s blood is checked. Rh sensitization is a risk if the father has Rh-positive blood. In these situations, the mother is given periodic blood tests during the pregnancy to check for Rh antibodies. Nothing further needs to be done as long as no antibodies are detected. If antibodies are detected, special tests on the mother and fetus are done during the pregnancy. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper Prevention Injection of immune globulin during pregnancy and after delivery To prevent Rh-negative women from developing antibodies against their fetus’s red blood cells, they are given an injection of an Rh0(D) immune globulin preparation at about 28 weeks of pregnancy and again within 72 hours after delivery. The immune globulin rapidly coats any Rh-positive fetal red blood cells that have entered the mother’s circulation so they are not recognized as “foreign” by the mother’s immune system and thus do not trigger formation of anti-Rh antibodies. This treatment usually prevents hemolytic disease of the newborn from developing. Treatment Before delivery, sometimes blood transfusion for the fetus After delivery, sometimes more transfusions Treatment of jaundice if present If anemia is diagnosed in the fetus, the fetus may be given a blood transfusion before birth. Transfusions may be done until the fetus has matured and can be delivered safely. Before delivery, the mother may be given corticosteroids to help the fetus’s lungs mature to prepare for the possible delivery of the fetus earlier than usual if necessary. After delivery, the newborn may need more transfusions. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper Severe anemia caused by hemolytic disease of the newborn is treated in the same way as any other anemia (see treatment of anemia). Doctors also observe the newborn for jaundice. Jaundice is likely to occur because the rapid breakdown of red blood cells produces a lot of bilirubin. Bilirubin is a yellow pigment, and it gives the newborn’s skin and whites of the eyes a yellow appearance. If the bilirubin level gets too high, it can injure the baby. High bilirubin levels can be treated by exposing the newborn to special bright lights (phototherapy or “bili lights”) or, occasionally, by having the newborn undergo an exchange transfusion. Very high levels of bilirubin in the blood can lead to brain damage (kernicterus), unless it is prevented by these measures. RAADP should be offered to all RhD negative, non-sensitised women. They should be supplied with clear written information and informed consent should be obtained. Both two-dose (at 28 and 34 weeks) and larger single-dose (at 28–30 weeks) prophylactic anti-D regimens reduce maternal sensitisation but there are no comparative data to confirm their relative efficacy. The single-dose regimen may achieve better compliance but anti-D levels at term may be low in some women. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper Recommended anti-D Ig doses for RAADP: Two-dose regimen – minimum of 500 IU at 28 and 34 weeks. Single-dose regimen – 1500 IU at 28–30 weeks. RAADP should be given even if the woman has received anti-D Ig prophylaxis for a potentially sensitising event earlier in the pregnancy. The transfusion laboratory should be informed of the administration of RAADP in case the woman requires pre-transfusion testing. It is not possible to differentiate between ‘prophylactic’ and ‘immune’ (allo-) anti-D in maternal blood in laboratory tests. 9.5.4: Anti-D Ig prophylaxis after the birth of a RhD positive baby or intrauterine death Following the birth of a child to a RhD negative woman, a cord blood sample should be tested to determine the baby’s ABO and Rh group. If the cord Rh group is unclear, or if a sample cannot be obtained, the baby should be assumed to be RhD positive for anti-D Ig administration purposes. A direct antiglobulin test (DAT) on the cord sample should only be performed if HDFN is suspected. If the baby is RhD positive, a minimum of 500 IU anti-D Ig should be administered to non-sensitised RhD negative women, within 72 hours of the birth. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper A maternal blood sample for confirmation of her ABO and RhD status and for FMH screening should be taken within 2 hours of delivery. A dose of 500 IU anti-D Ig given IM will cover a FMH of up to 4 mL. If an additional dose is required, it should be based on 125 IU/mL fetal red cells if given IM or 100 IU/mL if given IV (manufacturer’s instructions on dosing should be followed and anti-D Ig produced for IM use only must not be given IV). If a FMH of >4 mL is detected, follow-up maternal blood samples should be tested 72 hours after an IM dose (48 hours if given IV) to confirm clearance of fetal red cells from the maternal circulation. In the case of very large FMH, administration of IV anti-D Ig may be more convenient and less painful than large-volume or repeated IM administration. If anti-D Ig is inadvertently omitted, there may be some benefit in giving prophylaxis up to 10 days. If intraoperative cell salvage is used at Caesarean section, 1500 IU anti-D Ig should be administered immediately after the procedure if the baby is RhD positive and maternal FMH screening should be performed. 9.5.5: Inadvertent transfusion of RhD positive blood If RhD positive blood is inadvertently transfused to a non-sensitised RhD negative woman of child-bearing potential, the advice of a transfusion medicine specialist should be obtained and the appropriate dose of anti-D Ig administered (125 IU/mL fetal red cells if given IM or 100 IU/mL IV). For transfusions >15 mL, IV anti-D Ig is more practical. FMH testing should be carried out at 48-hour intervals and further anti-D Ig given until clearance of fetal cells is confirmed. If more than one unit of red cells has been transfused, red cell exchange should be considered to reduce the load of RhD positive cells and the dose of anti-D Ig required. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper Red cell alloantibodies in the mother occur as a result of previous pregnancies (where fetal red cells containing paternal blood group antigens cross the placenta) or blood transfusion. Naturally occurring IgG anti-A or anti-B antibodies in a group O mother can cross the placenta but rarely cause more than mild jaundice and anaemia in the neonate (ABO haemolytic disease). Recommendations for serological screening for maternal red cell antibodies in pregnancy are summarised in Table 9.1 (see also BCSH Guideline for Blood Grouping and Antibody Testing in Pregnancy – http://www.bcshguidelines.com). Knowledge of any maternal red cell alloantibodies is also important in providing compatible blood without delay in the event of obstetric haemorrhage. HDFN due to anti-D This is the most important cause of HDFN and may occur in RhD negative women carrying a RhD positive fetus. Around 15% of white Europeans are RhD negative. Typically, the mother is sensitised by the transplacental passage of RhD positive fetal red cells during a previous pregnancy – usually at delivery or during the third trimester. HDFN then occurs in subsequent RhD positive pregnancies when further exposure to fetal red cells causes a secondary immune response and increased levels of maternal IgG anti-RhD alloantibodies that can cross the placenta. Before the introduction of routine postnatal prophylaxis with anti-RhD immunoglobulin (anti-D Ig, standard dose 500 IU) in the 1970s, HDFN was a major cause of perinatal mortality in the UK (46/100 000 births). Rates of sensitisation fell further with the introduction of routine antenatal anti-D prophylaxis in the third trimester (RAADP) and mortality is now <1.6/100 000 births. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper 9.5.2: Potentially sensitising events RhD negative mothers can also produce anti-RhD in response to potentially sensitising events that may cause feto-maternal haemorrhage (FMH) during pregnancy or by blood transfusion. The BCSH Guideline for the Use of Anti-D Immunoglobulin for the Prevention of Haemolytic Disease of the Fetus and Newborn 2013 lists the following as potentially sensitising events in pregnancy: Amniocentesis, chorionic villus biopsy and cordocentesis Antepartum haemorrhage/vaginal bleeding in pregnancy External cephalic version Fall or abdominal trauma Ectopic pregnancy Evacuation of molar pregnancy Intrauterine death and stillbirth In utero therapeutic interventions (transfusion, surgery, insertion of shunts, laser) Miscarriage, threatened miscarriage Therapeutic termination of pregnancy Delivery – normal, instrumental or Caesarean section Intraoperative cell salvage. Recommendations for the administration of prophylactic anti-D Ig for potentially sensitising events are summarised in Table 9.2 and the reader is referred to the current BCSH Guideline for the Use of Anti-D Immunoglobulin for the Prevention of Haemolytic Disease of the Fetus and Newborn (http://www.bcshguidelines.com) and the Royal College of Obstetricians and Gynaecologists’ Green Top Guideline No. 22 on the use of anti-D immunoglobulin for Rhesus D prophylaxis (http://www.rcog.org.uk/files/rcog-corp/GTG22AntiDJuly2013.pdf) for up-to-date guidance. An intramuscular (IM) injection of 125 IU anti-D Ig, or 100 IU of the appropriate preparation given intravenously (IV), ‘covers’ a FMH of 1 mL red cells. Women with anomalous RhD typing results should be treated as RhD negative until confirmatory testing is completed. Anti-D Ig should be administered within 72 hours of the potentially sensitising event (although some benefit may occur up to 10 days if treatment is inadvertently delayed). Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper If the pregnancy has reached 20 weeks or more, administration of anti-D Ig should be accompanied by a test on the mother’s blood to estimate the volume of fetal red cells that have entered the maternal circulation (e.g. Kleihauer test) in case it exceeds that covered by the standard dose of anti-D Ig. The Kleihauer test detects fetal cells, which contain HbF, in the maternal blood. If the screening Kleihauer test suggests a FMH >2 mL then the FMH volume should be confirmed by flow cytometry, which accurately measures the population of RhD positive cells. Detailed guidance is given in the 2009 BCSH Guidelines on the Estimation of Fetomaternal Haemorrhage (http://www.bcshguidelines.com). Signs of hemolytic disease of the newborn include a positive direct Coombs test (also called direct agglutination test), elevated cord bilirubin levels, and hemolytic anemia. It is possible for a newborn with this disease to have neutropenia and neonatal alloimmune thrombocytopenia as well. Hemolysis leads to elevated bilirubin levels. After delivery bilirubin is no longer cleared (via the placenta) from the neonate’s blood and the symptoms of jaundice (yellowish skin and yellow discoloration of the whites of the eyes, or icterus) increase within 24 hours after birth. Like other forms of severe neonatal jaundice, there is the possibility of the neonate developing acute or chronic kernicterus, however the risk of kernicterus in HDN is higher because of the rapid and massive destruction of blood cells. It is important to note that isoimmunization is a risk factor for neurotoxicity and lowers the level at which kernicterus can occur. Untreated profound anemia can cause high-output heart failure, with pallor, enlarged liver and/or spleen, generalized swelling, and respiratory distress. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper HDN can be the cause of hydrops fetalis, an often-severe form of prenatal heart failure that causes fetal edema.[2] Complications Complications of HDN could include kernicterus, hepatosplenomegaly, inspissated (thickened or dried) bile syndrome and/or greenish staining of the teeth, hemolytic anemia and damage to the liver due to excess bilirubin. Similar conditions include acquired hemolytic anemia, congenital toxoplasma, congenital syphilis infection, congenital obstruction of the bile duct, and cytomegalovirus (CMV) infection. High at birth or rapidly rising bilirubin[3] Prolonged hyperbilirubinemia[3] Bilirubin Induced Neurological Dysfunction[4] Cerebral Palsy[5] Kernicterus[6] Neutropenia[7][8] Thrombocytopenia[7] Hemolytic anemia – Must NOT be treated with iron[9] Late onset anemia – Must NOT be treated with iron. Can persist up to 12 weeks after birth.[10][11][12] Pathophysiology Antibodies are produced when the body is exposed to an antigen foreign to the make-up of the body. If a mother is exposed to a foreign antigen and produces IgG (as opposed to IgM which does not cross the placenta), the IgG will target the antigen, if present in the fetus, and may affect it in utero and persist after delivery. The three most common models in which a woman becomes sensitized toward (i.e., produces IgG antibodies against) a particular antigen are hemorrhage, blood transfusion, and ABO incompatibility. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper Fetal-maternal hemorrhage, which is the movement of fetal blood cells across the placenta, can occur during abortion, ectopic pregnancy, childbirth, ruptures in the placenta during pregnancy (often caused by trauma), or medical procedures carried out during pregnancy that breach the uterine wall. In subsequent pregnancies, if there is a similar incompatibility in the fetus, these antibodies are then able to cross the placenta into the fetal bloodstream to attach to the red blood cells and cause their destruction (hemolysis). This is a major cause of HDN, because 75% of pregnancies result in some contact between fetal and maternal blood, and 15-50% of pregnancies have hemorrhages with the potential for immune sensitization. The amount of fetal blood needed to cause maternal sensitization depends on the individual’s immune system and ranges from 0.1 mL to 30 mL.[2] The woman may have received a therapeutic blood transfusion. ABO blood group system and the D antigen of the Rhesus (Rh) blood group system typing are routine prior to transfusion. Suggestions have been made that women of child-bearing age or young girls should not be given a transfusion with Rhc-positive blood or Kell1-positive blood to avoid possible sensitization, but this would strain the resources of blood transfusion services, and it is currently considered uneconomical to screen for these blood groups. HDFN can also be caused by antibodies to a variety of other blood group system antigens, but Kell and Rh are the most frequently encountered. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper The third sensitization model can occur in women of blood type O. The immune response to A and B antigens, that are widespread in the environment, usually leads to the production of IgM or IgG anti-A and anti-B antibodies early in life. Women of blood type O are more prone than women of types A and B to making IgG anti-A and anti-B antibodies, and these IgG antibodies are able to cross the placenta. For unknown reasons, the incidence of maternal antibodies against type A and B antigens of the IgG type that could potentially cause hemolytic disease of the newborn is greater than the observed incidence of “ABO disease.” About 15% of pregnancies involve a type O mother and a type A or type B child; only 3% of these pregnancies result in hemolytic disease due to A/B/O incompatibility. In contrast to antibodies to A and B antigens, Rhesus antibodies are generally not produced from exposure to environmental antigens.[citation needed] In cases where there is ABO incompatibility and Rh incompatibility, the risk of alloimmunization is decreased because fetal red blood cells are removed from maternal circulation due to anti-ABO antibodies before they can trigger an anti-Rh response.[2] Antibody Specific Information Anti-D is the only preventable form of HDN. Since the 1968 introduction of Rho-D immunoglobulin, (Rhogam), which prevents the production of maternal Rho-D antibodies, the incidence of anti-D HDN has decreased dramatically.[2][13] Anti-C and anti-c can both show a negative DAT but still have a severely affected infant.[14][15] An indirect Coombs must also be run. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper Anti-M also recommends antigen testing to rule out the presence of HDN as the direct coombs can come back negative in a severely affected infant.[16] Anti-Kell can cause severe anemia regardless of titer.[17] Anti-Kell suppresses the bone marrow,[18] by inhibiting the erythroid progenitor cells.[19][20] Kidd antigens are also present on the endothelial cells of the kidneys[21][22] One study done by Moran et al., found that titers are not reliable for anti-E. Their most severe case of hemolytic disease of the newborn occurred with titers 1:2. Moran states that it would be unwise routinely to dismiss anti-E as being of little clinical consequence.[23] Diagnosis The diagnosis of HDN is based on history and laboratory findings: Blood tests done on the newborn baby Biochemistry tests for jaundice Peripheral blood morphology shows increased reticulocytes. Erythroblasts (also known as nucleated red blood cells) occur in moderate and severe disease. Positive direct Coombs test (might be negative after fetal interuterine blood transfusion) Blood tests done on the mother Positive indirect Coombs test Blood tests done on the father Erythrocyte antigen status Types (classified by serology) Types of HDN are classified by the type of antigens involved. The main types are ABO HDN, Rhesus HDN, Kell HDN, and other antibodies. ABO hemolytic disease of the newborn can range from mild to severe, but generally it is a mild disease. It can be caused by anti-A and anti-B antibodies. Rhesus D hemolytic disease of the newborn (often called Rh disease) is the most common form of severe HDN. Rhesus c hemolytic disease of the newborn can range from a mild to severe disease – is the third most common form of severe HDN.[24] Rhesus e and rhesus C hemolytic disease of the newborn are rare. Combinations of antibodies, for example, anti-Rhc and a

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