Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper

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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.

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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

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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

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 anti-RhE occurring together can be especially severe. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper

Anti-Kell hemolytic disease of the newborn is most commonly caused by anti-K 1 antibodies, the second most common form of severe HDN. Over half of the cases of anti-K 1 related HDN are caused by multiple blood transfusions. Antibodies to the other Kell antigens are rare.[24]

Prevention
In cases of Rho(D) incompatibility, Rho(D) immunoglobulin is given to prevent sensitization. However, there is no comparable immunotherapy available for other blood group incompatibilities.[2]

Early pregnancy

IVIG – IVIG stands for Intravenous Immunoglobulin. It is used in cases of previous loss, high maternal titers, known aggressive antibodies, and in cases where religion prevents blood transfusion. IVIG can be more effective than IUT alone.[25] Fetal mortality was reduced by 36% in the IVIG and IUT group than in the IUT alone group. IVIG and plasmapheresis together can reduce or eliminate the need for an IUT.[26]
Plasmapheresis – Plasmapheresis aims to decrease the maternal titer by direct plasma replacement and physical removal of antibody.[16] Plasmapheresis and IVIG together can even be used on women with previously hydropic fetuses and fetal losses.[27][28]
Mid- to late- pregnancy

IUT – Intrauterine Transfusion (IUT) is done either by intraperitoneal transfusion (IPT) or intravenous transfusion (IVT).[29] IVT is preferred over IPT.[30] IUTs are only done until 35 weeks. After that, the risk of an IUT is greater than the risk from post birth transfusion.[31]
Steroids – Steroids are sometimes given to the mother before IUTs and early delivery to mature the fetal lungs.[31][32]
Phenobarbital – Phenobarbital is sometimes given to the mother to help mature the fetal liver and reduce hyperbilirubinemia.[32][33]
Early Delivery – Delivery can occur anytime after the age of viability.[30] Emergency delivery due to failed IUT is possible, along with induction of labor at 35–38 weeks.[31][34]
Rhesus-negative mothers who are pregnant with a rhesus-positive infant are offered Rho(D) immune globulin (RhIG, or RhoGam) at 28 weeks during pregnancy, at 34 weeks, and within 48 hours after delivery to prevent sensitization to the D antigen. It works by binding any fetal red blood cells with the D antigen before the mother is able to produce an immune response and form anti-D IgG.[2] A drawback to pre-partum administration of RhIG is that it causes a positive antibody screen when the mother is tested, which can be difficult to distinguish from natural immunological responses that result in antibody production.[citation needed] Without Rho(D) immunoglobulin, the risk of isoimmunization is approximately 17% Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper

Hemolytic disease of the newborn, also known as hemolytic disease of the fetus and newborn, HDN, HDFN, or erythroblastosis fetalis,[1] is an alloimmune condition that develops in a peripartum fetus, when the IgG molecules (one of the five main types of antibodies) produced by the mother pass through the placenta. Among these antibodies are some which attack antigens on the red blood cells in the fetal circulation, breaking down and destroying the cells (hemolysis). The fetus can develop reticulocytosis and anemia. This fetal disease ranges from mild to very severe, and fetal death from heart failure (hydrops fetalis) can occur. When the disease is moderate or severe, many erythroblasts (immature red blood cells) are present in the fetal blood, and so these forms of the disease can be called erythroblastosis fetalis (or erythroblastosis foetalis).

Hemolytic disease of the newborn (HDN) used to be a major cause of fetal loss and death among newborn babies. The first description of HDN is thought to be in 1609 by a French midwife who delivered twins—one baby was swollen and died soon after birth, the other baby developed jaundice and died several days later. For the next 300 years, many similar cases were described in which newborns failed to survive.

It was not until the 1950s that the underlying cause of HDN was clarified; namely, the newborn’s red blood cells (RBCs) are being attacked by antibodies from the mother. The attack begins while the baby is still in the womb and is caused by an incompatibility between the mother’s and baby’s blood.

By the 1960s, trials in the United States and the United Kingdom tested the use of therapeutic antibodies that could remove the antibodies that cause HDN from the mother’s circulation. The trials showed that giving therapeutic antibodies to women during their pregnancy largely prevented HDN from developing (1). By the 1970s, routine antenatal care included screening of all expectant mothers to find those whose pregnancy may be at risk of HDN, and giving preventative treatment accordingly. This has led to a dramatic decrease in the incidence of HDN, particularly severe cases that were responsible for stillbirth and neonatal death.

This chapter will discuss the causes of HDN and how the disease can be treated or minimized, if not prevented entirely. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper

Maternal antibodies cross the placenta and attack fetal red blood cells
During pregnancy, some of the mother’s antibodies are transported across the placenta and enter the fetal circulation. This is necessary because by the time of birth, newborns have only a primitive immune system, and the continuing presence of maternal antibodies helps ensure that they survive while their immune system matures. A downside to this protection is that by targeting fetal RBCs, maternal antibodies can also cause HDN.

A major cause of HDN is an incompatibility of the Rh blood group between the mother and fetus. Most commonly, hemolytic disease is triggered by the D antigen, although other Rh antigens, such as c, C, E, and e, can also cause problems.

Pregnancies at risk of HND are those in which an Rh D-negative mother becomes pregnant with an RhD-positive child (the child having inherited the D antigen from the father). The mother’s immune response to the fetal D antigen is to form antibodies against it (anti-D). These antibodies are usually of the IgG type, the type that is transported across the placenta and hence delivered to the fetal circulation.

HDN can also be caused by an incompatibility of the ABO blood group. It arises when a mother with blood type O becomes pregnant with a fetus with a different blood type (type A, B, or AB). The mother’s serum contains naturally occurring anti-A and anti-B, which tend to be of the IgG class and can therefore cross the placenta and hemolyse fetal RBCs.

HDN due to ABO incompatibility is usually less severe than Rh incompatibility. One reason is that fetal RBCs express less of the ABO blood group antigens compared with adult levels. In addition, in contrast to the Rh antigens, the ABO blood group antigens are expressed by a variety of fetal (and adult) tissues, reducing the chances of anti-A and anti-B binding their target antigens on the fetal RBCs. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper

Less common causes of HDN include antibodies directed against antigens of the Kell blood group (e.g., anti-K and anti-k), Kidd blood group (e.g., anti-Jka and anti-Jkb), Duffy blood group (e.g., anti-Fya), and MNS and s blood group antibodies. To date, antibodies directed against the P and Lewis blood groups have not been associated with HDN.

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Sensitization occurs during the first pregnancy
Sensitization to an antigen occurs when the immune system encounters an antigen for the first time and mounts an immune response. In the case of HDN caused by Rh incompatibility, an Rh D-negative mother may first encounter the D antigen while being pregnant with an Rh D-positive child, or by receiving a blood transfusion of Rh D-positive blood. Once a mother has been sensitized to the D antigen, her serum will contain anti-D. The direct Coombs test (see below) confirms the presence of anti-D and hence that the mother has been sensitized.

Only a small amount of fetal blood need enter the mother’s circulation for sensitization to occur. Typically, this occurs during the delivery of the first-born Rh D-positive child. Fetal-maternal hemorrhage is common during labor and is increased during a prolonged or complicated labor, which in turn increases the risk of sensitization. Sensitization can also occur earlier in the pregnancy, for example during a prenatal bleed or a miscarriage. It may also occur during medical procedures, such as a termination of pregnancy or chorionic villus sampling.

The risk of sensitization to the Rh D antigen is decreased if the fetus is ABO incompatible. This is because any fetal cells that leak into the maternal circulation are rapidly destroyed by potent maternal anti-A and/or anti-B, reducing the likelihood of maternal exposure to the D antigen. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper

HDN occurs in subsequent pregnancies
Initially, the maternal anti-D that is formed at the time of sensitization is of the IgM type, which can not cross the placenta. In subsequent pregnancies, a repeat encounter with the Rh D antigen stimulates the rapid production of type IgG anti-D, which can be transported across the placenta and enter the fetal circulation. Once in the fetal circulation, anti-D attaches to the Rh D antigens found on the fetal RBCs, marking them to be destroyed.

The rate of hemolysis determines whether the nature of HDN is mild, moderate, or severe. In mild cases, the small increase in the rate of hemolysis is tolerated by the fetus. At birth and during the newborn period, symptoms include a mild anemia and jaundice, both of which may resolve without treatment.

In cases where there is a greater increase in the rate of hemolysis, the level of bilirubin may still remain low during the pregnancy because of the ability of the placenta to remove bilirubin from the fetal circulation. However, after birth the neonate’s immature liver is unable to metabolize the increased amount of bilirubin that instead accumulates in his or her blood. Within 24 hours of birth, the level of bilirubin may rise dramatically. If levels continue to rise, bilirubin may enter the brain to cause kernicterus, a potentially fatal condition that leaves permanent neurological damage in the babies that survive.

An even greater rapid and prolonged destruction of RBCs leads to severe anemia in the fetus. The liver, spleen, and other organs increase their production of RBCs to compensate for their loss. The drive to produce RBCs causes the liver and spleen to increase in size (hepatosplenomegaly), and liver dysfunction can occur. Immature RBCs (erythroblasts) spill into the circulation, giving rise to the alternative name of this disease, erythroblastosis fetalis. A complication of severe HDN is hydrops fetalis, in which the fetal tissues become swollen (edematous). This condition is usually fatal, either in utero or soon after birth. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper

The Coombs test detects Rh incompatibility between mother and fetus
To detect HDN, the presence of maternal anti-Rh IgG must be identified. In vivo, these antibodies destroy Rh D-positive fetal RBCs, but in vitro, they do not lyse cells or even cause agglutination, making them difficult to identify. Therefore, the Coombs test is used. This test uses antibodies that bind to anti-D antibodies. The test is named for Robin Coombs, who first developed the technique of using antibodies that are targeted against other antibodies.

Direct Coombs test: diagnoses HDN
The direct Coombs test detects maternal anti-D antibodies that have already bound to fetal RBCs.

First, a sample of fetal RBCs is washed to remove any unbound antibody (Ig). When the test antibodies (anti-Ig) are added, they agglutinate any fetal RBCs to which maternal antibodies are already bound.

This is called the direct Coombs test because the anti-Ig binds “directly” to the maternal anti-D Ig that coats fetal RBCs in HDN.

Indirect Coombs test: used in the prevention of HDN
The indirect Coombs test finds anti-D antibodies in the mother’s serum. If these were to come into contact with fetal RBCs they would hemolyse them and hence cause HDN. By finding maternal anti-D before fetal RBCs have been attacked, treatment can be given to prevent or limit the severity of HDN.

For this test, the mother’s serum is incubated with Rh D-positive RBCs. If any anti-D is present in the mother’s serum, they will bind to the cells. The cells are then washed to remove all free antibodies. When anti-Ig antibodies are added, they will agglutinate any RBCs to which maternal antibodies are bound.

This is called the indirect Coombs test because the anti-Ig finds “indirect” evidence of harmful maternal antibodies, requiring the addition of fetal RBCs to show the capacity of maternal anti-D to bind to fetal RBCs.

See a diagram of the Direct and Indirect Coombs tests in Janeway & Travers Immunobiology Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper

Preventing HDN
Determine Rh status of the mother
As part of routine prenatal or antenatal care, the blood type of the mother (ABO and Rh) is determined by a blood test. A test for the presence of atypical antibodies in the mother’s serum is also performed. At present, Rh D incompatibility is the only cause of HDN for which screening is routine.

In the United States, the frequency of Rh D-negative status varies from about 17% in Caucasians to about 7% in Hispanics and Blacks. The frequency is much lower in people of Asian descent (including people from China, India, and Japan), averaging about 2% (2).

If the mother is not sensitized, reduce the risk of future sensitization
To find out whether a pregnant Rh D-negative mother has been sensitized to the Rh D antigen, an indirect Coombs test is done (see above). If anti-D is not found in the mother’s serum, it is likely that she has not been sensitized to the Rh D antigen.

The risk of future sensitization can be greatly reduced by giving all unsensitized mothers anti-D Ig, which “mops up” any fetal RBCs that may have leaked into the maternal circulation, reducing the risk of first-time exposure to the D antigen.

Usually, Rh D-negative mothers receive on injection of anti-D Ig at about 28 weeks gestation, which is about the time when fetal RBCs start to express the D antigen, and mothers receive another dose at about 34 weeks, a few weeks before labor begins during which the risk of fetomaternal hemorrhage is high. A final dose of anti-D Ig is given after the baby has been delivered. In addition, anti-D Ig is given to cover other events during the pregnancy that may lead to sensitization, e.g., antepartum bleeds and pre-eclampsia.

This prophylaxis regime against Rh D sensitization is effective. However, currently, there is no routine prophylaxis for HDN caused by incompatibility of other blood group antigens.

If the mother is sensitized, determine whether the fetus is at risk and monitor accordingly
Once the presence of maternal anti-D has been confirmed, the next step is to determine whether the fetal RBCs are a target, i.e., confirm the Rh status of the fetus. If the father is homozygous for the D allele (D/D), the fetus will be D positive. If however the father is heterozygous (D/d), there is a 50:50 chance that the fetus is D positive, and the only way to know the blood type for sure is to test a sample of fetal cells taken from the amniotic fluid or umbilical cord. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper

If the fetus is Rh D-positive, the pregnancy is carefully monitored for signs of HDN. Monitoring includes regular ultrasound scans of the fetus and monitoring of the amount of anti-D in the mother’s serum. Active hemolysis is indicated by a rise in anti-D. If a fetal blood test confirms fetal anemia, depending upon its severity, a blood transfusion can be done in utero to replace the lysed fetal RBCs.

Blood transfusions may also be needed to correct anemia in the newborn period. During this period there may also be a sharp rise in the level of bilirubin in the neonate, which can be lowered by phototherapy and exchange transfusions.

This often happens at birth when the placenta breaks away. But it may also happen any time the mother’s and baby’s blood cells mix. This can occur during a miscarriage or fall. It may also happen during a prenatal test. These can include amniocentesis or chorionic villus sampling. These tests use a needle to take a sample of tissue. They may cause bleeding. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper

The Rh negative mother’s immune system sees the baby’s Rh positive red blood cells as foreign. Your immune system responds by making antibodies to fight and destroy these foreign cells. Your immune system stores these antibodies in case these foreign cells come back again. This can happen in a future pregnancy. You are now Rh sensitized.

Rh sensitization normally isn’t a problem with a first pregnancy. Most problems occur in future pregnancies with another Rh positive baby. During that pregnancy, the mother’s antibodies cross the placenta to fight the Rh positive cells in the baby’s body. As the antibodies destroy the cells, the baby gets sick. This is called erythroblastosis fetalis during pregnancy. Once the baby is born, it’s called HDN.

Which children are at risk for HDN?
The following can raise your risk for having a baby with HDN:
You’re Rh negative and have an Rh positive baby but haven’t received treatment.
You’re Rh negative and have been sensitized. This can happen in a past pregnancy with an Rh positive baby. Or it can happen because of an injury or test in this pregnancy with an Rh positive baby.
HDN is about 3 times more common in Caucasian babies than in African-American babies.

What are the symptoms of HDN in a newborn?
Symptoms can occur a bit differently in each pregnancy and child.
During pregnancy, you won’t notice any symptoms. But your healthcare provider may see the following during a prenatal test: Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper

A yellow coloring of amniotic fluid. This color may be because of bilirubin. This is a substance that forms as blood cells break down.
Your baby may have a big liver, spleen, or heart. There may also be extra fluid in his or her stomach, lungs, or scalp. These are signs of hydrops fetalis. This condition causes severe swelling (edema).
After birth, symptoms in your baby may include:

Pale-looking skin. This is from having too few red blood cells (anemia).
Yellow coloring of your baby’s umbilical cord, skin, and the whites of his or her eyes (jaundice). Your baby may not look yellow right after birth. But jaundice can come on quickly. It often starts within 24 to 36 hours.
Your newborn may have a big liver and spleen.
A newborn with hydrops fetalis may have severe swelling of their entire body. They may also be very pale and have trouble breathing.
How is HDN diagnosed in a newborn?
HDN can cause symptoms similar to those caused by other conditions. To make a diagnosis, your child’s healthcare provider will look for blood types that cannot work together. Sometimes, this diagnosis is made during pregnancy. It will be based on results from the following tests:
Blood test. Testing is done to look for for Rh positive antibodies in your blood.
Ultrasound. This test can show enlarged organs or fluid buildup in your baby.
Amniocentesis. This test is done to check the amount of bilirubin in the amniotic fluid. In this test, a needle is put into your abdominal and uterine wall. It goes through to the amniotic sac. The needle takes a sample of amniotic fluid.
Percutaneous umbilical cord blood sampling. This test is also called fetal blood sampling. In this test, a blood sample is taken from your baby’s umbilical cord. Your child’s healthcare provider will check this blood for antibodies, bilirubin, and anemia. This is done to check if your baby needs an intrauterine blood transfusion.
The following tests are used to diagnose HDN after your baby is born:

Testing of your baby’s umbilical cord. This can show your baby’s blood group, Rh factor, red blood cell count, and antibodies.
Testing of the baby’s blood for bilirubin levels.
How is HDN treated in a newborn?
Treatment will depend on your child’s symptoms, age, and general health. It will also depend on how severe the condition is.
During pregnancy, treatment for HDN may include the following.

Monitoring
A healthcare provider will check your baby’s blood flow with an ultrasound. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper

Intrauterine blood transfusion
This test puts red blood cells into your baby’s circulation. In this test, a needle is placed through your uterus. It goes into your baby’s abdominal cavity to a vein in the umbilical cord. Your baby may need sedative medicine to keep him or her from moving. You may need to have more than 1 transfusion.

Early delivery
If your baby gets certain complications, he or she may need to be born early. Your healthcare provider may induce labor may once your baby has mature lungs. This can keep HDN from getting worse.

After birth, treatment may include the following.

Blood transfusions
This may be done if your baby has severe anemia.

Intravenous fluids
This may be done if your baby has low blood pressure.

Phototherapy
In this test, your baby is put under a special light. This helps your baby get rid of extra bilirubin.

Help with breathing
Your baby may need oxygen, a substance in the lungs that helps keep the tiny air sacs open (surfactant), or a mechanical breathing machine to breathe better. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper

Exchange transfusion
This test removes your baby’s blood that has a high bilirubin level. It replaces it with fresh blood that has a normal bilirubin level. This raises your baby’s red blood cell count. It also lowers his or her bilirubin level. In this test, your baby will alternate giving and getting small amounts of blood. This will be done through a vein or artery. Your baby may need to have this procedure again if his or her bilirubin levels stay high.

Intravenous immunoglobulin (IVIG)
IVIG is a solution made from blood plasma. It contains antibodies to help the baby’s immune system. IVIG reduces your baby’s breakdown of red blood cells. It may also lower his or her bilirubin levels.

What are possible complications of HDN in a newborn?
When your antibodies attack your baby’s red blood cells, they are broken down and destroyed (hemolysis).
When your baby’s red blood cells break down, bilirubin is formed. It’s hard for babies to get rid of bilirubin. It can build up in their blood, tissues, and fluids. This is called hyperbilirubinemia. Bilirubin makes a baby’s skin, eyes, and other tissues to turn yellow. This is called jaundice.

When red blood cells breakdown, this makes your baby anemic. Anemia is dangerous. In anemia, your baby’s blood makes more red blood cells very quickly. This happens in the bone marrow, liver, and spleen. This causes these organs to get bigger. The new red blood cells are often immature and can’t do the work of mature red blood cells. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper

Complications of HDN can be mild or severe.

During pregnancy, your baby may have the following:

Mild anemia, hyperbilirubinemia, and jaundice. The placenta gets rid of some bilirubin. But it can’t remove all of it.
Severe anemia. This can cause your baby’s liver and spleen to get too big. This can also affect other organs.
Hydrops fetalis. This happens when your baby’s organs aren’t able to handle the anemia. Your baby’s heart will start to fail. This will cause large amounts of fluid buildup in your baby’s tissues and organs. Babies with this condition are at risk for being stillborn.
After birth, your baby may have the following:

Severe hyperbilirubinemia and jaundice. Your baby’s liver can’t handle the large amount of bilirubin. This causes your baby’s liver to grow too big. He or she will still have anemia.
Kernicterus. This is the most severe form of hyperbilirubinemia. It’s because of the buildup of bilirubin in your baby’s brain. This can cause seizures, brain damage, and deafness. It can even cause death.
What can I do to prevent hemolytic disease of the newborn?
HDN can be prevented. Almost all women will have a blood test to learn their blood type early in pregnancy.
If you’re Rh negative and have not been sensitized, you’ll get a medicine called Rh immunoglobulin (RhoGAM). This medicine can stop your antibodies from reacting to your baby’s Rh positive cells. Many women get RhoGAM around week 28 of pregnancy.

If your baby is Rh positive, you’ll get a second dose of medicine within 72 hours of giving birth. If your baby is Rh negative, you won’t need a second dose

Key points about hemolytic disease of the newborn
HDN occurs when your baby’s red blood cells break down at a fast rate. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper
HDN happens when an Rh negative mother has a baby with an Rh positive father.
If the Rh negative mother has been sensitized to Rh positive blood, her immune system will make antibodies to attack her baby.
When the antibodies enter the baby’s bloodstream, they will attack the red blood cells. This causes them to break down. This can cause problems.
This condition can be prevented. Women who are Rh negative and haven’t been sensitized can receive medicine. This medicine can stop your antibodies from reacting to your baby’s Rh positive cells.

Monitoring
A healthcare provider will check your baby’s blood flow with an ultrasound.

After birth, treatment may include the following.

Blood transfusions
This may be done if your baby has severe anemia.

Intravenous fluids
This may be done if your baby has low blood pressure.

Phototherapy
In this test, your baby is put under a special light. This helps your baby get rid of extra bilirubin.

Complications of HDN can be mild or severe.

During pregnancy, your baby may have the following:

If your baby is Rh positive, you’ll get a second dose of medicine within 72 hours of giving birth. If your baby is Rh negative, you won’t need a second dose

Key points about hemolytic disease of the newborn
HDN occurs when your baby’s red blood cells break down at a fast rate.
HDN happens when an Rh negative mother has a baby with an Rh positive father.
If the Rh negative mother has been sensitized to Rh positive blood, her immune system will make antibodies to attack her baby.
When the antibodies enter the baby’s bloodstream, they will attack the red blood cells. This causes them to break down. This can cause problems.
This condition can be prevented. Women who are Rh negative and haven’t been sensitized can receive medicine. This medicine can stop your antibodies from reacting to your baby’s Rh positive cells.

Normally, red blood cells last for about 120 days in the body. In this disorder, red blood cells in the blood are destroyed earlier than normal. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper

Causes
During pregnancy, red blood cells from the unborn baby can cross into the mother’s blood through the placenta. HDN occurs when the immune system of the mother sees a baby’s red blood cells as foreign. Antibodies then develop against the baby’s red blood cells. These antibodies attack the red blood cells in the baby’s blood and cause them to break down too early.

HDN may develop when a mother and her unborn baby have different blood types. The types are based on small substances (antigens) on the surface of the blood cells.

There is more than one way in which the unborn baby’s blood type may not match the mother’s.

A, B, AB, and O are the 4 major blood types. This is the most common form of a mismatch. In most cases, this is not very severe.
If the mother is Rh-negative and the baby in the womb has Rh-positive cells. When this form does occur, it can cause very severe anemia in the baby. It can be prevented in most cases.
There are other, much less common, types of mismatch between minor blood group antigens. These can also cause severe problems.Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper

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