Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper
Hemolytic Disease of the Newborn
What is hemolytic disease of the newborn (HDN)?
Hemolytic disease of the newborn is also called erythroblastosis fetalis. This condition occurs when there is an incompatibility between the blood types of the mother and baby.
“Hemolytic” means breaking down of red blood cells
“Erythroblastosis” refers to making of immature red blood cells Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper
“Fetalis” refers to fetus
What causes hemolytic disease of the newborn (HDN)?
HDN most frequently occurs when an Rh negative mother has a baby with an Rh positive father. When the baby’s Rh factor is positive, like the father’s, problems can develop if the baby’s red blood cells cross to the Rh negative mother. This usually happens at delivery when the placenta detaches. However, it may also happen anytime blood cells of the two circulations mix, such as during a miscarriage or abortion, with a fall, or during an invasive prenatal testing procedure (such as an amniocentesis or chorionic villus sampling).
The mother’s immune system sees the baby’s Rh positive red blood cells as “foreign.” Just as when bacteria invade the body, the immune system responds by developing antibodies to fight and destroy these foreign cells. The mother’s immune system then keeps the antibodies in case the foreign cells appear again, even in a future pregnancy. The mother is now “Rh sensitized.”
In a first pregnancy, Rh sensitization is not likely. Usually, it only becomes a problem in a future pregnancy 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 red blood cells, the baby can become sick. This is called erythroblastosis fetalis during pregnancy. In the newborn, the condition is called hemolytic disease of the newborn. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper
Who is affected by hemolytic disease of the newborn?
Babies affected by HDN are usually in a mother’s second or higher pregnancy, after she has become sensitized with a first baby. HDN due to Rh incompatibility is about three times more likely in Caucasian babies than African-American babies.
Why is hemolytic disease of the newborn a concern?
When the mother’s antibodies attack the red blood cells, they are broken down and destroyed (hemolysis). This makes the baby anemic. Anemia is dangerous because it limits the ability of the blood to carry oxygen to the baby’s organs and tissues. As a result:
The baby’s body responds to the hemolysis by trying to make more red blood cells very quickly in the bone marrow and the liver and spleen. This causes these organs to get bigger. The new red blood cells, called erythroblasts, are often immature and are not able to do the work of mature red blood cells.
As the red blood cells break down, a substance called bilirubin is formed. Babies are not easily able to get rid of the bilirubin and it can build up in the blood and other tissues and fluids of the baby’s body. This is called hyperbilirubinemia. Because bilirubin has a pigment or coloring, it causes a yellowing of the baby’s skin and tissues. This is called jaundice.
Complications of hemolytic disease of the newborn can range from mild to severe. The following are some of the problems that can result: Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper
Mild anemia, hyperbilirubinemia, and jaundice. The placenta helps rid some of the bilirubin, but not all.
Severe anemia with enlargement of the liver and spleen. When these organs and the bone marrow cannot compensate for the fast destruction of red blood cells, severe anemia results and other organs are affected.
Hydrops fetalis. This occurs as the baby’s organs are unable to handle the anemia. The heart begins to fail and large amounts of fluid build up in the baby’s tissues and organs. A fetus with hydrops is at great risk of being stillborn.
Severe hyperbilirubinemia and jaundice. The baby’s liver is unable to handle the large amount of bilirubin that results from red blood cell breakdown. The baby’s liver is enlarged and anemia continues.
Kernicterus. Kernicterus is the most severe form of hyperbilirubinemia and results from the buildup of bilirubin in the brain. This can cause seizures, brain damage, deafness, and death.
What are the symptoms of hemolytic disease of the newborn?
The following are the most common symptoms of hemolytic disease of the newborn. However, each baby may experience symptoms differently. During pregnancy symptoms may include:
With amniocentesis, the amniotic fluid may have a yellow coloring and contain bilirubin.
Ultrasound of the fetus shows enlarged liver, spleen, or heart and fluid buildup in the fetus’s abdomen, around the lungs, or in the scalp. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper
After birth, symptoms may include:
A pale coloring may be evident, due to anemia.
Jaundice, or yellow coloring of amniotic fluid, umbilical cord, skin, and eyes may be present. The baby may not look yellow immediately after birth, but jaundice can develop quickly, usually within 24 to 36 hours.
The newborn may have an enlarged liver and spleen.
Babies with hydrops fetalis have severe edema (swelling) of the entire body and are extremely pale. They often have difficulty breathing.
How is hemolytic disease of the newborn diagnosed?
Because anemia, hyperbilirubinemia, and hydrops fetalis can occur with other diseases and conditions, the accurate diagnosis of HDN depends on determining if there is a blood group or blood type incompatibility. Sometimes, the diagnosis can be made during pregnancy based on information from the following tests:
Testing for the presence of Rh positive antibodies in the mother’s blood
Ultrasound – to detect organ enlargement or fluid buildup in the fetus. Ultrasound is a diagnostic imaging technique which uses high-frequency sound waves and a computer to create images of blood vessels, tissues, and organs. Ultrasound is used to view internal organs as they function, and to assess blood flow through various vessels.
Amniocentesis – to measure the amount of bilirubin in the amniotic fluid. Amniocentesis is a test performed to determine chromosomal and genetic disorders and certain birth defects. The test involves inserting a needle through the abdominal and uterine wall into the amniotic sac to retrieve a sample of amniotic fluid.
Sampling of some of the blood from the fetal umbilical cord during pregnancy to check for antibodies, bilirubin, and anemia in the fetus.
Once a baby is born, diagnostic tests for HDN may include the following: Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper
Testing of the baby’s umbilical cord blood for blood group, Rh factor, red blood cell count, and antibodies
Testing of the baby’s blood for bilirubin levels
Treatment for hemolytic disease of the newborn
Once HDN is diagnosed, treatment may be needed. Specific treatment for hemolytic disease of the newborn will be determined by your baby’s doctor based on:
Your baby’s gestational age, overall health, and medical history
Extent of the disease
Your baby’s tolerance for specific medications, procedures, or therapies
Expectations for the course of the disease
Your opinion or preference
During pregnancy, treatment for HDN may include:
Intrauterine blood transfusion of red blood cells into the baby’s circulation. This is done by placing a needle through the mother’s uterus and into the abdominal cavity of the fetus or directly into the vein in the umbilical cord. It may be necessary to give a sedative medication to keep the baby from moving. Intrauterine transfusions may need to be repeated.
Early delivery if the fetus develops complications. If the fetus has mature lungs, labor and delivery may be induced to prevent worsening of HDN.
After birth, treatment may include:
Blood transfusions (for severe anemia)
Intravenous fluids (for low blood pressure)
Help for respiratory distress using oxygen, surfactant, or a mechanical breathing machine
Exchange transfusion to replace the baby’s damaged blood with fresh blood. The exchange transfusion helps increase the red blood cell count and lower the levels of bilirubin. An exchange transfusion is done by alternating giving and withdrawing blood in small amounts through a vein or artery. Exchange transfusions may need to be repeated if the bilirubin levels remain high. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper
Intravenous immunoglobin(IVIG). IVIG is a solution made from blood plasma that contains antibodies to help the baby’s immune system. IVIG may help reduce the breakdown of red blood cells and lower bilirubin levels.
Prevention of hemolytic disease of the newborn
Fortunately, HDN is a very preventable disease. Because of the advances in prenatal care, nearly all women with Rh negative blood are identified in early pregnancy by blood testing. If a mother is Rh negative and has not been sensitized, she is usually given a drug called Rh immunoglobulin (RhIg), also known as RhoGAM. This is a specially developed blood product that can prevent an Rh negative mother’s antibodies from being able to react to Rh positive cells. Many women are given RhoGAM around the 28th week of pregnancy. After the baby is born, a woman should receive a second dose of the drug within 72 hours, if her baby is Rh positive. If her baby is Rh negative, she does not need another dose.
Prevention of haemolytic disease of the fetus and newborn (HDFN)
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.
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
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 Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper
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.
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: Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper
Amniocentesis, chorionic villus biopsy and cordocentesis
Antepartum haemorrhage/vaginal bleeding in pregnancy
External cephalic version
Fall or abdominal trauma
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).
For recurrent or intermittent uterine bleeding, a minimum of 500 IU anti-D Ig should be given at 6-weekly intervals. Estimation of FMH haemorrhage by the Kleihauer technique should be carried out at 2-weekly intervals and additional anti-D Ig administered if required.
Haemolytic disease of the newborn (HDN), or haemolytic disease of the fetus and newborn (HDFN) used to be a major cause of fetal loss and neonatal death. It is an alloimmune condition, meaning that an individual develops immunity against antigens of another individual. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper
In HDN, the mother produces IgG-type antibodies against red cell antigens on fetal red blood cells (RBC); these antibodies pass through the placenta into the fetal circulation. Once in the fetal circulation, the offending antibodies attach to corresponding antigens on fetal RBC, marking them to be destroyed by haemolysis. The rate of haemolysis determines whether the clinical picture of HDN is mild, moderate or severe.
Mild cases may have only mild anaemia and jaundice at birth. In severe cases, the bilirubin level may rise dramatically within 24 hours of birth, and enter the brain to cause kernicterus, a potentially fatal condition.
The most important cause of HDN is antibody to the rhesus D antigen (RhD), which will be the focus of this article.
Sensitisation to an antigen occurs when the immune system encounters that antigen for the first time and mounts an immune response. As maternal and fetal circulations are separate, for HDN to occur, fetal RhD-positive cells must enter the RhD-negative maternal circulation, allowing her immune system to see the foreign red cell antigen and form an antibody against it.
Only a small amount of fetal blood need enter the mother’s circulation for sensitisation to occur. HDN does not usually affect the first pregnancy unless there is a sensitising event or the mother already has RhD antibodies.
Potential sensitising events are listed in the box below. In subsequent pregnancies, pre-sensitised RhD-negative mothers, carrying RhD-positive babies, boost antibody production progressively, putting later pregnancies at increasing risk.
In all expectant mothers, blood type (ABO and Rh groups) should be determined and serum screened for atypical antibodies (that will recognise antigens on fetal RBC), in the first trimester and again at 28 weeks’ gestation to identify at-risk pregnancies.
In RhD-negative women with a negative antibody screen, the risk of sensitisation is reduced by administering anti-RhD immunoglobulin when sensitising events occur and routinely in the third trimester (routine antenatal anti-D prophylaxis); this should be offered to all RhD-negative women, as per NICE recommendations. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper
Anti-D immunoglobulin destroys the RhD-positive RBC and prevents active immunisation, thus preventing production of RhD antibodies.
Following delivery, a repeat maternal group and antibody screen is performed and the baby’s blood group determined. If the baby is grouped RhD-positive then the mother should receive further anti-D immunoglobulin within 72 hours and a Kleihauer test should be performed on maternal blood to look for evidence of fetomaternal haemorrhage (FMH) occurring at birth.
Further anti-D immunoglobulin may be required depending on the amount of FMH detected in the Kleihauer, as set out in guidelines for the estimation of fetomaternal haemorrhage (see resources). The baby should also be monitored and treated for anaemia and jaundice.
In addition, in the UK, RhD-negative girls and women of childbearing age should never receive RhD-positive cellular blood products if they require transfusion, to prevent sensitisation occurring.
This use of anti-D immunoglobulin has led to a dramatic decrease in the incidence of HDN, particularly severe cases, and the mortality rate has decreased from 1.2 to 0.02 per 1,000 births.
Management of sensitised mothers
Where the presence of maternal anti-D is confirmed in a pregnancy, the next step is to determine whether fetal RBCs are a target. Determining the paternal rhesus genotype will answer this question, if the father is homozygous for the D allele.
If the father is heterozygous (D/d) then fetal genotyping is required. There are two methods of obtaining fetal cells. The non-invasive method for RhD analyses fetal DNA that is present in the plasma of pregnant women. The second method, for RhD and also other antigens, analyses fetal DNA in amniotic fluid or chorionic villus biopsy. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper
If the fetus is RhD-positive, the pregnancy is monitored for signs of HDN by regular fetal ultrasound scans and measurement of anti-D titres in the mother’s serum. Rising anti-D levels indicates active haemolysis.
If a fetal blood test confirms anaemia, an in utero blood transfusion may be required. In the neonatal period anaemia and hyperbilirubinaemia may require blood transfusions and phototherapy or exchange transfusion.
The RhD antibody remains the most frequent cause of severe HDN but other alloimmune antibodies of the Kell, Duffy, Kidd and MNS systems can cause HDN.
Routine antibody screening of all mothers will identify other antibodies of clinical significance to the fetus. The antibody should be quantified and follow-up tests performed as recommended in British Committee for Standards in Haematology (BCSH) guidelines for antibody testing in pregnancy.
Dr Bonney is a consultant paediatric heamatologist, Royal Manchester Children’s Hospital
Signs and symptoms
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
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.
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.
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. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper
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:
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. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper
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.
A healthcare provider will check your baby’s blood flow with an ultrasound.
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.
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.
This may be done if your baby has severe anemia.
This may be done if your baby has low blood pressure.
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.
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. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper
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.
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: Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper
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.
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.
HDN can be the cause of hydrops fetalis, an often-severe form of prenatal heart failure that causes fetal edema.
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. Hemolytic Disease of the Newborn and Clinical Manifestations Essay Paper
High at birth or rapidly rising bilirubin
Bilirubin Induced Neurological Dysfunction
Hemolytic anemia – Must NOT be treated with iron
Late onset anemia – Must NOT be treated with iron. Can persist up to 12 weeks after birth.
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.
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. 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