The document summarizes Rh disease, which occurs when a Rh-negative pregnant woman is exposed to Rh-positive fetal blood cells. This can sensitize the mother's immune system and cause hemolytic anemia in future Rh-positive babies. Key points include the mechanisms of sensitization, effects on the fetus including anemia and jaundice, methods to prevent sensitization like RhIgG antibodies after pregnancy events, and management of sensitized pregnancies including fetal monitoring and possible interventions.
This presentation describes in detail about managing Rh negative pregnancy- to identify and manage Rh non-isommunized and Rh isoimmunized pregnancies, with recent advances
The document discusses Rhesus incompatibility, which occurs when a mother with Rh-negative blood is carrying a baby with Rh-positive blood. This can lead to the mother's immune system developing antibodies against the baby's blood. The summary is:
Rhesus incompatibility occurs when a mother with Rh-negative blood is carrying an Rh-positive baby. This can cause the mother's body to produce antibodies against the baby's blood cells. For subsequent pregnancies, these antibodies can cross the placenta and destroy the baby's red blood cells, causing anemia or other severe complications like hydrops fetalis. Screening, prevention, and management aim to identify at-risk mothers and babies to provide treatments like
This document discusses Rhesus isoimmunization, which occurs when a Rh-negative mother develops antibodies against Rh-positive fetal red blood cells. It covers the epidemiology, pathophysiology, causes including the "grandmother effect", investigations such as the Kleihauer-Betke and Coombs' tests, management of sensitized mothers through surveillance and potential fetal transfusions, and treatment of affected newborns including phototherapy and exchange transfusions. Prevention relies on administering Rhogam prophylaxis to unsensitized Rh-negative mothers.
1. Hemolytic Disease of the Fetus and Neonate (HDFN) is caused by Rh isoimmunization, which occurs when an Rh-negative mother carries an Rh-positive fetus. The mother's antibodies attack the fetus's red blood cells.
2. HDFN stages include fetalis, which causes fetal anemia over 7g/dL Hb deficit, and hydrops fetalis, severe edema when Hb is below 5g/dL. Hydrops occurs due to mechanisms like increased capillary permeability and lymphatic blockade.
3. Preventing HDFN involves routine antenatal anti-D prophylaxis for Rh-negative mothers between 28-34 weeks and within 72 hours of delivery or
Rh isoimmunization occurs when an Rh-negative mother develops antibodies against Rh-positive blood cells from her baby. This can cause hemolytic disease of the fetus and newborn. Sensitization occurs during pregnancy or delivery when fetal blood cells enter the mother's bloodstream. Subsequent pregnancies with an Rh-positive baby are then at risk, as the antibodies can destroy the baby's red blood cells. Prophylactic anti-D immunoglobulin injections are given during and after pregnancy to prevent sensitization by neutralizing any fetal Rh-positive blood cells. Testing monitors antibody levels and fetal health in sensitized pregnancies. Early delivery may be needed to prevent fetal complications like anemia.
1) Rh isoimmunization occurs when an Rh-negative mother is exposed to Rh-positive fetal blood cells, leading to production of IgG antibodies that can cross the placenta and destroy fetal red blood cells.
2) Prevention involves identifying at-risk Rh-negative mothers and administering anti-D immunoglobulin within 72 hours of potential fetal-maternal hemorrhage to suppress immunization.
3) For sensitized pregnancies, fetal anemia is monitored through Doppler ultrasound or invasive tests, and treated with intrauterine transfusions if severe anemia is detected before 35 weeks.
This ppt may help in understanding Rh negative women during pregnancy, labour and postpartum. Great advancements have been made in the detection and management of this condition, and many of our Rh-negative women can now have a happy obstetric career.
Hemolytic disease of the fetus and newborn (HDFN), also known as erythroblastosis fetalis, is caused by maternal antibodies crossing the placenta and destroying fetal red blood cells. Rh incompatibility occurs when an Rh-negative mother has an Rh-positive baby. This can sensitize the mother's immune system and cause hemolytic anemia in subsequent Rh-positive babies. Management involves monitoring for signs of fetal anemia, performing intrauterine blood transfusions if needed, and delivering the baby when it is mature. After birth, affected babies may require phototherapy, exchange transfusions, or other treatments to prevent complications from hemolysis and jaundice. RhoGAM injections during and after pregnancy
This presentation describes in detail about managing Rh negative pregnancy- to identify and manage Rh non-isommunized and Rh isoimmunized pregnancies, with recent advances
The document discusses Rhesus incompatibility, which occurs when a mother with Rh-negative blood is carrying a baby with Rh-positive blood. This can lead to the mother's immune system developing antibodies against the baby's blood. The summary is:
Rhesus incompatibility occurs when a mother with Rh-negative blood is carrying an Rh-positive baby. This can cause the mother's body to produce antibodies against the baby's blood cells. For subsequent pregnancies, these antibodies can cross the placenta and destroy the baby's red blood cells, causing anemia or other severe complications like hydrops fetalis. Screening, prevention, and management aim to identify at-risk mothers and babies to provide treatments like
This document discusses Rhesus isoimmunization, which occurs when a Rh-negative mother develops antibodies against Rh-positive fetal red blood cells. It covers the epidemiology, pathophysiology, causes including the "grandmother effect", investigations such as the Kleihauer-Betke and Coombs' tests, management of sensitized mothers through surveillance and potential fetal transfusions, and treatment of affected newborns including phototherapy and exchange transfusions. Prevention relies on administering Rhogam prophylaxis to unsensitized Rh-negative mothers.
1. Hemolytic Disease of the Fetus and Neonate (HDFN) is caused by Rh isoimmunization, which occurs when an Rh-negative mother carries an Rh-positive fetus. The mother's antibodies attack the fetus's red blood cells.
2. HDFN stages include fetalis, which causes fetal anemia over 7g/dL Hb deficit, and hydrops fetalis, severe edema when Hb is below 5g/dL. Hydrops occurs due to mechanisms like increased capillary permeability and lymphatic blockade.
3. Preventing HDFN involves routine antenatal anti-D prophylaxis for Rh-negative mothers between 28-34 weeks and within 72 hours of delivery or
Rh isoimmunization occurs when an Rh-negative mother develops antibodies against Rh-positive blood cells from her baby. This can cause hemolytic disease of the fetus and newborn. Sensitization occurs during pregnancy or delivery when fetal blood cells enter the mother's bloodstream. Subsequent pregnancies with an Rh-positive baby are then at risk, as the antibodies can destroy the baby's red blood cells. Prophylactic anti-D immunoglobulin injections are given during and after pregnancy to prevent sensitization by neutralizing any fetal Rh-positive blood cells. Testing monitors antibody levels and fetal health in sensitized pregnancies. Early delivery may be needed to prevent fetal complications like anemia.
1) Rh isoimmunization occurs when an Rh-negative mother is exposed to Rh-positive fetal blood cells, leading to production of IgG antibodies that can cross the placenta and destroy fetal red blood cells.
2) Prevention involves identifying at-risk Rh-negative mothers and administering anti-D immunoglobulin within 72 hours of potential fetal-maternal hemorrhage to suppress immunization.
3) For sensitized pregnancies, fetal anemia is monitored through Doppler ultrasound or invasive tests, and treated with intrauterine transfusions if severe anemia is detected before 35 weeks.
This ppt may help in understanding Rh negative women during pregnancy, labour and postpartum. Great advancements have been made in the detection and management of this condition, and many of our Rh-negative women can now have a happy obstetric career.
Hemolytic disease of the fetus and newborn (HDFN), also known as erythroblastosis fetalis, is caused by maternal antibodies crossing the placenta and destroying fetal red blood cells. Rh incompatibility occurs when an Rh-negative mother has an Rh-positive baby. This can sensitize the mother's immune system and cause hemolytic anemia in subsequent Rh-positive babies. Management involves monitoring for signs of fetal anemia, performing intrauterine blood transfusions if needed, and delivering the baby when it is mature. After birth, affected babies may require phototherapy, exchange transfusions, or other treatments to prevent complications from hemolysis and jaundice. RhoGAM injections during and after pregnancy
Rh isoimmunization occurs when a Rh-negative mother develops antibodies against Rh-positive fetal red blood cells. This can cause hemolytic disease in future Rh-positive pregnancies. Prophylaxis with Rh immunoglobulin is highly effective at preventing sensitization. For sensitized pregnancies, maternal anti-D titers and fetal middle cerebral artery Doppler are used to monitor for anemia. Severe anemia may require cordocentesis or intrauterine transfusions. After delivery, affected newborns may need exchange transfusions or other supportive care to manage hyperbilirubinemia and anemia. Prompt and specialized treatment can help prevent complications in isoimmunized pregnancies.
1. Blood group is defined by the ABO system (O, A, B, AB) and the Rhesus system (Rh positive or negative).
2. Rh disease occurs when an Rh-negative mother is pregnant with an Rh-positive baby. Her immune system develops antibodies that can cross the placenta and destroy the baby's red blood cells.
3. Management involves routine antenatal anti-D prophylaxis for Rh-negative mothers and monitoring of sensitized mothers through antibody titers and fetal Doppler testing. Intrauterine transfusions may be needed to treat severe fetal anemia.
This document discusses Rh isoimmune disease, which occurs when a pregnant woman has Rh-negative blood and her baby has Rh-positive blood. It begins by explaining the differences between isoimmune and autoimmune diseases. It then covers blood group systems like ABO and Rh, how they are inherited, and the importance of compatibility for transfusions. The majority of the document focuses on Rh incompatibility during pregnancy, how it can harm the fetus, diagnosis, and treatments like intrauterine transfusions, early delivery, and phototherapy or exchange transfusions for the newborn. It emphasizes the need for Rh-negative mothers to receive Rh immunoglobulin injections during and after pregnancy to prevent sensitization.
This document discusses Rh isoimmunization in pregnancy. The key points are:
- Rh isoimmunization occurs when an Rh-negative mother is exposed to Rh-positive blood cells from her baby during pregnancy or delivery, triggering an immune response.
- The first baby is usually unaffected, but subsequent pregnancies are at risk if the mother's IgG antibodies cross the placenta and destroy the baby's red blood cells.
- Management involves prophylaxis with anti-D globulin injections after delivery or abortion. Severe cases may require antenatal treatments like plasmapheresis or intrauterine transfusions. High-risk babies require intensive monitoring and possible exchange transfusions.
Rh incompatibility occurs when an Rh-negative pregnant woman is exposed to Rh-positive blood cells, usually from her fetus. This can cause the woman to develop Rh antibodies which can then cross the placenta and destroy fetal red blood cells. The most common cause is fetal blood exposure during pregnancy or delivery from the first Rh-positive baby. Subsequent pregnancies are at higher risk of more severe anemia or death for the baby. Treatment involves administering Rh immunoglobulin injections during and after pregnancy to prevent antibody formation. Early prenatal care and Rh immunoglobulin have reduced the risk from 10-20% to less than 1%.
Rhesus factor is a protein found on red blood cells. If present, one is Rh positive; if absent, Rh negative. Rh factor is inherited from parents. Rh incompatibility occurs when an Rh negative mother is exposed to Rh positive blood, risking complications for her Rh positive baby like hydrops fetalis or jaundice. Management includes screening, anti-D immunoglobulin, monitoring, and timing delivery to prevent baby anemia. Sensitized mothers require additional monitoring and may need intrauterine transfusions or early delivery.
Rh isoimmunization occurs when an Rh-negative pregnant mother develops antibodies against Rh-positive fetal red blood cells. This most commonly happens due to fetomaternal hemorrhage during pregnancy or delivery when fetal cells enter the mother's circulation. The antibodies can then cross the placenta during subsequent pregnancies and destroy fetal red blood cells, causing anemia or even hydrops fetalis. Management of at-risk pregnancies includes determining paternal and fetal Rh status, monitoring antibody titers, and assessing fetal anemia using Doppler ultrasound or invasive tests like amniocentesis if high titers are present. Timely administration of RhIg prophylaxis can prevent sensitization in Rh-negative mothers carrying Rh-positive fet
This document discusses immune conflict that can occur during pregnancy between an Rh-negative mother and Rh-positive fetus. Specifically, it describes Rh isoimmunization, where antibodies produced by the mother's immune system in response to Rh antigens on fetal red blood cells can cross the placenta and destroy fetal red blood cells. If left untreated, this hemolytic process can lead to fetal anemia, jaundice, edema, and even hydrops fetalis. The document outlines methods for diagnosing and preventing Rh isoimmunization.
An Rh-negative pregnant woman is at risk of developing antibodies against her Rh-positive baby's red blood cells. This can cause hemolytic disease in future pregnancies.
The document outlines protocols for testing, prevention, and management. All Rh-negative pregnant women should be tested for antibodies at first visit. Anti-D immunoglobulin is given postpartum/abortion to prevent sensitization if the baby is Rh-positive. Precautions like gentle delivery and placenta removal can minimize fetal-maternal bleeding. Developed antibodies can cause anemia, jaundice or fluid buildup in subsequent Rh-positive babies.
This document discusses Rh negative pregnancy and management of Rh sensitization. It explains that Rh factor is a red blood cell antigen, with the D antigen being most important in determining Rh positivity. If a Rh negative mother carries a Rh positive fetus, some Rh positive fetal red blood cells can enter the mother's circulation, causing her to develop antibodies against the D antigen. This sensitization can lead to fetal anemia and hydrops if the fetus in a subsequent pregnancy is Rh positive. Prophylactic anti-D injections are given during and after pregnancy to prevent sensitization. For sensitized pregnancies, careful fetal monitoring and potential intrauterine blood transfusions are needed to manage the risk of fetal anemia.
Immune hydrops fetalis is a condition where excess fluid builds up in fetal tissues due to maternal antibodies destroying fetal red blood cells. It can be caused by Rh incompatibility between mother and fetus. The excess hemolysis of fetal red blood cells leads to anemia, liver and spleen damage, heart failure and fluid buildup. Ultrasound is used to diagnose hydrops fetalis by detecting fluid in two fetal compartments. Treatment involves monitoring the fetus and performing intrauterine blood transfusions if needed to improve fetal hemoglobin levels and resolve hydrops. Routine Rh immunoprophylaxis can prevent Rh sensitization and immune hydrops in subsequent pregnancies.
Hemolytic Disease of the Newborn (HDN) is caused by maternal antibodies destroying fetal red blood cells. The most common cause is Rh disease, where an Rh-negative mother produces antibodies against Rh+ antigens from the father. These antibodies cross the placenta and cause anemia or hydrops fetalis in the fetus or newborn. Diagnosis involves serological testing of the mother's blood type and antibody screen during pregnancy. Management may include Rh immunoglobulin injections for the mother or intrauterine transfusions for severe cases of fetal anemia.
Hemolytic disease of the newborn (HDN), also known as erythroblastosis fetalis, occurs when maternal antibodies attack and destroy fetal red blood cells due to blood group incompatibilities between mother and fetus, most commonly Rh incompatibility, which can cause fetal anemia, jaundice, and in severe cases heart failure or death; diagnosis involves blood tests of the mother and newborn and management focuses on monitoring the pregnancy, preventing sensitization in unsensitized mothers, and treating the newborn if necessary.
Rh Incompatibility a Gynecological disordervirengeeta
Rh incompatibility occurs when a mother has Rh-negative blood and the fetus has Rh-positive blood. This can lead to hemolytic disease in subsequent pregnancies as the mother's immune system produces antibodies against the Rh-positive fetal blood cells. Key aspects of management include Rh immunoglobulin injections for Rh-negative mothers after pregnancy events or delivery of an Rh-positive baby to prevent sensitization, monitoring of sensitized mothers and treatment of affected fetuses or newborns which may include intrauterine transfusions, induction of early delivery, exchange transfusions, and phototherapy.
Manifestation of hdfn & prophylaxis of rh isoimmunizationabangroy94
Slideshow about manifestation of the hemolytic disease of the fetus & newborn (HDFN)
Hydrops Fetalis
Diagnostic Features
Icterus Gravis Neonatorum
Congenital Anemia of Newborn
Prevention of Rh-immunization
Hemolytic disease of newborn Lecture Final Year MBBS Sajjad Sabir
Hemolytic disease of the newborn (HDN), also known as erythroblastosis fetalis, is a condition where a pregnant woman's red blood cells are destroyed by antibodies produced by the fetus or newborn baby. It occurs when the mother is Rh negative and the baby's father is Rh positive, causing the mother to form antibodies against the baby's Rh positive blood cells. These antibodies can then cross the placenta and destroy the baby's red blood cells. Symptoms in severe cases include jaundice, anemia, enlarged liver and spleen, fluid in the lungs or abdomen, and heart failure. Diagnosis involves blood typing of the mother and baby. Management may include RhIG injections during pregnancy to prevent
Rh incompatibility occurs when a pregnant woman with Rh negative blood is carrying a baby with Rh positive blood. During pregnancy or delivery, the baby's Rh positive blood can enter the mother's bloodstream and trigger an immune response. This response produces antibodies that can destroy the baby's red blood cells if the mother has a subsequent Rh positive baby. Rh incompatibility can cause jaundice, anemia and in severe cases hydrops fetalis in the baby. Diagnosis involves blood tests to check the mother's Rh status and antibody levels. Treatment may include Rh immunoglobulin injections during pregnancy to prevent sensitization.
HDN is caused by maternal IgG antibodies crossing the placenta and destroying fetal red blood cells. The most common causes are Rh and ABO incompatibility. This leads to fetal anemia, jaundice, liver/spleen enlargement, hydrops fetalis, and potentially kernicterus. Management involves prevention with RhIg in Rh-negative mothers, and treatment of the fetus with intrauterine transfusions or the newborn with phototherapy or exchange transfusions. Testing of mothers and fetuses helps monitor the condition.
This document summarizes Rh isoimmunization, which occurs when a pregnant woman with Rh-negative blood is carrying a baby with Rh-positive blood. Fetal blood can enter the mother's circulation, causing her to form antibodies against the Rh antigen. On subsequent pregnancies, these antibodies can cross the placenta and destroy the fetus's red blood cells, potentially causing hydrops fetalis or jaundice in the newborn. Anti-D immunoglobulin injections are given to Rh-negative mothers during and after pregnancy to prevent antibody formation by blocking the Rh antigen. Proper management can prevent severe complications in future pregnancies from Rh isoimmunization.
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Rh isoimmunization occurs when a Rh-negative mother develops antibodies against Rh-positive fetal red blood cells. This can cause hemolytic disease in future Rh-positive pregnancies. Prophylaxis with Rh immunoglobulin is highly effective at preventing sensitization. For sensitized pregnancies, maternal anti-D titers and fetal middle cerebral artery Doppler are used to monitor for anemia. Severe anemia may require cordocentesis or intrauterine transfusions. After delivery, affected newborns may need exchange transfusions or other supportive care to manage hyperbilirubinemia and anemia. Prompt and specialized treatment can help prevent complications in isoimmunized pregnancies.
1. Blood group is defined by the ABO system (O, A, B, AB) and the Rhesus system (Rh positive or negative).
2. Rh disease occurs when an Rh-negative mother is pregnant with an Rh-positive baby. Her immune system develops antibodies that can cross the placenta and destroy the baby's red blood cells.
3. Management involves routine antenatal anti-D prophylaxis for Rh-negative mothers and monitoring of sensitized mothers through antibody titers and fetal Doppler testing. Intrauterine transfusions may be needed to treat severe fetal anemia.
This document discusses Rh isoimmune disease, which occurs when a pregnant woman has Rh-negative blood and her baby has Rh-positive blood. It begins by explaining the differences between isoimmune and autoimmune diseases. It then covers blood group systems like ABO and Rh, how they are inherited, and the importance of compatibility for transfusions. The majority of the document focuses on Rh incompatibility during pregnancy, how it can harm the fetus, diagnosis, and treatments like intrauterine transfusions, early delivery, and phototherapy or exchange transfusions for the newborn. It emphasizes the need for Rh-negative mothers to receive Rh immunoglobulin injections during and after pregnancy to prevent sensitization.
This document discusses Rh isoimmunization in pregnancy. The key points are:
- Rh isoimmunization occurs when an Rh-negative mother is exposed to Rh-positive blood cells from her baby during pregnancy or delivery, triggering an immune response.
- The first baby is usually unaffected, but subsequent pregnancies are at risk if the mother's IgG antibodies cross the placenta and destroy the baby's red blood cells.
- Management involves prophylaxis with anti-D globulin injections after delivery or abortion. Severe cases may require antenatal treatments like plasmapheresis or intrauterine transfusions. High-risk babies require intensive monitoring and possible exchange transfusions.
Rh incompatibility occurs when an Rh-negative pregnant woman is exposed to Rh-positive blood cells, usually from her fetus. This can cause the woman to develop Rh antibodies which can then cross the placenta and destroy fetal red blood cells. The most common cause is fetal blood exposure during pregnancy or delivery from the first Rh-positive baby. Subsequent pregnancies are at higher risk of more severe anemia or death for the baby. Treatment involves administering Rh immunoglobulin injections during and after pregnancy to prevent antibody formation. Early prenatal care and Rh immunoglobulin have reduced the risk from 10-20% to less than 1%.
Rhesus factor is a protein found on red blood cells. If present, one is Rh positive; if absent, Rh negative. Rh factor is inherited from parents. Rh incompatibility occurs when an Rh negative mother is exposed to Rh positive blood, risking complications for her Rh positive baby like hydrops fetalis or jaundice. Management includes screening, anti-D immunoglobulin, monitoring, and timing delivery to prevent baby anemia. Sensitized mothers require additional monitoring and may need intrauterine transfusions or early delivery.
Rh isoimmunization occurs when an Rh-negative pregnant mother develops antibodies against Rh-positive fetal red blood cells. This most commonly happens due to fetomaternal hemorrhage during pregnancy or delivery when fetal cells enter the mother's circulation. The antibodies can then cross the placenta during subsequent pregnancies and destroy fetal red blood cells, causing anemia or even hydrops fetalis. Management of at-risk pregnancies includes determining paternal and fetal Rh status, monitoring antibody titers, and assessing fetal anemia using Doppler ultrasound or invasive tests like amniocentesis if high titers are present. Timely administration of RhIg prophylaxis can prevent sensitization in Rh-negative mothers carrying Rh-positive fet
This document discusses immune conflict that can occur during pregnancy between an Rh-negative mother and Rh-positive fetus. Specifically, it describes Rh isoimmunization, where antibodies produced by the mother's immune system in response to Rh antigens on fetal red blood cells can cross the placenta and destroy fetal red blood cells. If left untreated, this hemolytic process can lead to fetal anemia, jaundice, edema, and even hydrops fetalis. The document outlines methods for diagnosing and preventing Rh isoimmunization.
An Rh-negative pregnant woman is at risk of developing antibodies against her Rh-positive baby's red blood cells. This can cause hemolytic disease in future pregnancies.
The document outlines protocols for testing, prevention, and management. All Rh-negative pregnant women should be tested for antibodies at first visit. Anti-D immunoglobulin is given postpartum/abortion to prevent sensitization if the baby is Rh-positive. Precautions like gentle delivery and placenta removal can minimize fetal-maternal bleeding. Developed antibodies can cause anemia, jaundice or fluid buildup in subsequent Rh-positive babies.
This document discusses Rh negative pregnancy and management of Rh sensitization. It explains that Rh factor is a red blood cell antigen, with the D antigen being most important in determining Rh positivity. If a Rh negative mother carries a Rh positive fetus, some Rh positive fetal red blood cells can enter the mother's circulation, causing her to develop antibodies against the D antigen. This sensitization can lead to fetal anemia and hydrops if the fetus in a subsequent pregnancy is Rh positive. Prophylactic anti-D injections are given during and after pregnancy to prevent sensitization. For sensitized pregnancies, careful fetal monitoring and potential intrauterine blood transfusions are needed to manage the risk of fetal anemia.
Immune hydrops fetalis is a condition where excess fluid builds up in fetal tissues due to maternal antibodies destroying fetal red blood cells. It can be caused by Rh incompatibility between mother and fetus. The excess hemolysis of fetal red blood cells leads to anemia, liver and spleen damage, heart failure and fluid buildup. Ultrasound is used to diagnose hydrops fetalis by detecting fluid in two fetal compartments. Treatment involves monitoring the fetus and performing intrauterine blood transfusions if needed to improve fetal hemoglobin levels and resolve hydrops. Routine Rh immunoprophylaxis can prevent Rh sensitization and immune hydrops in subsequent pregnancies.
Hemolytic Disease of the Newborn (HDN) is caused by maternal antibodies destroying fetal red blood cells. The most common cause is Rh disease, where an Rh-negative mother produces antibodies against Rh+ antigens from the father. These antibodies cross the placenta and cause anemia or hydrops fetalis in the fetus or newborn. Diagnosis involves serological testing of the mother's blood type and antibody screen during pregnancy. Management may include Rh immunoglobulin injections for the mother or intrauterine transfusions for severe cases of fetal anemia.
Hemolytic disease of the newborn (HDN), also known as erythroblastosis fetalis, occurs when maternal antibodies attack and destroy fetal red blood cells due to blood group incompatibilities between mother and fetus, most commonly Rh incompatibility, which can cause fetal anemia, jaundice, and in severe cases heart failure or death; diagnosis involves blood tests of the mother and newborn and management focuses on monitoring the pregnancy, preventing sensitization in unsensitized mothers, and treating the newborn if necessary.
Rh Incompatibility a Gynecological disordervirengeeta
Rh incompatibility occurs when a mother has Rh-negative blood and the fetus has Rh-positive blood. This can lead to hemolytic disease in subsequent pregnancies as the mother's immune system produces antibodies against the Rh-positive fetal blood cells. Key aspects of management include Rh immunoglobulin injections for Rh-negative mothers after pregnancy events or delivery of an Rh-positive baby to prevent sensitization, monitoring of sensitized mothers and treatment of affected fetuses or newborns which may include intrauterine transfusions, induction of early delivery, exchange transfusions, and phototherapy.
Manifestation of hdfn & prophylaxis of rh isoimmunizationabangroy94
Slideshow about manifestation of the hemolytic disease of the fetus & newborn (HDFN)
Hydrops Fetalis
Diagnostic Features
Icterus Gravis Neonatorum
Congenital Anemia of Newborn
Prevention of Rh-immunization
Hemolytic disease of newborn Lecture Final Year MBBS Sajjad Sabir
Hemolytic disease of the newborn (HDN), also known as erythroblastosis fetalis, is a condition where a pregnant woman's red blood cells are destroyed by antibodies produced by the fetus or newborn baby. It occurs when the mother is Rh negative and the baby's father is Rh positive, causing the mother to form antibodies against the baby's Rh positive blood cells. These antibodies can then cross the placenta and destroy the baby's red blood cells. Symptoms in severe cases include jaundice, anemia, enlarged liver and spleen, fluid in the lungs or abdomen, and heart failure. Diagnosis involves blood typing of the mother and baby. Management may include RhIG injections during pregnancy to prevent
Rh incompatibility occurs when a pregnant woman with Rh negative blood is carrying a baby with Rh positive blood. During pregnancy or delivery, the baby's Rh positive blood can enter the mother's bloodstream and trigger an immune response. This response produces antibodies that can destroy the baby's red blood cells if the mother has a subsequent Rh positive baby. Rh incompatibility can cause jaundice, anemia and in severe cases hydrops fetalis in the baby. Diagnosis involves blood tests to check the mother's Rh status and antibody levels. Treatment may include Rh immunoglobulin injections during pregnancy to prevent sensitization.
HDN is caused by maternal IgG antibodies crossing the placenta and destroying fetal red blood cells. The most common causes are Rh and ABO incompatibility. This leads to fetal anemia, jaundice, liver/spleen enlargement, hydrops fetalis, and potentially kernicterus. Management involves prevention with RhIg in Rh-negative mothers, and treatment of the fetus with intrauterine transfusions or the newborn with phototherapy or exchange transfusions. Testing of mothers and fetuses helps monitor the condition.
This document summarizes Rh isoimmunization, which occurs when a pregnant woman with Rh-negative blood is carrying a baby with Rh-positive blood. Fetal blood can enter the mother's circulation, causing her to form antibodies against the Rh antigen. On subsequent pregnancies, these antibodies can cross the placenta and destroy the fetus's red blood cells, potentially causing hydrops fetalis or jaundice in the newborn. Anti-D immunoglobulin injections are given to Rh-negative mothers during and after pregnancy to prevent antibody formation by blocking the Rh antigen. Proper management can prevent severe complications in future pregnancies from Rh isoimmunization.
Similar to Rhesus Isoimmunisation Dr Adegoke.pptx (20)
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3. INTRODUCTION
• The Rh factor (Rhesus factor) is a red blood cell surface antigen that was
named after the monkeys in which it was first discovered.
• Rh incompatibility, also known as Rh disease, is a condition that occurs
when a woman with Rh-negative blood type is exposed to Rh-positive
blood cells, leading to the development of Rh antibodies.
• There are two main mechanisms by which Rh incompatibility can occur:
1. The most common type occurs when a Rhesus negative pregnant mother
is exposed to Rh-positive fetal red blood cells secondary to fetomaternal
hemorrhage during the course of pregnancy from spontaneous or
induced abortion, trauma, invasive obstetric procedures, or normal
delivery.
4. INTRODUCTION(cont’d)
2. Rh incompatibility can also occur when a Rh-negative female
receives a Rh-positive blood transfusion
• The most common cause of Rh incompatibility is exposure from a Rh-
negative mother by Rh-positive fetal blood during pregnancy or
delivery.
• As a consequence, blood from the fetal circulation may leak into the
maternal circulation, and, after a significant exposure, sensitization
occurs leading to maternal antibody production against the foreign Rh
antigen.
5. INTRODUCTION(cont’d)
• Once produced, maternal Rh immunoglobulin G (IgG) antibodies
persist for life and may cross freely from the placenta to the fetal
circulation, where they form antigen-antibody complexes with Rh-
positive fetal erythrocytes and eventually are destroyed, resulting in a
fetal alloimmune-induced hemolytic anemia.
• Although the Rh blood group systems consist of many antigen
subtypes (eg, D, C, c, E, e), the D antigen is the most immunogenic;
therefore, it most commonly is involved in Rh incompatibility.
6. RHESUS SYSTEM
• Rhesus genes = chromosome 1. (short arm)
• Rh genes C, D, and E (dominant genes)
• c, d, and e genes (recessive genes).
• Each chromosome has a C locus, a D locus, and an E locus
• Rhesus D antigen (or Rhesus factor) is the most important or antigenic of all the
Rh antigens.
• Absence = rhesus negative.
• Rhesus system is inherited by Mendelian model of Inheritance. The genotype can
be as follows:
• CDe/cDE Homozygous Rh (D) positive
• CDe/cde Heterozygous Rh (D) positive
• Cde/cde Rhesus negative
7. • Heterozygous Rh (D) positive - 55%
• Homozygous Rh (D) positive - 45%
N.B: Rhesus c and E antigens can also cause maternal
sensitization.
8. EPIDEMIOLOGY
• The incidence of rhesus negativity varies.
• Basque of Spain 30-35%,
• Caucasians 15-16%,
• American Blacks 8%,
• African Blacks 4%, and
• Mongoloid nil
9. AETIOLOGY OF RHESUS ISOIMMUNISATION
• Rhesus disease = Rh –ve woman is sensitized = antibodies cross the
placenta to affect the fetus.
• The sensitization of the Rh –ve woman:
• Transfusion of incompatible blood
• Feto-maternal haemorrhage
• Sensitizing conditions include:
• Silent feto-maternal haemorrhage = 1-2%
• Vaginal delivery
• Abortions: - spontaneous (3-4% risk)
- induced abortions (5-25% risk)
10. AETIOLOGY(Cont’d)
• Antepartum haemorrhage – placenta praevia and placental abruption
• Manual removal of the placenta
• Caesarean section
• External version
• Invasive prenatal testing – chorion villus sampling, amniocentesis and
cordocentesis
11. PATHOGENESIS
• Development of antibodies depends on some factors:
1. Inborn ability to respond to Rh antigenic stimulus = 2/3 of the Rh –
ve women are responsive.
2. ABO incompatibility is protective = reduces the incidence from
about 16% to about 1.5-2%.
3. Variation in the strength of the Rh antigenic stimulus = CDe/cde
genotype seems to be relatively ‘strong’.
4. Volume of fetal blood entering the maternal circulation.
Critical sensitising volume is 0.25ml although sensitization can occur with as
little as 0.1ml
12. • 5. When conditions are favourable for the formation of antibodies:
• IgM (Saline Ab), (abt 7 days after stimulation).
• IgG (Albumin antibody), 7S immunoglobulin, 21 days after stimulation = IgG
crosses the placenta
13. EFFECTS ON THE FETUS
• Haemolysis – the coated fetal RBCs = reticulo-endothelial cells
• anaemia and release of increased amount of unconjugated bilirubin
• increased extramedullary erythropoiesis with immature erythroblasts in the
fetal circulation
• unconjugated bilirubin passes through the placenta into the maternal blood
• Severe anaemia: it occurs when destruction of fetal RBCs far exceeds
production
• Placental hyperplasia 2o to hypoxia
15. EFFECTS ON THE NEONATE
• Severe anaemia = HF, ascites, edema etc
• Hyperbilirubinaemia = immature liver (low level of
glucuronyltransferase)
16. MANAGEMENT OF UNSENSITISED RHESUS
NEGATIVE PREGNANCY
• First visit = Rhesus status and screening test for immune antibodies
(ICT). If Rhesus negative,
• Test paternal Rhesus status. If Rh –ve, no risk of Rh +ve fetus or Rh
disease. If Rh +ve,
• Monitor atypical antibody level at
• 24 weeks
• 28 weeks. If negative, give RhIgG
• 35 or 36 weeks
17. • Postpartum, take fetal cord for Rhesus status, PCV, DCT and bilirubin
level. If rhesus +ve,
• Give standard dose of anti-D IgG (RhIgG) within 72 hrs of delivery
(give up to 28 days, if necessary).
• Kleihauer-Betke test (acid elution test) on maternal blood = estimate
volume of fetal blood = fetal RBCs in x50 LPF (80 fetal RBCs = 4mLof
fetal blood, 0.05ml = 1 cell).
• 1500 IU(300μg) of RhIgG(RhoGAM) neutralizes 15mL of Rh +ve blood
• Anti-D IgG prophylaxis reduces risk of isoimmunisation to 0.2%
18. ]FG00PPPP
• Give RhIgG in case of some fetomaternal risk states:
• Abortion: 1st trimester = 50μg (250 IU)
2nd trimester = 300μg
• Amniocentesis, CVS, Cordocentesis = 300 μg
• APH – placenta praevia, placental abruption = 300 μg stat, repeat if pregnancy
is carried more than 12 weeks after the administration of the anti-D IgG
• ECV = 300 μg RhIgG. It carries 2-6% risk of fetomaternal haemorrhage.
• Avoid manual removal of placenta as much as possible during CS in a
Rh –ve woman.
• Pack off the uterus from peritoneal cavity
• Amniocentesis = under direct ultrasound guidance
19. • COOMB’s TEST – an antiglobulin test.
• Coomb’s reagent is an immune anti-globulin .
• DCT (DAGT) = detects an affected fetus at birth
• Cells from fetal cord + reagent = agglutination if affected.
• ICT (IAGT) = detects and measures antibody in the maternal serum.
• Maternal serum + test cells = coated cells + reagent = agglutination if
sensitized.
• Dilute maternal serum to quantify antibody (titre)
20. MANAGEMENT OF PREGNANCY
COMPLICATED BY RHESUS IMMUNISATION
• Depends on two factors:
• Whether the patient has a history of an affected fetus in a previous
pregnancy.
• Maternal antibody titre
• a) No history of previous fetus affected by Rh isoimmunisation
• Monitor antibody titre at booking, 20 weeks, then 4 weekly.
• If antibody titre is >15IU/mL or ≥ 1:32 by ICT, amniocentesis should be carried
out
21. • b) Has history of prior fetus affected by Rh isoimmunisation
• stillbirth or neonatal death
• Severely affected baby (cord Hb < 10g/dL)
• Fetal transfusion in previous pregnancy
• No need for serial antibody monitoring
• 1st amniocentesis or cordocentesis = performed 10 weeks earlier
than the gestation in the previous pregnancy when Rh-associated
morbidity/mortality was first identified (Action line method of
Whitfield)
• Cordocentesis (fetal haematocrit and rhesus status) is preferable < 28
weeks
• If no serious outcome in previous pregnancy, 1st amniocentesis
should be btw 28 and 30 weeks. Repeat in 3 -4 weeks = establish the
trend and eliminate error from bloody tap or from measurement
22. • The concentration of bilirubin in the amniotic fluid
• Spectrophotometry = optical density deviation of 450nm
• Liley’s chart = delta OD450 plotted against GA. Has zones 1-3.
• N.B: Liley’s prediction zones are valid only in 3rd trimester.
• Manage based on the zone
• Biophysical Surveillance
• UltraGFsound to monitor
• Features of hydrops fetalis – ascites, hydrothorax, pericardial effusion, or generalized
edema
• Fetal heart size
• Amniotic fluid index - polyhydramnios
• Fetal movement
• Doppler USS = increase blood flow velocities in umbilical vein, middle cerebral artery
and descending aorta = fetal anaemia
23. • FHR tracing
• Sinusoidal rhythm = severe anaemia
• Abnormal CTG
• Non-reactive
• Reduced variability
• N.B: Clinical and USS features of fetal anaemia only become evident
when fetal Hb >5-7g/dL less than the mean for gestation or become
obvious when the Hb < 5-6g/dL.
24. INTERVENTION
• Depends on result of investigation
• Mildly affected / unaffected fetus
• Zone 1 of Liley’s curve
• Repeat amniocentesis 2-3 weekly
• Deliver near term or after the fetus has achieved pulmonary maturity
• Moderately affected fetus
• Zone 2
• Amniocentesis 1-2 weekly
• Preterm delivery as soon as pulmonary maturity is achieved (naturally or
facilitated)
25. • Severely affected fetus
• Zone 3
• Intrauterine intervention necessary
• Weekly amniocentesis
• Close ultrasound monitoring
• Intrauterine transfusion may be required every 7-10 days until pulmonary
maturity is achieved
26. DELIVERY OF AN AFFECTED FETUS
• Paediatrician should be present.
• - Induction of labour preferable
• - Low threshold for C/S with signs of fetal distress
• - Anaemia predisposes to fetal distress
• - Hypoxia and acidosis impair baby’s ability to conjugate bilirubin
• - Get blood ready for possible exchange transfusion
• - Take cord blood for PCV, blood group and rhesus status, Direct
Coomb’s test, and bilirubin level.
27. POSTPARTUM COUNSELLING AND
CONTRACEPTION
• Counsel patient based on prognosis
• Rh mortality rate range from:
• 2% when no previous baby has been affected to
• 30% when there has been a previous Rhesus death despite intensive
management by experienced Rh team
• Advise on contraception