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Rh incompatibility
- 2. • Proteins (antigens) occurring only on surface of RBC’s • Rh + if proteins present • Rh – if proteins absent • A+, A-, B+, B-, AB+, AB-, O+, O- • Most important for pregnancy • Inheritance is Autosomal Dominant • 15% Caucasian population are Rh- Rh FACTOR
- 3. INTRODUCTION • During Pregnancy, the mother and the fetus have different Rh protein factors, this condition is called Rh incompatibility. • Like our blood type, we inherit our Rh factor type from our parents. Most people are Rh-positive, but a small percentage of people are Rh-negative • Rh factor doesn’t directly affect the health. • However, Rh factor becomes important during pregnancy.
- 4. • Rhesus disease is a condition where antibodies in a pregnant woman's blood destroy her baby's blood cells. It's also known as haemolytic disease of the fetus and newborn (HDFN). • If the mother is Rh-negative and her baby is Rh-positive, during pregnancy (and especially during labor and delivery) some of the fetus's Rh-positive red blood cells may get into the mother's bloodstream. • SENSITIZATION – The process in which mother’s body will try to fight them off by producing antibodies against them. Rh DISEASE?
- 5. Potential sensitizing events for Rhesus Disease • Miscarriage • Termination of pregnancy • Antepartum haemorrhage • Invasive prenatal testing (amniocentesis, cordocentesis etc.) • Delivery • Ectopic pregnancy
- 9. CAUSES •Ectopic pregnancy •Partial molar pregnancy •Blighted ovum •Antepartum bleeding •External version •Platelet transfusion •Placenta previa •Placental abruption •Abdominal/pelvic trauma •In utero fetal death •Any invasive obstetric procedure (eg, amniocentesis) •Lack of prenatal care •Postpartum (Rh+baby) •Spontaneous abortion
- 10. Rh incompatibility can cause symptoms ranging from very mild to deadly. In its mildest form, Rh incompatibility causes the destruction of red blood cells. There are no other effects. After birth, the infant may have: •Yellowing of the skin and whites of the eyes (jaundice) •Low muscle tone (hypotonia) •Lethargy •Swelling or edema (hydrops fetalis) SYMPTOMS
- 11. Signs of fetal anemia • Polyhydramnios • Enlarged fetal heart • Ascites and pericardial effusions • Hyperdynamic fetal circulation (MCA doppler) • Reduced fetal movements • Abnormal CTG with reduced variability
- 12. Diagnosis • MCA doppler • Cell free DNA • Kleihauer test • Amniocentesis and liley graph • Direct coomb’s test
- 13. SCREENING TESTS • ABO & Rh Ab at 1st prenatal visit • At 28 weeks • Postpartum Bleeding • Antepartum bleeding and before giving any immune globulin • Neonatal bloods ABO, Rh GOLD STANDARD TESTS • Indirect Coombs: mix Rh(D)+ cells with maternal serum anti-Rh(D) Ab will adhere RBC’s then washed & suspended in Coombs serum RBC’s coated with Ab will be agglutinated • Direct Coombs: mix infant’s RBC’s with Coombs serum maternal Ab present if cells agglutinate
- 16. Non Reliable Parameters: • Placental thickness • Umbilical vein diameter • Hepatic size • Splenic size • Polyhydramnios Visualization of walls of fetal bowel from small amounts intra abdominal fluid may be 1st sign of impending hydrops U/S reliable for hydrops (ascites, pleural effusions, skin edema) – Hgb < 70 Ultrasound Parameters
- 17. COMPLICATIONS DURING PREGNANCY •Mild anemia, hyperbilirubinemia and jaundice. •Severe anemia with enlargement of the liver and spleen. •Hydrops fetalis. AFTER BIRTH •Severe hyperbilirubinemia and jaundice. •Kernicterus
- 18. Management • Anti D immunoglobulin • Fetal blood transfusion (fetal Hct <30%) • Phototherapy
- 19. • Routes of administration- • Into umbilical vein at the point of cord insertion • Into intrahepatic vein • Into peritoneal cavity • Into fetal heart • Transfused blood- • RhD negative • Crossmatched with a maternal sample • Densely packed (Hb around 30g/L) • White cell depleted and irradiated • Screened for infection including CMV
- 20. •Prophylactic vaccinations- • During every pregnancy • After a miscarriage or abortion • After prenatal tests such as amniocentesis and chorionic villus biopsy • After injury to the abdomen during pregnancy
Editor's Notes
- 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. Rh incompatibility can occur by 2 main mechanisms. The most common type occurs when an Rh-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,[1] invasive obstetric procedures, or normal delivery. Rh incompatibility can also occur when an Rh-negative female receives an Rh-positive blood transfusion. In part, this is the reason that blood banks prefer using blood type "O negative" or "type O, Rh negative," as the universal donor type in emergency situations when there is no time to type and crossmatch blood. The most common cause of Rh incompatibility is exposure from an 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. Once produced, maternal Rh immunoglobulin G (IgG) antibodies 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.[2] Although the Rh blood group systems consist of several antigens (eg, D, C, c, E, e), the D antigen is the most immunogenic; therefore, it most commonly is involved in Rh incompatibility. This means that if blood cells from your baby cross your bloodstream, which can happen during pregnancy, labor, and delivery, your immune system will make antibodies against your baby’s red blood cells. Antibodies are parts of your body’s immune system. They destroy foreign substances. If you have an Rh-negative blood type, you’re considered sensitized to your baby once your body has made these antibodies. This means that your body might send these antibodies across the placenta to attack your baby’s red blood cells. Your placenta is the organ that connects you and your baby.
- This is a disease that destroys an unborn baby's blood cells, potentially resulting in newborns being born with jaundice (yellowing of the skin and eyes) and anemia. In some cases the results could be brain damage, heart failure, and even death. But today, doctors are able to detect and treat Rh disease in the fetus, so about 95 percent of babies with severe Rh disease survive. Sensitization - Amniocentesis Chorionic villus sampling (CVS) Bleeding during pregnancy Manual rotation of a baby in a breech presentation before labor Blunt trauma to the abdomen during pregnancy It also is possible to develop antibodies after a miscarriage, an ectopic pregnancy, or an induced abortion. If an Rh-negative woman becomes pregnant after one of these events, she does not receive treatment, and the fetus is Rh positive, the fetus may be at risk of Rh-related problems.
- Once sensitized, it takes approximately one month for Rh antibodies in the maternal circulation to equilibrate in the fetal circulation. In 90% of cases, sensitization occurs during delivery. The amount of fetal blood necessary to produce Rh incompatibility varies. In one study, less than 1 mL of Rh-positive blood was shown to sensitize volunteers with Rh-negative blood. Conversely, other studies have suggested that 30% of persons with Rh-negative blood never develop Rh incompatibility, even when challenged with large volumes of Rh-positive blood. Once sensitized, it takes approximately one month for Rh antibodies in the maternal circulation to equilibrate in the fetal circulation. In 90% of cases, sensitization occurs during delivery. Therefore, most firstborn infants with Rh-positive blood type are not affected because the short period from first exposure of Rh-positive fetal erythrocytes to the birth of the infant is insufficient to produce a significant maternal IgG antibody response. The risk and severity of sensitization response increases with each subsequent pregnancy involving a fetus with Rh-positive blood. In women who are prone to Rh incompatibility, the second pregnancy with an Rh-positive fetus often produces a mildly anemic infant, whereas succeeding pregnancies produce more seriously affected infants who ultimately may die in utero from massive antibody-induced hemolytic anemia. Risk of sensitization depends largely upon the following 3 factors: Volume of transplacental hemorrhage Extent of the maternal immune response Concurrent presence of ABO incompatibility The incidence of Rh incompatibility in the Rh-negative mother who is also ABO incompatible is reduced dramatically to 1-2% and is believed to occur because the mother's serum contains antibodies against the ABO blood group of the fetus. The few fetal red blood cells that are mixed with the maternal circulation are destroyed before Rh sensitization can proceed to a significant extent. Fortunately, ABO incompatibility usually does not cause serious sequela. Rh incompatibility is only of medical concern for females who are pregnant or plan to have children in the future. Rh-positive antibodies circulating in the bloodstream of an Rh-negative woman otherwise have no adverse effects.
- partial molar pregnancy is a variation of a molar pregnancy, an abnormal pregnancy in which an embryo (the fertilized egg) either develops incompletely, or doesn’t develop at all. Instead, a cluster of grape-like cysts (known as a hydatidiform mole) grows in the uterus. A blighted ovum occurs when a fertilized egg implants in the uterus but doesn't develop into an embryo. It is also referred to as an anembryonic (no embryo) pregnancy and is a leading cause of early pregnancy failure or miscarriage. Often it occurs so early that you don't even know you are pregnant. A blighted ovum causes about one out of two miscarriages in the first trimester of pregnancy. A miscarriage is when a pregnancy ends on its own within the first 20 weeks. Placenta previa (pluh-SEN-tuh PREH-vee-uh) occurs when a baby's placenta partially or totally covers the opening in the mother's cervix — the lower end of the uterus that connects to the top of the vagina. Placenta previa can cause severe bleeding before or during delivery.
- Direct Coombs test The direct Coombs test finds antibodies attached to your red blood cells. The antibodies may be those your body made because of disease or those you get in a blood transfusion. The direct Coombs test also may be done on a newborn baby with Rh-positive blood whose mother has Rh-negative blood. The test shows whether the mother has made antibodies and if the antibodies have moved through the placenta to her baby. Indirect Coombs test The indirect Coombs test finds certain antibodies that are in the liquid part of your blood (serum). These antibodies can attack red blood cells but are not attached to your red blood cells. The indirect Coombs test is commonly done to find antibodies in a recipient's or donor's blood before a transfusion. A test to determine whether a woman has Rh-positive or Rh-negative blood (Rh antibody titer) is done early in pregnancy. If she is Rh-negative, steps can be taken to protect the baby.
- During pregnancy: 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. After birth: 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.