Effects on the fetus & neonate Symptoms and complications will only affect the fetus.
The complications occur when standard preventive measures are not taken.
🔹
The symptoms can vary from mild to severe.
🔹 Hemolytic anemia
🔹
🔹
Numerous erythroblast in fetal circulation
Generalized edema (hydrops fetalis)
🔹 Enlargement of fetal liver & spleen in its most severe form
Severity of the anemia resulted in cardiac failure, with widespread edema, ascites and pleural effusion.
🔻 A complication of untreated jaundice is kernicterus, a syndrome which can affect the baby's nervous system. Contact doctor
right away if the baby:
-Has a yellow or orange appearance to the skin
-Does not sleep
- Is hard to wake up
- Is not breastfeeding or has difficulty sucking from a bottl
- Is restless or fussy
Investigation
Kleihauer–Betke test The diagnosis is based on the presence of anti-Rh (D) antibody in maternal serum. Methods of detecting Anti D
Antibodies in maternal serum:
The Enzymatic Method
The Antibody Titer In Saline, In Albumin
The Indirect Coombs Tests.
🔻 Maternal blood
The Kleihauer–Betke test or flow cytometry on a postnatal maternal blood sample can confirm that fetal blood
has passed into the maternal circulation and can also be used to estimate the amount of fetal blood that has passed
into the maternal circulation and the dose of the anti Rhesus antibody will be adjusted accordingly.
🔹 ISO:
🔹is the
is a prefix means similar, equal or uniform.
🔸
It depends on the fact that fetal hemoglobin is more resistant than adult’s hemoglobin to the acid elution.
The indirect Coombs test is used to screen blood from antenatal women for IgGantibodies that may pass through
the placenta and cause hemolytic disease of thenewborn.
Isoimmunization:
process of immunizing a species with antigen derived fromthe same
🔹
subject
🔻
🔹Fetal blood (or umbilical cord blood)
The direct coombs test is done after birth to detect the presence of maternal antibody on the neonate's RBCs.
Rhesus :
major blood group antigen of importance during pregnancy.Incompatibility
DIAGNOSIS
🔹RhRhoGAM®
indirect Coombs test The infant's RBCs are placed in Coomb’s serum. If the cells are agglutinated this indicate the presence of maternal between mother (-) and fetus (+) may led to hemolytic diseaseof the newborn.
Definitions: :
🔹
antibody. Is used to confirm that the fetus or neonate has an immune mediated hemolytic anemia.
🔹 Full blood count—the hemoglobin level and platelet count are important immunoglobulin given to gravidas who are Rh negative if there is suspicion
🔹 Bilirubin (total and indirect) of fetal maternal bleeding for example : if there is bleeding during any
Fetal Rhesus Determination: trimester and after delivery.
-Type and zygosity (if Rh-positive) of the father
-Amniocentesis to determine the fetal blood type using the polymerase chain reaction (PCR) 🔹 Rh disease (also known as Rhesus isoimmunization, Rh (D) disease,
Rhesusincompatibility, Rhesus disease, Hemolytic Disease of the Newborn,
-Detection of free fetal RhD DNA (FRHD) sequences in maternal plasma or serum using PCR
-Flow cytometry of maternal blood for fetal cells Rhesus DHemolytic Disease of the Newborn) is one of the causes of hemolytic
Methods of diagnosis and evaluation of Fetal Rh Isoimmunization: disease of thenewborn.
-Measurements Of Antibodies in Maternal Serum
-Determination of Fetal Rh Blood Group
direct coombs test
-Ultrasonography
-Amniocentesis 🔹 Incidence
-Fetal Blood Sampling
🔹
varies based on prevalance of RBC antigen in different population
🔻
Prevalence(varies with race)
Ultrasonography INCIDENCE & PREVALENCE: Asian 99% D-positive (either DD & Dd genotype)African american 92-93%White
To establish the correct Gestational Age. american 87%Incidence higher in white due to relatively higher percentage of the
🔹
In guiding invasive procedures and monitoring fetal growth and well-being. population who do not carry the D-antigen on their RBC. Hence, more Rh-negative
Ultrasonographic parameters to determine Fetal Anemia: mother (dd)
o Placental Thickness.
o Umbilical Vein Diameter
o Hepatic Size.
o Splenic Size. The Rh Antigen- Biochemical Aspects:-
o Polyhydramnios. The Rh antigen is a complex lipoprotein. - It has a molecular weight of approximately 30,000.- It is distributed
o Fetal Hydrops (e.g. Ascites, Pleural Effusions, Skin Edema). throughout the erythrocyte membrane in a nonrandom fashion. -The surface antigens cannot be seen by routine
🔻
ultrasounogrphy microscopy, but can be identified byspecific Antisera
Doppler Velocimetry of the Fetal Middle Cerebral Artery (MCA) The RH Antigen- Genetic Aspect
Anemic fetus preserves oxygen delivery to the brain by increasing cerebral flow of its already low viscosity blood. The Rh gene complex is located on the distal end of the short arm of chromosome one. A given Rh antigen
For predicting fetal anemia To predict the timing of a Second intrauterine fetal transfusion complex is determined by a specific gene sequence inherited in a Mendelian fashion from the parents. One
haploid from the mother and one from the father. Three genetic loci, determine the Rh antigen (i.e. Rh blood
🔻 Invasive Techniques (Amniocentesis and Fetal Blood Sampling):
Rh Antigen:
group).
Each chromosome will be D positive or D negative (there is no "d" antigen), C or c positive, and E or e positive.
🔹
Indications
A Critical Anti-D Titer:
A Titer associated with a significant
🔹
Factors Affect The Expression Of The Rh Antigen:
The Number Of Specific Rh-antigen Sites:
🔹
risk for fetal hydrops. Anti-D titer value between 8 And 32
Previous Seriously Affected Fetus Or Infant
- The Gene Dose,
- The Relative Position of the Alleles,
🔻
(e.g. Intrauterine fetal transfusion, early delivery, fetal hydrops, neonatal exchange transfusion).
🔹 Amniocentesis 🔹
- The Presence or Absence of Regulator Genes.
Interaction of Other Components of the Rh Blood Group. Erythrocytes ofIndividuals of Genotype Cde/cde
Fetal blood sampling
🔹 Normally bilirubin in amniotic fluid decreases with advanced gestation.
🔹 ItItsderives from fetal pulmonary and tracheal effluents.
level rises in correlation with fetal hemoly
🔹
Express Less D Antigen than Do theErythrocytes of Individuals of Genotype cDE/cde.
The Exposure of the D Antigen on the Surface of the Red Cell Membrane
Interpretation of Amniotic Fluid Bilirubin:
-A falling curve: is reassuring: i.e. an unaffected or RhD-negative fetus.
-A plateauing or rising curve: suggests active hemolysis (require close monitoring and may require fetal blood
sampling and/or early delivery). 🔹 The Rh blood system (CDE) consists of five major antigens, D, C, c, E and e, all of which can produce erythrocyte
-A curve that reaches to or beyond the 80th percentile of zone II on the lileygraph or enters the “ intrauterine Rh alloimmunization.
transfusion" zone of the Queenan curve: necessitates investigation by fetal blood sampling
INCOMPATIBILITY 🔹
The erythrocyte D antigen is strongly immunogenic and therefore more important and more common than the other antigens.
Rh factor is a protein that may be found on the surface of red blood cells.
🔻 Fetal blood sampling:
-If she carries this protein, her blood is Rh positive.
Is the gold standard for detection of fetal anemia. Reserved for cases with:
- With an increased MCA-PSV(Peak systolic velocity of the fetal middle cerebral artery)
🔹
-If not carry this protein, her blood is Rh negative.
Sometimes a mother with Rh-negative blood is pregnant with a fetus that has Rh-positive blood. This can cause a problem if
the fetal blood enters the mother's blood flow (fetomaternal haemrrhage).
- Increased ΔOD 450 The Rh-positive blood from the fetus will make the mother's body create antibodies. This is called isoimmunization. The antibodies will
Fetal blood sampling — Ultrasound-directed fetal blood sampling (i.e., percutaneous umbilical blood sampling, attack any Rh-positive blood cells. However, the antibodies can pass to the developing fetus and destroy some of the baby's blood
cordocentesis, funipuncture) allows direct access to the fetal circulation to obtain important laboratory values such
as hematocrit, direct Coombs, fetal blood type, reticulocyte count, and total bilirubin 🔹
cells
The disease ranges from mild to severe, and typically occurs only in some second or subsequent pregnancies of Rh negative
🔷 Fetal blood sampling Complications:
-Total risk of fetal loss rate 2.7% (fetal death is 1.4% before 28 weeks and the perinatal death rate is 1.4% after 28
women where the fetus's father is Rh positive,leading to a Rh+ pregnancy.
During birth, the mother may be exposed to the infant's blood, and this causes the development of antibodies, which may affect the
weeks). -Bleeding from the puncture site in 23% to 53% of cases. -Bradycardia in 3.1% to 12%.
-Fetal-maternal hemorrhage: occur in 65.5% if the placenta is anterior and 16.6% if the placenta is posterior. PATHOGENESIS 🔹
health of subsequent Rh+ pregnancies.
After anti-Rh antibodies formed in the mother, they diffuse slowly through the placental membrane into the fetus’s blood and
cause agglutination of the fetus’s blood.
-Infection and abruptio placentae are rare complications -The agglutinated RBC subsequently hemolyze,releasing Hb into the blood.
🔷 Complications of Fetal-Neonatal Anemia:
Fetal hydrops and stillbirth
-The fetus macrophages then convert the Hb into bilirubin,which cause the baby skin to become yellow/ jaundiced.
-The ab can also attack and damaged the other cells of the body.
Hepatosplenomegaly
Neonatal jaundice
🔹
-The jaundiced or erythroblastosis newborn babyis usually anemic at birth
The anti Rh ab from the mother usually circulate in the infant blood for another 1 to 2 months after birth, destroying more and more
Compilations of neonatal kernicterus (lethargy, hypertonicity, hearing loss, cerebral palsy and learning disability)
Neonatal anemia
🔹
RBCThe hematopoietic tissues of the infant attempt to replace the hemolyzed RBC.
The liver and spleen become greatly enlarged and produced RBC in the same manner that they normally produced during the
middle of gestation. Because of rapid production of RBC, many early forms of RBC passed from the baby’s bone marrow into the
circulatory system and because of the presence of these nucleated blastic RBC the disease is called erythroblastosis fetal is
Although severe anemia of the erythroblastosis fetalis is usually the cause of the death, many children who barely survive the anemia
🔹
exhibit permanent mentalimpairment or damage to the motor areas of the brain because of precipitation of bilirubin in neuronal cells.
🔹 In mild cases, the fetus may have mild anaemia with reticulocytosis.
In moderate or severe cases the fetus may have a more marked anaemia and erythroblastosis (erythroblastosis fetalis). When the
🔻
management:
1. Rhesus negative without antibodies
(a) First visit: Rhesus group and screening test for immune antibodies.
disease is very severe it may cause haemolytic disease of the newborn hydrops fetalis or stillbirth
(b) Repeat antibody check monthly from 24 to 36 weeks.
(c) Give anti D immunoglobulin for complications.
(d) Delivery: Mother's blood — antibody check and Kleihauer Betke test.
🔻 2. Rhesus negative with antibodies Fetal RBC with Rh +ve antigen →Maternal circulation 🔹 The Primary Response:
Is a slow response (6 weeks to 6 months). IgM
a) First visit — antibody identified and measured and preferably, direct quantitationof antibody level. of an Rh –ve mother→The Rh+ve antigen will be
cleared by macrophages; processed and transferred antibodies A molecular weight of 900,000 that
(b) Antibody test repeated monthly or until management decided on by other investigations e.g. amniocentesis.
to plasmastem cell precursors (Develop an almost does not cross the placenta.
(c) Rhesus genotyping of partner — if heterozygous Rhesus positive the possibility of an unaffected child exists.
The Mechanism of Development of the Rh
(d) Amniocentesis — the bilirubin level in the liquor, measured by spectrophotometry, is a useful prognostic indicator as it
reflects the excretion of bilirubin by the baby and thus the degree of haemolysis.
Immune Response:
permanent immunologic memory) →(Primary
immune response)→ With subsequent exposure the 🔹 The Secondary Response:
Is a Rapid response
(e) Ultrasound — can detect fetal ascites and oedema, indicating a severely affectedfetus, at a very early stage in the plasma cell lineproliferate to produce humeral
pregnancy, e.g. less than 20 weeks. Such findings indicate the need for fetal blood sampling by cordocentesis. IgG antibodies
antibodies→ (Secondary immune response).
(f) Cordocentesis --Blood may be obtained from the fetus in patients with a history of severe early rhesus disease and in A molecular weight of 160,000 that cross the
those in whom ultrasound has demonstrated ascites. placenta.
A haematocrit reading is at once available and treatment by direct intravascular transfusion can be given if indicated by the
result.
• Postnatal
A baby's Rh status is determined from the mother and father.
-Phototherapy for neonatal jaundice in mild disease CAUSES If the mother is Rh negative and the father is Rh positive, the baby has at least a 50% chance of being Rhpositive.
-Exchange transfusion if the neonate has moderate or severe disease (the blood for transfusion must be less than a week old, MANAGEMENT However, Rh isoimmunization will only happen if the baby's Rh-positive blood enters the mother's blood flow. In most pregnancies,
Rh negative, ABO compatible with both the fetus and the mother, and be cross matched against the mother's serum)
PREVENTION
🔹
the mother's and baby's blood will not mix. The baby's blood may come into contact with the mother's blood flow during:
🔹 Bleeding during pregnancy (Miscarriage & APH)
Most Rh disease can be prevented by treating the mother during pregnancy (28wks & 34 wks) or promptly (within 72 hours) 🔹
🔹
Spontaneous/Induced abortion
Ectopic pregnancy
🔹
after childbirth. The mother has an intramuscular injection of anti-Rh antibodies (Rho(D) Immune Globulin),so that the fetal Trauma during pregnancy
🔹
Rhesus D positive erythrocytes are destroyed before her immunesystem can discover them. This is passive immunity and the External cephalic version
🔹
effect of the immunity will wear off after about 4 to 6 weeks (or longer depending on injected dose) as the anti-Rh antibodies Cesarean-section
🔹
gradually decline to zero in the maternalblood. Use of anti-D and smaller family size Amniocentesis, Chorionic villus sampling (CVS) or other invasive testing procedures related to pregnancy.
Normal deliveryThe mix in blood happens most often at the end of pregnancy. This means it is rarely a problem in a woman's first
When is RhIg given? pregnancy. The mother's antibodies could affect a future pregnancy with a baby with Rh-positive blood even if the blood is not mixed.A
🔹
Rh Ig is given to Rh-negative women in the following situations:
🔹 At around the 28th week of pregnancy to prevent Rh sensitization for the rest of the pregnancy.
woman can also become sensitized to Rh-positive blood if she receives an incompatible blood transfusion .
🔹
🔹
Within 72 hours after the delivery of an Rh-positive infant.
After a miscarriage, abortion, or ectopic pregnancy.
RISK FACTORS Factors
🔹
that put pregnant woman at risk for Rh incompatibility include Rh-negative pregnant woman who:
After amniocentesis or chorionic villus sampling.
Dosage: 🔹
🔹
Had a prior pregnancy with a baby that was Rh positive
Had a prior blood transfusion or amniocentesis
Did not receive Rh immunization prophylaxis during a prior pregnancy with an Rh-positive baby
1 vial (300ug) IM or micro dose of
-50ug IM.50 ug: after CVS, ectopic pregnancy, miscarriage or abortion < 13 weeks.
-300 ug: miscarriage/abortion>13 weeks, amniocentesis, abruption ,trauma, bleeding, at 28 wks and within 72 hr of delivery.
->300 ug after large placenta hemorrhage or mismatched blood transfusion.
by fatema okoff
The complications occur when standard preventive measures are not taken.
🔹
The symptoms can vary from mild to severe.
🔹 Hemolytic anemia
🔹
🔹
Numerous erythroblast in fetal circulation
Generalized edema (hydrops fetalis)
🔹 Enlargement of fetal liver & spleen in its most severe form
Severity of the anemia resulted in cardiac failure, with widespread edema, ascites and pleural effusion.
🔻 A complication of untreated jaundice is kernicterus, a syndrome which can affect the baby's nervous system. Contact doctor
right away if the baby:
-Has a yellow or orange appearance to the skin
-Does not sleep
- Is hard to wake up
- Is not breastfeeding or has difficulty sucking from a bottl
- Is restless or fussy
Investigation
Kleihauer–Betke test The diagnosis is based on the presence of anti-Rh (D) antibody in maternal serum. Methods of detecting Anti D
Antibodies in maternal serum:
The Enzymatic Method
The Antibody Titer In Saline, In Albumin
The Indirect Coombs Tests.
🔻 Maternal blood
The Kleihauer–Betke test or flow cytometry on a postnatal maternal blood sample can confirm that fetal blood
has passed into the maternal circulation and can also be used to estimate the amount of fetal blood that has passed
into the maternal circulation and the dose of the anti Rhesus antibody will be adjusted accordingly.
🔹 ISO:
🔹is the
is a prefix means similar, equal or uniform.
🔸
It depends on the fact that fetal hemoglobin is more resistant than adult’s hemoglobin to the acid elution.
The indirect Coombs test is used to screen blood from antenatal women for IgGantibodies that may pass through
the placenta and cause hemolytic disease of thenewborn.
Isoimmunization:
process of immunizing a species with antigen derived fromthe same
🔹
subject
🔻
🔹Fetal blood (or umbilical cord blood)
The direct coombs test is done after birth to detect the presence of maternal antibody on the neonate's RBCs.
Rhesus :
major blood group antigen of importance during pregnancy.Incompatibility
DIAGNOSIS
🔹RhRhoGAM®
indirect Coombs test The infant's RBCs are placed in Coomb’s serum. If the cells are agglutinated this indicate the presence of maternal between mother (-) and fetus (+) may led to hemolytic diseaseof the newborn.
Definitions: :
🔹
antibody. Is used to confirm that the fetus or neonate has an immune mediated hemolytic anemia.
🔹 Full blood count—the hemoglobin level and platelet count are important immunoglobulin given to gravidas who are Rh negative if there is suspicion
🔹 Bilirubin (total and indirect) of fetal maternal bleeding for example : if there is bleeding during any
Fetal Rhesus Determination: trimester and after delivery.
-Type and zygosity (if Rh-positive) of the father
-Amniocentesis to determine the fetal blood type using the polymerase chain reaction (PCR) 🔹 Rh disease (also known as Rhesus isoimmunization, Rh (D) disease,
Rhesusincompatibility, Rhesus disease, Hemolytic Disease of the Newborn,
-Detection of free fetal RhD DNA (FRHD) sequences in maternal plasma or serum using PCR
-Flow cytometry of maternal blood for fetal cells Rhesus DHemolytic Disease of the Newborn) is one of the causes of hemolytic
Methods of diagnosis and evaluation of Fetal Rh Isoimmunization: disease of thenewborn.
-Measurements Of Antibodies in Maternal Serum
-Determination of Fetal Rh Blood Group
direct coombs test
-Ultrasonography
-Amniocentesis 🔹 Incidence
-Fetal Blood Sampling
🔹
varies based on prevalance of RBC antigen in different population
🔻
Prevalence(varies with race)
Ultrasonography INCIDENCE & PREVALENCE: Asian 99% D-positive (either DD & Dd genotype)African american 92-93%White
To establish the correct Gestational Age. american 87%Incidence higher in white due to relatively higher percentage of the
🔹
In guiding invasive procedures and monitoring fetal growth and well-being. population who do not carry the D-antigen on their RBC. Hence, more Rh-negative
Ultrasonographic parameters to determine Fetal Anemia: mother (dd)
o Placental Thickness.
o Umbilical Vein Diameter
o Hepatic Size.
o Splenic Size. The Rh Antigen- Biochemical Aspects:-
o Polyhydramnios. The Rh antigen is a complex lipoprotein. - It has a molecular weight of approximately 30,000.- It is distributed
o Fetal Hydrops (e.g. Ascites, Pleural Effusions, Skin Edema). throughout the erythrocyte membrane in a nonrandom fashion. -The surface antigens cannot be seen by routine
🔻
ultrasounogrphy microscopy, but can be identified byspecific Antisera
Doppler Velocimetry of the Fetal Middle Cerebral Artery (MCA) The RH Antigen- Genetic Aspect
Anemic fetus preserves oxygen delivery to the brain by increasing cerebral flow of its already low viscosity blood. The Rh gene complex is located on the distal end of the short arm of chromosome one. A given Rh antigen
For predicting fetal anemia To predict the timing of a Second intrauterine fetal transfusion complex is determined by a specific gene sequence inherited in a Mendelian fashion from the parents. One
haploid from the mother and one from the father. Three genetic loci, determine the Rh antigen (i.e. Rh blood
🔻 Invasive Techniques (Amniocentesis and Fetal Blood Sampling):
Rh Antigen:
group).
Each chromosome will be D positive or D negative (there is no "d" antigen), C or c positive, and E or e positive.
🔹
Indications
A Critical Anti-D Titer:
A Titer associated with a significant
🔹
Factors Affect The Expression Of The Rh Antigen:
The Number Of Specific Rh-antigen Sites:
🔹
risk for fetal hydrops. Anti-D titer value between 8 And 32
Previous Seriously Affected Fetus Or Infant
- The Gene Dose,
- The Relative Position of the Alleles,
🔻
(e.g. Intrauterine fetal transfusion, early delivery, fetal hydrops, neonatal exchange transfusion).
🔹 Amniocentesis 🔹
- The Presence or Absence of Regulator Genes.
Interaction of Other Components of the Rh Blood Group. Erythrocytes ofIndividuals of Genotype Cde/cde
Fetal blood sampling
🔹 Normally bilirubin in amniotic fluid decreases with advanced gestation.
🔹 ItItsderives from fetal pulmonary and tracheal effluents.
level rises in correlation with fetal hemoly
🔹
Express Less D Antigen than Do theErythrocytes of Individuals of Genotype cDE/cde.
The Exposure of the D Antigen on the Surface of the Red Cell Membrane
Interpretation of Amniotic Fluid Bilirubin:
-A falling curve: is reassuring: i.e. an unaffected or RhD-negative fetus.
-A plateauing or rising curve: suggests active hemolysis (require close monitoring and may require fetal blood
sampling and/or early delivery). 🔹 The Rh blood system (CDE) consists of five major antigens, D, C, c, E and e, all of which can produce erythrocyte
-A curve that reaches to or beyond the 80th percentile of zone II on the lileygraph or enters the “ intrauterine Rh alloimmunization.
transfusion" zone of the Queenan curve: necessitates investigation by fetal blood sampling
INCOMPATIBILITY 🔹
The erythrocyte D antigen is strongly immunogenic and therefore more important and more common than the other antigens.
Rh factor is a protein that may be found on the surface of red blood cells.
🔻 Fetal blood sampling:
-If she carries this protein, her blood is Rh positive.
Is the gold standard for detection of fetal anemia. Reserved for cases with:
- With an increased MCA-PSV(Peak systolic velocity of the fetal middle cerebral artery)
🔹
-If not carry this protein, her blood is Rh negative.
Sometimes a mother with Rh-negative blood is pregnant with a fetus that has Rh-positive blood. This can cause a problem if
the fetal blood enters the mother's blood flow (fetomaternal haemrrhage).
- Increased ΔOD 450 The Rh-positive blood from the fetus will make the mother's body create antibodies. This is called isoimmunization. The antibodies will
Fetal blood sampling — Ultrasound-directed fetal blood sampling (i.e., percutaneous umbilical blood sampling, attack any Rh-positive blood cells. However, the antibodies can pass to the developing fetus and destroy some of the baby's blood
cordocentesis, funipuncture) allows direct access to the fetal circulation to obtain important laboratory values such
as hematocrit, direct Coombs, fetal blood type, reticulocyte count, and total bilirubin 🔹
cells
The disease ranges from mild to severe, and typically occurs only in some second or subsequent pregnancies of Rh negative
🔷 Fetal blood sampling Complications:
-Total risk of fetal loss rate 2.7% (fetal death is 1.4% before 28 weeks and the perinatal death rate is 1.4% after 28
women where the fetus's father is Rh positive,leading to a Rh+ pregnancy.
During birth, the mother may be exposed to the infant's blood, and this causes the development of antibodies, which may affect the
weeks). -Bleeding from the puncture site in 23% to 53% of cases. -Bradycardia in 3.1% to 12%.
-Fetal-maternal hemorrhage: occur in 65.5% if the placenta is anterior and 16.6% if the placenta is posterior. PATHOGENESIS 🔹
health of subsequent Rh+ pregnancies.
After anti-Rh antibodies formed in the mother, they diffuse slowly through the placental membrane into the fetus’s blood and
cause agglutination of the fetus’s blood.
-Infection and abruptio placentae are rare complications -The agglutinated RBC subsequently hemolyze,releasing Hb into the blood.
🔷 Complications of Fetal-Neonatal Anemia:
Fetal hydrops and stillbirth
-The fetus macrophages then convert the Hb into bilirubin,which cause the baby skin to become yellow/ jaundiced.
-The ab can also attack and damaged the other cells of the body.
Hepatosplenomegaly
Neonatal jaundice
🔹
-The jaundiced or erythroblastosis newborn babyis usually anemic at birth
The anti Rh ab from the mother usually circulate in the infant blood for another 1 to 2 months after birth, destroying more and more
Compilations of neonatal kernicterus (lethargy, hypertonicity, hearing loss, cerebral palsy and learning disability)
Neonatal anemia
🔹
RBCThe hematopoietic tissues of the infant attempt to replace the hemolyzed RBC.
The liver and spleen become greatly enlarged and produced RBC in the same manner that they normally produced during the
middle of gestation. Because of rapid production of RBC, many early forms of RBC passed from the baby’s bone marrow into the
circulatory system and because of the presence of these nucleated blastic RBC the disease is called erythroblastosis fetal is
Although severe anemia of the erythroblastosis fetalis is usually the cause of the death, many children who barely survive the anemia
🔹
exhibit permanent mentalimpairment or damage to the motor areas of the brain because of precipitation of bilirubin in neuronal cells.
🔹 In mild cases, the fetus may have mild anaemia with reticulocytosis.
In moderate or severe cases the fetus may have a more marked anaemia and erythroblastosis (erythroblastosis fetalis). When the
🔻
management:
1. Rhesus negative without antibodies
(a) First visit: Rhesus group and screening test for immune antibodies.
disease is very severe it may cause haemolytic disease of the newborn hydrops fetalis or stillbirth
(b) Repeat antibody check monthly from 24 to 36 weeks.
(c) Give anti D immunoglobulin for complications.
(d) Delivery: Mother's blood — antibody check and Kleihauer Betke test.
🔻 2. Rhesus negative with antibodies Fetal RBC with Rh +ve antigen →Maternal circulation 🔹 The Primary Response:
Is a slow response (6 weeks to 6 months). IgM
a) First visit — antibody identified and measured and preferably, direct quantitationof antibody level. of an Rh –ve mother→The Rh+ve antigen will be
cleared by macrophages; processed and transferred antibodies A molecular weight of 900,000 that
(b) Antibody test repeated monthly or until management decided on by other investigations e.g. amniocentesis.
to plasmastem cell precursors (Develop an almost does not cross the placenta.
(c) Rhesus genotyping of partner — if heterozygous Rhesus positive the possibility of an unaffected child exists.
The Mechanism of Development of the Rh
(d) Amniocentesis — the bilirubin level in the liquor, measured by spectrophotometry, is a useful prognostic indicator as it
reflects the excretion of bilirubin by the baby and thus the degree of haemolysis.
Immune Response:
permanent immunologic memory) →(Primary
immune response)→ With subsequent exposure the 🔹 The Secondary Response:
Is a Rapid response
(e) Ultrasound — can detect fetal ascites and oedema, indicating a severely affectedfetus, at a very early stage in the plasma cell lineproliferate to produce humeral
pregnancy, e.g. less than 20 weeks. Such findings indicate the need for fetal blood sampling by cordocentesis. IgG antibodies
antibodies→ (Secondary immune response).
(f) Cordocentesis --Blood may be obtained from the fetus in patients with a history of severe early rhesus disease and in A molecular weight of 160,000 that cross the
those in whom ultrasound has demonstrated ascites. placenta.
A haematocrit reading is at once available and treatment by direct intravascular transfusion can be given if indicated by the
result.
• Postnatal
A baby's Rh status is determined from the mother and father.
-Phototherapy for neonatal jaundice in mild disease CAUSES If the mother is Rh negative and the father is Rh positive, the baby has at least a 50% chance of being Rhpositive.
-Exchange transfusion if the neonate has moderate or severe disease (the blood for transfusion must be less than a week old, MANAGEMENT However, Rh isoimmunization will only happen if the baby's Rh-positive blood enters the mother's blood flow. In most pregnancies,
Rh negative, ABO compatible with both the fetus and the mother, and be cross matched against the mother's serum)
PREVENTION
🔹
the mother's and baby's blood will not mix. The baby's blood may come into contact with the mother's blood flow during:
🔹 Bleeding during pregnancy (Miscarriage & APH)
Most Rh disease can be prevented by treating the mother during pregnancy (28wks & 34 wks) or promptly (within 72 hours) 🔹
🔹
Spontaneous/Induced abortion
Ectopic pregnancy
🔹
after childbirth. The mother has an intramuscular injection of anti-Rh antibodies (Rho(D) Immune Globulin),so that the fetal Trauma during pregnancy
🔹
Rhesus D positive erythrocytes are destroyed before her immunesystem can discover them. This is passive immunity and the External cephalic version
🔹
effect of the immunity will wear off after about 4 to 6 weeks (or longer depending on injected dose) as the anti-Rh antibodies Cesarean-section
🔹
gradually decline to zero in the maternalblood. Use of anti-D and smaller family size Amniocentesis, Chorionic villus sampling (CVS) or other invasive testing procedures related to pregnancy.
Normal deliveryThe mix in blood happens most often at the end of pregnancy. This means it is rarely a problem in a woman's first
When is RhIg given? pregnancy. The mother's antibodies could affect a future pregnancy with a baby with Rh-positive blood even if the blood is not mixed.A
🔹
Rh Ig is given to Rh-negative women in the following situations:
🔹 At around the 28th week of pregnancy to prevent Rh sensitization for the rest of the pregnancy.
woman can also become sensitized to Rh-positive blood if she receives an incompatible blood transfusion .
🔹
🔹
Within 72 hours after the delivery of an Rh-positive infant.
After a miscarriage, abortion, or ectopic pregnancy.
RISK FACTORS Factors
🔹
that put pregnant woman at risk for Rh incompatibility include Rh-negative pregnant woman who:
After amniocentesis or chorionic villus sampling.
Dosage: 🔹
🔹
Had a prior pregnancy with a baby that was Rh positive
Had a prior blood transfusion or amniocentesis
Did not receive Rh immunization prophylaxis during a prior pregnancy with an Rh-positive baby
1 vial (300ug) IM or micro dose of
-50ug IM.50 ug: after CVS, ectopic pregnancy, miscarriage or abortion < 13 weeks.
-300 ug: miscarriage/abortion>13 weeks, amniocentesis, abruption ,trauma, bleeding, at 28 wks and within 72 hr of delivery.
->300 ug after large placenta hemorrhage or mismatched blood transfusion.
by fatema okoff
