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Erythroblastosi 115157

Erythroblastosis fetalis is a condition caused by Rh incompatibility between the mother and fetus, leading to severe anemia and potential fetal death. It is characterized by the destruction of fetal red blood cells by maternal antibodies, resulting in symptoms such as jaundice, hemolytic anemia, and kernicterus. Diagnosis involves blood tests and ultrasound, while treatment options include blood transfusions, phototherapy, and immunoglobulin administration, with prevention strategies focusing on screening and the use of Rh factor immunoglobulins.

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0% found this document useful (0 votes)
12 views30 pages

Erythroblastosi 115157

Erythroblastosis fetalis is a condition caused by Rh incompatibility between the mother and fetus, leading to severe anemia and potential fetal death. It is characterized by the destruction of fetal red blood cells by maternal antibodies, resulting in symptoms such as jaundice, hemolytic anemia, and kernicterus. Diagnosis involves blood tests and ultrasound, while treatment options include blood transfusions, phototherapy, and immunoglobulin administration, with prevention strategies focusing on screening and the use of Rh factor immunoglobulins.

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ERYTHROBLASTO

SIS FETALIS

MEDIC PRAISE .I.


OUTLINE
 Introduction
 Causes
 Pathophysiology
 Signs and symptoms
 Diagnosis
 Treatment
 Prevention
INTRODUCTION

Erythroblastosis fetalis occured due to


Rh incompatibility between the mother
and the fetus, resulting in severe anaemia
and sometimes death of the fetus.
Erythroblastosis fetalis, also called hemolytic
disease of the newborn (HDN), usually occurs
in the fetus, but can also occur in the neonate
(erythroblastosis neonatorum). It is a type of
anemia in which the red blood cells (RBC) of
the fetus are destroyed by maternal antibodies
in an immune response targeted against the
fetus.
This occurs due to incompatibility of the
blood groups of the mother and fetus, which
arises when the fetus inherits a certain blood
group factor from the father that is absent in
the mother. As a result, the baby can suffer
from severe anemia, brain damage, or even
death.
CAUSES
Erythroblastosis fetalis can be caused due to
incompatibility of either of two major blood
types. These include Rh incompatibility and
ABO incompatibility.
PATHOPHYSIOLOGY
Following maternal exposure to RhD-positive
blood, B-lymphocyte clones that recognize
the RBC antigen are established. The primary
maternal immune response is the production
of IgM isotype. Maternal IgG response occurs
later in subsequent pregnancies .
Maternal anti-D (IgG) antibodies cross the placenta
and attach to Rh antigens on fetal RBCs. RBC
destruction occurs by lysis of antibody-coated RBCs
by macrophage lysosomal enzymes. The fetus
initially responds to the subsequent anemia and
tissue hypoxia through reticulocytosis, and a rise in
umbilical artery lactate indicates severe fetal anemia.
Erythroblastosis fetalis results when RBC
destruction exceeds production.
SIGNS AND SYMPTOMS
1.Jaundice: This occurs due to the deposition
of bilirubin (breakdown product of
hemoglobin from RBC) in the skin and the
whites of the eyes. This imparts a yellowish
color to these structures.
2. Hemolytic Anemia: This occurs due to the
destruction of RBCs. Untreated anemia can
cause heart failure, enlarged liver and/or
spleen, generalized swelling and respiratory
distress.
3.Kernicterus: This occurs due to the
deposition of bilirubin in the brain and spinal
cord. This can lead to nerve cell degeneration,
hearing loss, mental retardation, and even
death.
4. Hydrops Fetalis: This is the severest form of the
disease in newborns and is characterized by extreme
edema (abnormal accumulation of serous fluid) in
unusual places like the abdominal cavity, heart and
lungs. This can lead to congestive heart failure as the
extra fluid causes increased pressure on the heart,
reducing its pumping ability. Moreover, fluid
accumulation in the lungs prevents normal breathing,
because the lungs cannot expand fully.
DIAGNOSIS
Blood Tests

1. Indirect Coombs test: is done on the mother’s


blood if she is found to be Rh-, during the antenatal
visit and the father is Rh+. It measures the number of
antibodies in the maternal blood. If the Rh¯ mother
does not have antibodies during initial testing, then
she will be tested again at 18 to 20 weeks of
pregnancy and again at 26 to 27 weeks. If anti-Rh
antibodies are detected at any of these time-points,
then treatment is initiated.
2. Direct Coombs test is carried out on the
fetal blood sample which measures the level
of maternal antibodies attached to the baby’s
RBCs. This test is done if the fetus shows
features of anemia and jaundice.
3.Doppler Ultrasound

The doctor may recommend a non-invasive


test to detect fetal middle cerebral artery
blood flow by means of Doppler ultrasound.
If the baby’s blood flow is affected, then
erythroblastosis fetalis is suspected.
4. Amniocentesis

This procedure is used to sample the amniotic fluid


that surrounds the developing fetus inside the uterus.
A needle is inserted into the amnion (the sack filled
with amniotic fluid) using ultrasound guidance to
take a fluid sample. This is tested in the lab to assess
the baby’s risk of anemia.
Moreover, analysis of the amniotic fluid can
measure the bilirubin concentration to predict
the severity of the disease. If the levels are
elevated, then intrauterine transfusion with
Rh¯ blood can be given until premature
delivery can be induced.
TREATMENT
1.Blood Transfusion: The baby may require
blood transfusions before birth in order to
treat anemia. Intrauterine blood transfusion is
given through the umbilical cord.
2. Pre-term Delivery: In certain situations, the
baby needs to be born before its full-term.
Therefore, when the baby’s lungs and heart
mature enough for delivery, the doctor may
advise delivering the baby pre-term (usually
between 32 to 35 weeks).
3. Exchange Transfusion: This is a special type of
transfusion in which the baby’s blood is exchanged
with that of the donor’s blood. In this procedure, the
anti-Rh antibodies (produced by the mother’s
incompatible blood) that are destroying the baby’s
RBC are removed, along with excess bilirubin. Small
samples of the baby’s blood are taken out and
simultaneously replaced with the donor’s blood. This
procedure may have to be repeated several times
4. Phototherapy: This is also called light
therapy and is used to treat jaundice. The light
treatment helps to convert the bilirubin in the
baby’s skin to a form that can be excreted by
the baby. The baby is usually placed on its
back and illuminated from above by a special
light. Nowadays, flexible light pads are also
available that wrap around the baby. The eyes
are kept covered to protect from contact with
the light.
5. Immunoglobulin: Intravenous
immunoglobulin (IVIG) to neutralize
maternal anti-D antibodies. These can be
administered with the aim of reducing RBC
breakdown and lowering the levels of
circulating bilirubin. IVIG can be used to
reduce the need for exchange transfusion and
to shorten the length of phototherapy.
PREVENTION
1. Screening: The pregnant mother’s blood type
should be tested at the first prenatal visit. Besides
testing for Rh type, other blood types may also be
tested. In case of previous pregnancies or a history of
blood transfusions, further tests may be required.
The father’s blood may also be tested for ABO and
Rh types. During pregnancy, the baby’s blood may
also need to be tested for ABO and Rh types and as
well as to see if it reacts with the maternal blood.
2. Rh Factor Immunoglobulins: If the
pregnant mother is at risk of Rh sensitization,
it is recommended that Rho (D)
immunoglobulin (RhoGAM) be administered
at 28 weeks of gestation and within 72 hours
of delivery. This medicine contains high titers
of anti-Rh antibodies, which neutralize Rh+
fetal RBCs.
The standard dose is 300 µg of RhoGAM by
the intramuscular (IM) route. A rosette test
can be used to rule out significant fetal-
maternal hemorrhage (FMH).
THANK

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