anemia , rhesus and blood group incompatibility in
TRANSCRIPT
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Dr. Dina Garniasih, SpA, Mkes.
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Hematologic physiology of the
newbornNormal development: The physiologic anemia
of infancy
In utero the fetal aortic O2 saturation is45%; erythropoietin levels are high, RBC
production is rapid, and reticulocyte valuesare 3 to 7%.
After birththe O2 saturation is 95%, anderythropoietin is undetectable.
RBC production by day 7 is < 1/10 the levelin utero. Reticulocyte counts are low, andthe Hb level falls.
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normal development: The
physiologic anemia of infancy
At 8 to 12 weeksHb nadir
O2 delivery to the tissue is impaired,
erythropoietin production is stimulated,
and RBC production increases.
Active erythropoiesisiron stores are
rapidly utilized.
The reticuloendothelial system hasadequate iron for 15 to 20 weeks in term
infants.
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Anemia of prematurity
RBC mass is decreased at birth.
The Hb nadir is reach earlier, because:
RBC survival is decreased.
There is a relatively more rapid rate of
growth.
Vit E deficiency is common.
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anemia of prematurity
Erythropoietin is produced by: Term infant at a Hb level of 10-11 g/dL
Premature infant at a Hb level of 7 to 9 g/dL.
Iron administration before the age of 10-14weeks does not increase the nadir of thehemoglobin level or diminish its rate ofreduction.
Once the nadir is reached RBCproduction is stimulated an iron storesare rapidly depleted because less iron isstored in premature infant.
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Etiology of anemia in the
neonateBLOOD LOSS:
/normal Ht
/normal reticulocyte count
Normal bilirubin level
Obstetric cause of blood loss, includingmalformations of plasenta and cord
Occult blood loss: Fetomaternal bleeding Fetoplacental bleeding
Twin-to-twin transfusion
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etiology of anemia in the
neonateHEMOLYSIS
Ht
reticulocyte
bilirubin level
Immune hemolysis: Rh incompatibility
ABO incompatibility Minor blood group incompatibility
Maternal disease
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etiology of anemia in the
neonate
Bleeding in the neonatal period:
Intracranial bleeding
Massive cephalhematoma
Retroperitoneal bleeding
Ruptured liver or spleen
Adrenal or renal hemorrhage
Gastrointestinal bleeding Bleeding fromumbilicus
Iatrogenic cause
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etiology of anemia in the
neonate
Hereditary RBC disorders:
RBC membran defects
Metabolic defect
Hemoglobinopathies
Acquired hemolysis:
Infectionbacterial or virus
DIC Vit E deficiency or other nutritional anemias
Microangiopathic hemolytic anemia
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etiology of anemia in the
neonateDIMINISHED RBC PRODUCTION
Ht
reticulocyte
normal bilirubin level
Diamond-Blackfan syndrome
Congenital leukemia or other tumor
Infections, especially rubella and parvovirus
Osteopetrosis, leading to inadequateerythropoiesis
Physiologic anemia or anemia of prematurity
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Diagnostic approach to anemia
in the newborn
The family history
The obstetric history
The physical examination:
Acute blood loss Chronic blood loss
Chronic hemolysis
Complete blood count Reticulocyte count
Blood smear
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Diagnostic approach to anemia
in the newborn
Coombs test and bilirubin level
Apt test on gastrointestinal blood ofuncertain origin
Kleihauer-Betke preparation of themothers blood.
Ultrasound of abdomen and head
Test on parents Studies for infection
Bone marrow (rarely used)
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Therapy
TRANSFUSION
Indications for transfusion: Infants with significant respiratory disease or
CHD
Healthy, asymptomatic newborns will self-correct a mild anemia
Infants with ABO incompatibility who do nothave an exchange transfusion may haveprotracted hemolysis
Premature babies may have be quitecomfortable with hemoglobin levels of 6.5 to 7.0mg/dL
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therapy
Blood products and methods of
transfusion
Packed RBCs
Whole blood
Exchange transfusion with packed RBCs
Irradiated or frozen RBCs
Direct-donor transfusion Transfusing stored red blood cells from a
single unit reserved for an infant.
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therapy
PROPHYLAXIS
Term infant should be sent home from
hospital on iron-fortified formula (2
mg/kg per day) if they are notbreastfeeding.
Premature infants (preventing or
ameliorating the anemia of prematurity). Iron supplementation in the preterm infant
prevents late iron deficiency.
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therapy
Mothers milk or formulas similar to mothers
milk
Vitamin E (15 to 25 IU of water-soluble form)
is given daily until the baby is 38 to 40weeks postconceptional age
These infants should be followed carefully
Recombinant human erythropoietin (REPO)
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RHESUS
ISOIMMUNIZATIONClinical Features
Anemia, mild to severe
Jaundice (indirect hyperbilirubinemia)
Presents during first 24 hours. May cause kernicterus
(1) Exchange transfusion
(2) Factors that predispose to the development
of kernicterus at lower levels of bilirubin
prematurity, hypoproteinemia, metabolicacidosis, drugs (sulfonamides, caffeine, sodiumbenzoate), and hypoglycemia.
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rhesus isoimmunization
Hepatosplenomegaly; varies with
severity.
Petechiae (only in severely affected
infants).
Severe illness with birth of infant with
hydrops fetalis, stillbirth, or death in
utero and delivery of a macerated fetus. Late hyporegenerative anemia with
absent reticulocytes.
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rhesus isoimmunization
Laboratory Findings Serologic abnormalities (incompatibility
between blood group of infant and mother;direct Coombs test positive in infant;
mothers serum has the presence ofimmune antibodies detected by the indirectCoombs test)
Hb level, reticulocyte count, smear-
increased nucleated red cells, markedpolychromasia, and anisocytosis
indirect bilirubin level.
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Determine zygosity of the father
Examination of the amniotic fluid for
spectrophotometric analysis of bilirubin.
The following are indications for amniocentesis:
a. History of previous Rh disease severe
enough to require an exchange transfusion or to
cause stillbirth.
b. Maternal titer of anti-D, anti-c, or anti-Kell (or
other irregular antibodies) of 1:8 to 1:64 or
greater by indirect Coombs test or albumin
titration and depending on previous history.
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PostnatalHyperbilirubinemia exchange transfusion.
phototherapy
In hydropic infant at birth: Adequate ventilation.
Partial exchange transfusion.
Double-volume exchange transfusion.
Clinical signs suggesting kernicterus at anytime at any bilirubin level are an indication forexchange transfusion.
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Prevention of Rh Hemolytic
DiseaseRh hemolytic disease can be prevented by the use of Rh Ig at a dose of
300 mg, which is indicated in the following circumstances:
For all Rh-negative, Rh0 (Du)-negative mothers who are
unimmunized to the Rh factor.
For all unimmunized Rh-negative mothers who have undergone
spontaneous or induced abortion. After ruptured tubal pregnancies in unimmunized Rh-negative
mothers
Following any event during pregnancy that may lead to
transplacental hemorrhage or antepartum hemorrhage in
unimmunized Rh-negative women
Following tubal ligation or hysterotomy after the birth of an Rh-
positive child in unimmunized Rh-negative women.
Following chorionic villus sampling at 1012 weeks gestation. In
these patients 50 mg of Rh immunoglobulin should be given.
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ABO Isoimmunization
Clinical Features
Jaundice (indirect hyperbilirubinemia)
usually within first 24 hours; may be of
sufficient severity to cause kernicterus
Anemia
Hepatosplenomegaly.
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ABO Isoimmunization
Diagnosis Hemoglobin decreased
Smear: spherocytosis in 80% of infants,reticulocytosis, marked polychromasia
Elevated indirect bilirubin level Demonstration of incompatible blood group
Group O mother may have an infant who is group Aor B.
Rarely, mother may be A and baby B or AB or
mother may be B and baby A or AB. Direct Coombs test on infants red cells
usually positive
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ABO Isoimmunization
Demonstration of antibody in infantsserum These antibodies can be demonstrated by
the indirect Coombs test in the infantsserum using adult erythrocytes possessingthe corresponding A or B antigen.
Antibody can be eluted from the infants redcells and identified.
Demonstration of antibodies in maternalserum.
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ABO Isoimmunization
Treatment
Antenatal management or premature
delivery is not required.
After deliverycontrolling the
hyperbilirubinemia by frequent
determination of unconjugated bilirubin
levels, with a view to the need forphototherapy or exchange transfusion.
Whole blood.
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