Hemolytic disease of newborn lecture final yr mbbs

1. (ERYTHROBLASTOSIS FETALIS)
Dr. Muhammad Sajjad Sabir
MBBS, DCH, MCPS, FCPS
Assistant Prof. Paediatrics

2. Hemolytic disease of newborn
The term Hemolytic disease of the new
born and fetus (HDN) is a destruction of
the red blood cells (RBCs) of the fetus
and neonate by antibodies produced by
the mother

3. Hemolytic disease of newborn
It is a condition in which the life span of the
fetal/neonatal RBC is shortened due to
maternal allo-antibodies against red cell
antigens acquired from the father
SO
Rate of RBCs destruction is accelerated BUT
ability of bone marrow to respond is NORMAL
It was a major cause of fetal loss and death
among newborn babies

4. EtiologyRh incompatibility:
 Hemolytic disease occurs most frequently
 develops when an Rh –ve mother conceives a fetus
which is Rh +ve
ABO incompatibility:
• mother has blood type O and the fetus has blood type A or
B or AB
Other causes:
 Other Minor blood group antigens(kell, kid )
 Thalassemia
 Autoimmune Hemolytic Anemia

5.  The Rh factor , Rh+ and Rh- usually refers
to presence or absence of antigen-D
There are two alleles of antigen: D and d
A person who is Rh -ve has two recessive
traits, dd
Anyone who has at least one D (DD or Dd)
is Rh+ve

6. Rh incompatibility:
 Rh incompatibility is a condition which
develops when an Rh negative mother
conceives a fetus which is Rh positive.
Isoimmunization:
When the mother produces Abs directed against fetus RBC
surface Ag
Cause Feto- maternal Bleed
Risk Factors of Feto-maternal Bleed:
 Amniocentesis
Ectopic pregnancy
Fetal RBC Rh Antigen : Rh “ D ’’ Ag
 Mother produces: Anti Rh (D) Abs

7. PATHOGENISIS

8. DEFINITION:
Rh incompatibility is a condition which
develops when there is a difference in
Rh blood type between that of the
pregnant mother (Rh negative) and
that of the fetus (Rh positive)

9.  A person's Rh type is generally most relevant
with respect to pregnancies
 If the pregnant woman is Rh -ve and her
husband Rh+ve, there is possibility of Rh
incompatibility
 If the pregnant woman and her husband are
Rh negative, there is no reason to worry about
Rh incompatibility

10. • Usually placenta is barrier to fetal blood
entering maternal circulation.
•Sometimes during pregnancy or birth,
fetomaternal haemorrhage (FMH) can occur
•The woman’s immune system reacts by
producing anti-D antibodies that cause
sensitisation

12. •Subsequent pregnancies antibodies can
cross placenta and destroy fetal
erythrocytes.

13. Conditions affecting 1st pregnancy :
 Miscarriage
 Abortion
 Feto-maternal haemorrage
•The haemolytic disease of fetus and new born
caused by Rh isoimmunisation can occur during
the first pregnancy, but
•Usually sensitisation during the first pregnancy
or birth leads to extensive destruction of fetal
RBC during subsequent pregnancies

14. Pathogenesis
Fetomaternal Hemorrhage
Maternal Antibodies formed against fetus derived
antigens
During subsequent pregnancy, placental passage of
maternal IgG antibodies
Maternal antibody attaches to fetal red blood cells
Fetal red blood cell hemolysis

15. Pathogenesis; before
birth

16. Pathogenesis; after
delivery

17. Clinical
Presentation

18.  Hemolysis → ↑ed bilirubin levels
 Rh incompatibility can cause symptoms ranging from
very mild to fatal.
 After delivery bilirubin is no longer cleared (via
placenta) from the neonate's blood → Jaundice
(within 24 hours of life)
 Possibility of acute or chronic Kernicterus

19. Sign &symptom
• Mildest form- Rh incompatibility:
1-Hemolysis with the release of free hemoglobin into the
infant's circulation
2- Jaundice

20.  Prenatal manifestations :
Hydrops fetalis / Erythroblastosis Fetalis
Massive fetal RBC destruction →Profound anemia
 pallor
 high-output heart failure (CCF)
 Enlarged liver / spleen
 Generalized Edema
 Ascites and
 Respiratory distress
Severe form- Rh incompatibility

21. Severe form- Rh incompatibility
1- severe forms → petechiae and purpura
2- Severe anemiaFetal heart failure stillborn
or
Death of infant shortly after delivery

22. 2- Total body swelling
3- Respiratory distress
(if infant has been delivered)
4- Circulatory collapse
5- Kernicterus. (bilirubin encephalopathy)
(Neurological syndrome in extremely high levels of
indirect bilirubin (>20 mg/dL).
6- It occurs several days after delivery and is
characterized initially by...
A) Loss of the Moro reflex.
B)Poor Feeding.
C) Decreased activity

23. LATER 
 At last it may lead to death of the child
immediately after its birth

24. Investigations

25. Blood grouping
 Mother: Rh Negative
 Father: Rh Positive
 Baby: Rh Positive
 Direct Coombs test: Positive in INFANT
 Indirect Coombs test: Positive in MOTHER
Biochemical test
 Hyperbilirubinemia
 Hypoalbuminemia
 LDH: Increase
 Haptoglobin Decrease

26. Blood Smear
 Polychromasia
 Anisocytosis
 ↑ Erythroblasts (nucleated RBCs)
 No Spherocytes
CBC
 TLC: normal
 Hb: ↓Hb
 MCV, MCH, HCHC : Normal or Increase
 Platelets: Normal to Decrease
 ↑ Reticulocytosis (6 to 40%)

27. Coombs test
Direct Coombs test: diagnoses HDN
 The direct Coombs test detects maternal anti-D
antibodies that have already bound to fetal
RBCs
 This is called the direct Coombs test because
the anti-Ig binds "directly" to the maternal anti-D
Ig that coats fetal RBCs in HDN

28.  Finds anti-D antibodies in mother's serum. If
these were to come into contact with fetal
RBCs they would hemolyse them and hence
cause HDN.
 This is called the indirect Coombs test
because the anti-Ig finds "indirect" evidence of
harmful maternal antibodies, requiring the
addition of fetal RBCs to show the capacity of
maternal anti-D to bind to fetal RBCs
Indirect Coombs test: used in the prevention of HDN

29. Management

30. If there is evidence of erythroblastosis
Notify Pediatrics team for possibilitye
delivery of a compromised newborn
Management

31. Management
Before birth(Antenatal) options:
 Intrauterine RCC transfusion - blood transfused into
fetal umbilical vein or
 Early induction of labor when
 Pulmonary maturity has been attained,
 Fetal distress is present, or
 35 to 37 weeks of gestation have passed
 The mother may also undergo plasma exchange to
reduce circulating levels of antibody by as much as
75%

32. After birth(Postnatal)
Treatment depends on the severity of condition:
 Phototherapy
 Transfusion with compatible RCC,
 Exchange transfusion with a blood type compatible
with both the infant and the mother
 Supportive care
 Temperature stabilization
 Monitoring
 Sodium bicarbonate ( correction of acidosis)
 O2/ assisted ventilation

33. Management:
Phototherapy for neonate
with mild jaundice
 Exchange transfusion in
Severe cases

34. For Mother (Antenatal)
Rh -ve mothers (pregnant with a Rh+ve infant are
given)
Rh immune globulin (RhIG) to prevent
sensitization to D antigen RhoGAM protects
against the effects of early transplacental
hemorrhage (as recommended by the American
College of Gynecologists).
 at 28 weeks during pregnancy
 at 34 weeks “ “
 Plasma exchange to reduce circulating levels of
antibody by as much as 75%
 Close monitoring of fetal well-being, as reflected by
Rh titers, amniocentesis results, and sonography

35. For Mother (Postenatal)
Rh -ve mothers with Rh+ve infant
Inj RhoGAM must given within 72
hours of delivery of the newborn.

36. Preventing HDN
 Determine Rh status of the mother
 If the mother is not sensitized, reduce the risk of
future sensitization
 If the mother is sensitized, determine whether
the fetus is at risk and monitor accordingly
 To prevent Isoimmuization of yet unimmunized
mother give Anti Rh D IgG (Rhogam) IntraMuscular at 28
weeks of gestation.

37. Summary:

38. Mother
must be
Rh -
Dad must
be Rh +
Coombs
test must
be positive
Abs must
be
associated
with
Hemolysis
Ab titer
must be
above 1:8
Is the baby at risk?
• Anti Lewis Abs Non-Hemolytic
ABS
• Anti KELL Abs
• Anti RH(D) Abs
Hemolytic
ABS

39. THANK YOU