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Hemolytic disease
of newborn
Muhammad Abdullah
2021-BS-MLS-040.
Hemolytic disease of newborn
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
It is a condition in which the life span of the
fetal/neonatal red cells is shortened due to
maternal allo-antibodies against red cell
antigens acquired from the father
■Accelerated red cell destruction stimulate
increases production of red cells ,many of
which enter the circulation prematurely as
nucleated cells hence the term
“erythroblastosis fetalis”.
■ Also called Hydrops fetalis as Severly
affected fetuses may develop generalized
edema, called “Hydrops fetalis”
Types of HDN
■ABO hemolytic disease of New born
■Other blood group HDN
E.g. Rh blood group, kell blood group, kid
etc
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
Pathogenesis; before
birth
Pathogenesis; after
delivery
Factors affecting immunization and
severity
■ Antigenic exposure
■ Host factors
■ Antibody specificity
Clinical Presentation
■
■
■
■ Varies from mild jaundice and anemia to hydrops fetalis (with
ascites, pleural and pericardial effusions)
Chief risk to the fetus is anemia.
Extramedullary hematopoiesis due to anemia results in
hepatosplenomegaly.
Postnatal problems include:
□ Asphyxia
□ Pulmonary hypertension
□ Pallor (due to anemia)
□ Edema (hydrops, due to low serum albumin)
□ Respiratory distress
□ Coagulopathies (
↓
platelets & clotting factors)
□ Jaundice
□ Kernicterus (from hyperbilirubinemia)
Laboratory Findings
■ CBC:
TLC: normal
Hb: Decrease
MCV, MCH, HCHC : Normal or Increase
Platelets: Normal to Decrease
Reticulocytosis (6 to 40%)
Blood Smear
■
■
■
■
Polychromasia
Anisocytosis
Increase NRBCs
no spherocytes
■ Blood Banking test:
Blood grouping
■ Mother: Rh Negative
■ Father: Rh Positive
■ Baby: Rh Positive
■ Direct coomb,s test: Positive
Biochemical test
■ Hyperbilirubinemia
■ Hypoalbuminemia
■ LDH: Increase
■ Haptoglobin Decrease
ABO HDN
In a group O mother with naturally occurring anti-
A and anti-B of the IgG subclass which can cross
the placenta.
HDN due to ABO incompatibility occurs when a
group O mother with IgG anti-A or IgG anti-B is
carrying a fetus of blood group A or blood group
B respectively.
The most common presentation of ABO HDN is
jaundice (un-conjugated hyperbilirubinaemia).
ABO HDN contd.
■ Signs and symptoms
■ Two mechanism protects the fetus against anti-A and anti-B
□ Relative weak A and B antigens o fetal red cells
□ Widespread distribution of A & B antigen in fetal tissue diverting
antibodies away from fetal RBCs
■ Anemia is most of the time mild
■ ABO- HDN may be seen in the first pregnancy
hdnnonmlt-151222085444.pptx

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hdnnonmlt-151222085444.pptx

  • 1. Hemolytic disease of newborn Muhammad Abdullah 2021-BS-MLS-040.
  • 2. Hemolytic disease of newborn 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 It is a condition in which the life span of the fetal/neonatal red cells is shortened due to maternal allo-antibodies against red cell antigens acquired from the father
  • 3. ■Accelerated red cell destruction stimulate increases production of red cells ,many of which enter the circulation prematurely as nucleated cells hence the term “erythroblastosis fetalis”.
  • 4. ■ Also called Hydrops fetalis as Severly affected fetuses may develop generalized edema, called “Hydrops fetalis”
  • 5. Types of HDN ■ABO hemolytic disease of New born ■Other blood group HDN E.g. Rh blood group, kell blood group, kid etc
  • 6. 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
  • 9. Factors affecting immunization and severity ■ Antigenic exposure ■ Host factors ■ Antibody specificity
  • 10.
  • 11. Clinical Presentation ■ ■ ■ ■ Varies from mild jaundice and anemia to hydrops fetalis (with ascites, pleural and pericardial effusions) Chief risk to the fetus is anemia. Extramedullary hematopoiesis due to anemia results in hepatosplenomegaly. Postnatal problems include: □ Asphyxia □ Pulmonary hypertension □ Pallor (due to anemia) □ Edema (hydrops, due to low serum albumin) □ Respiratory distress □ Coagulopathies ( ↓ platelets & clotting factors) □ Jaundice □ Kernicterus (from hyperbilirubinemia)
  • 12. Laboratory Findings ■ CBC: TLC: normal Hb: Decrease MCV, MCH, HCHC : Normal or Increase Platelets: Normal to Decrease Reticulocytosis (6 to 40%)
  • 14. ■ Blood Banking test: Blood grouping ■ Mother: Rh Negative ■ Father: Rh Positive ■ Baby: Rh Positive ■ Direct coomb,s test: Positive
  • 15. Biochemical test ■ Hyperbilirubinemia ■ Hypoalbuminemia ■ LDH: Increase ■ Haptoglobin Decrease
  • 16. ABO HDN In a group O mother with naturally occurring anti- A and anti-B of the IgG subclass which can cross the placenta. HDN due to ABO incompatibility occurs when a group O mother with IgG anti-A or IgG anti-B is carrying a fetus of blood group A or blood group B respectively. The most common presentation of ABO HDN is jaundice (un-conjugated hyperbilirubinaemia).
  • 17. ABO HDN contd. ■ Signs and symptoms ■ Two mechanism protects the fetus against anti-A and anti-B □ Relative weak A and B antigens o fetal red cells □ Widespread distribution of A & B antigen in fetal tissue diverting antibodies away from fetal RBCs ■ Anemia is most of the time mild ■ ABO- HDN may be seen in the first pregnancy