Department of Medical Laboratory Technology

Mother Patern College of Health Sciences

Stella Maris Polytechnic University
UN Drive and Randall Street

COURSE: IMMUNOHEMATOLOGY 202

Topic: Hemolytic Disease of the Newborn

GROUP PRESENTATION

BY: GROUP SIX MEMBERS

NAMES ID Numbers
 J. STONE BEFOH-SIEH 10914
 AGATHA S. JAMES 08958

TO: MR. EZEKIEL KANUE FARDOLO

COURSE LECTURER
 CONTENTS

INTRODUCTION
HISTORY
CAUSES
Rh INCOMPATIBILITY
ABO INCOMPATIBILITY
DIAGNOSIS
MANAGEMENT
SUMMARY
REFERENCES
 INTRODUCTION
Hemolytic Disease of the and Newborn (HDN) is a condition characterized
by the destruction of red blood cells in the fetus or newborn due to
incompatibility between maternal and fetal blood types.
This condition can lead to severe complications, including anemia, jaundice
and in some cases, fetal and neonatal death.
The mother can be stimulated to form the antibodies by previous pregnancy
or transfusion and sometimes during the second and third trimester of
pregnancy.
This research aims to provide a comprehensive overview of HDN, including
its causes, diagnosis and management strategies.
 Using systemic approach to gather relevant information on HDN, Rh and
ABO incompatibilities, as well as other less common causes such as Kell,
Duffy, and Kidd blood group systems. We will also look at laboratory tests
used to identify HDN, including maternal antibody screening, fetal blood
sampling, etc. and interventions such as intrauterine transfusion, phototherapy,
and immunoglobulin therapy.
 HISTORY OF HDN
HDN used to be a major caused of fetal loss and death among
newborn babies
1609 French midwife – twins.
 One baby being swollen and died soon after birth, the
other baby developed jaundice and died several days later.
1950 the underlying caused was identified
Newborn’s red blood cells are being attacked by antibodies
from the mother.
1970, routine antenatal care included screening of all expectant
mothers to find whose pregnancy may be at risk of HDN and
provide preventive treatment
Currently, dramatic decrease in the incidence of HDN,
particularly severe cases that were responsible for stillbirth and
needed urgent medical attention.
 HDN CAUSES – RHESUS INCOMPATIBILITY
Occurs when the mother and infant are incompatible with the Rh factor, with the
mother Rh (D) negative and the infant Rh (D) positive.
The first Rh-incompatible infant is usually unaffected, as the number of fetal cells
crossing the placenta is small.
The severity of the disease increases with each Rh-positive pregnancy.
IgG anti-D is found predominantly in subclasses IgG1 and IgG3, which plays an
effective role in erythrocytolysis in vivo.

Rh-D negative mother and Rh-D positive child

Mother is exposed to babies blood and produces anti-D antibodies (sensitization)

Antibodies cross the placenta> hemolysis of fetal RBCs
HDN worsens in subsequent pregnancies
Anti-D antibody injection after sensitization event

Factors affecting immunization and severity includes:

Antigenic Exposure
Host Factors
Antibody specificity
Immunoglobulin class
 HDN CAUSES – ABO INCOMPATIBILITY

ABO incompatibility between mother and newborn

or infant causes HDN
Maternal ABO antibodies that are IgG can cross the
placenta and attach to the ABO incompatible antigen of
the fetal RBCs.
Destruction of fetal RBCs leading to severe anemia
is rare, more commonly the disease is manifested by
the unset of hyperbilirubinaemia and jaundice with 12
to 48 hours of birth
HDN due to ABO incompatibility is usually less
severe than Rh incompatibility.
 DIAGNOSIS OF HDN

ABO Blood Grouping

Rh Typing
 Direct Antiglobulin Test (DAT)

Antenatal- Positive maternal antibody screening and / hydropic foetus

Postnatal- Rapidly developing or significant hyperbilirubinaemia not
predicted by maternal antenatal antibody screening
Jaundice – either physiological / pathological, but is always
pathological if it develops in the first 24 hours.

Laboratory findings- Positive direct anti-globulin test (DAT), hemolysis

on blood film
 Management / Treatment of HDN

The management or treatment of HDN includes the

following:

Intrauterine Transfusion
Phototherapy
Intravenous Immune Globulin
Exchange Transfusion
 INTRAUTERINE TRANSFUSION
Intrauterine Transfusion is necessary when the following are
observed:
Anemia
Fetal Hydrops
Cordocentesis blood sample hemoglobin below 10g/dl
High amniotic fluid results
Intrauterine transfusion suppresses fetal bone marrow RBC
production and additional RBCs may be required during the first
weeks after birth.
Major risk factor may include:
Infection
Premature labor
Trauma to the placenta, which may cause increased antibody
titers due to antigenic challenge to the mother
 PHOTOTHERAPY

After delivery, the neonate can develop

hyperbilirubinemia of unconjugated bilirubin.

Phototherapy at 460 to 490 nm is used to change

the unconjugated bilirubin to isomers, which are less
lipophilic and less toxic to the brain.

In infants with mild-to-moderate hemolysis or

history of intrauterine transfusion, phototherapy is
generally sufficient.
 EXCHANGE TRANSFUSION

Exchange transfusion is the use of whole blood or

equivalent to replace the neonate’s circulating blood.
Exchange transfusion is rarely required because of
advances in phototherapy and the use of IVIG.

Exchange transfusions are used primarily to remove

high levels of unconjugated bilirubin and thus prevent
kernicterus.

Premature newborns are more likely than full-term

infants to require exchange transfusions for elevated
bilirubin because their livers are less able to conjugate
bilirubin
 Intravenous Immune Globulin

Intravenous immune globulin (IVIG) is increasingly used

to treat hyperbilirubinemia of the newborn caused by
HDN.

 The IVIG competes with the mother’s antibodies for the

FC receptors on the macrophages in the infant’s spleen,
reducing the amount of hemolysis.
 SUMMARY

History of HDN

Pathophysiology – Rhesus and ABO incompatibilities

ABO more common and less severe

Maternal IgG1 and IgG3 antibodies crossing the placenta and causing
breakdown of Infants RBCs.

Diagnosis- antenatal, postnatal and laboratory findings

Jaundice in 12 to 48 hours but most especially 24 hours

Treatment- phototherapy, exchange transfusion, intravenous immune

globulin and intrauterine transfusion
 REFERENCES

Denise, M. H. (2012). Modern Blood Banking and Transfusion

Practices

 Arthur, J.(2021). Hemolytic disease of the newborn.

Birhaneselassie, M. et al. (2004). Immunohematology

Zipursky, A. (2008). Hemolytic disease of the newborn: Current

issues in diagnosis and treatment

MoiseJr, K.J. (2008). Hemolytic disease of the fetus and newborn