Hemolytic disease of new born.ppt.......

Haemolytic transfusion reaction

1. SUBJECT:
BLOOD TRANSFUSION SCIENCES
TOPIC
HAEMOLYTIC DISEASE OF NEWBORN

Adnan Hussein
Senior Lecturer

2. Defn: Is a condition in which the life span of infants red blood cells is
shortened by the action of specific antibodies derived form the mother
by placental transfer
In this condition there’s usually anaemia of the newborn due to the
destruction of foetal red cells
Other names of HDNB are:-
1.Neonatal jaudice
2.Erythroblastosis foetalis
The foeatal erythropoetic system is affected causing the presence of
erythroblasts to appear in circulation hence the disease formerly used
to be called Erythroblastosis foetalis

3. Usually HDNB starts in the intrauterine life and may cause death in
utero.
 The main cause of the disease is due to blood group incompatibility
through inheritance.
 Mother Father
dd Dd
Dd

4. The disease results for the passage of IgG antibodies for the maternal
circulation across the placenta into the circulation of the foetus
The ab’s attach onto the infants red cells causing destruction of the
cells
The foetal bone marrow in its course of replacing the destroyed cells
release blast into the circulation resulting into anaemia
 TYPES OF HDNB
1.Rhesus HDNB
2.ABO HDNB

5.  RHESUS HDNB
The disease occurs when a Rhesus –ve mother immunized to the
rhesus D antigen become pregnant with a rhesus +ve foetus
Always the mother is rhesus –ve
The most often cause of immunization is form a previous pregnancy or
a blood transfusion Other causes are abortion
Immunization due to pregnancy results from the passage of foetal
rhesus antigen form the foetus –ve mother
The mother become immunized and produce a maternal antibody
against the rhesus +ve foetus
The baby is affected due to the ability of the antibodies crossing the
placenta because of their molecular weight or sizes where they coat the
baby cells and are thus removed by the RES

6. Products such as bilirubin when the foetus is in utero thus bilirubin from
the foetus pass thru the placenta and is processed by the maternal liver
and excreted by the mother
The serious stage of HDNB comes after birth, when the infant has to
process the bilirubin
Since the baby is too young, it will not produce enough enzyme
glucuronyltransferase necessary for bilirubin conjugation hence implies
that a lot of bilirubin will circulate freely in the baby;s circulation
It is this free bilirubin which is toxic, has high affinity for the brain nerve
cells which are fat in nature
When bilirubin deposits on the brain nerve cells, kernicterus results
which is dangerous and may casue death or a mental retardation
The 1
st
baby is not usually affected unless the mother had previously been
sensitized e.g. previous blood transfusion

7. ABO HDNB
HDNB due to ABO incompatibility is caused by immune anti A or anti B
hwere the mother is blood group O and the foetus is group A or B
 Factors limiting primary immunization
Placenta barrier
The placenta acts as a filler and hence prevents large 1gG form passing
through placenta
It forms at the site of implantation of the fertilized ovum usually high
on the uterine wall. It consists of blood vessels, vascular space and small
amount of collective tissue
The mother and the foetal circulation are separate but there is an
extensive surface of contact since the chorionic villi containing the
foetal vessels extends into the intervillous space filled up with the maternal
blood

8. The main function is the exchange o f substances between the mother and
the foetus by simple diffusion
During delivering the placental villi and connective tissue rapture allowing
the foetal cells to escape into the maternal circulation and vice versa, this is
where immunization begins if the foetus and the mother are of different
rhesus group
 DIAGNOSIS OF HDNB
Clinical Symptoms:
Pallor, jaundice which may occur after birth or 3-5 days later
Anaemia, hepatomegally, splenomegally, oedema, hyperbilirubinaemia.
Severity of anaemia depends on the deficiency of the bone marrow and
other rbc’s producing sites in compensation
Occasionally, in more severe cases the foetus may die in utero resulting into
still birth

9. LABORATORY DIAGNOSIS
1.Perform ABO and rhesus grouping on both mother and the child.
2.Perform DCT on the body cells to detect inviro sensitization.
3.Perform ICT on the mothers serum. If positive indicates the mother has
an immune antibody
4.Do AST on the mothers serum to detect the type of antibody i.e. the
temperature and medium at which it reacts.
5.Do Ab identification test to identify the antibody
6.Perfom Ab titration test to determine the strength or titre of the antibody
7.Perform bilirubin estimation – if it is over 20mgs % and exchange
transfusion should be done
8.Do Hb estimation – it will be low
9.Perform reticulocyte count – increased

10.  TREATMENT OF HDNB
1.Exchange transfusion
2.Intrauterine transfusion
3.Early labour induction
4.Phototherapy
5.Albumin infusion

11. EXCHANGE TRANSFUSION
Normally carried out after the diagnosis has been established
Involves removal of blood from the infants and replacing it with cells that
will enjoy normal survival. The aim of exchange transfusion in HDNB is
oRemove the infants sensitized cells and replace them with cells which
will enjoy normal survival in the infant, and a supply of oxygen to the
tissues.
oLower or reduce the bilirubin level in the circulation and reduce the
risk of developing kernicterus
oRestore normal cardiac function and correct anaemia without
expanding the blood volume.
oReduce the amount of incompatible antibody present in the infants
circulation.

12. CRITERIA FOR EXCHANGE TRANSFUSION
1.The DCT on the infants cells must be +ve
2.The ICT on the mothers serum must be +ve
3.The serum bilirubin level of the infant must be over 20mg%
4.The cord Hb level must be low
5.The clinical symptoms must be assessed by the physician
6.Results of amniocentensis should be considered e.g. the titre of
maternal antibody

13.  SELECTION OF BLOOD FOR EXCHANGE TRANSFUSION
Blood should be a fresh as possible, less than 5 days old
Fresh blood is important because of the need to minimize the amount
of potassium level which is formed when cells stay for a long time
Blood used for exchange transfusion should lack red cell antigen (s)
corresponding to the maternal antibody
e.g. a rhesus +ve infant suffering from HDNB due to maternal antigen
should receive rh –ve blood
Hence the blood should be x-matched with the maternal antibody
When CPD and ACD are used in blood collection in exchange
transfusion, citrate toxicity is neutralized by calcium gluconate

14. Mother Baby Bld for
exchange
transfusion
Group O O
A O
B
Group A O O
B
A A or O
AB

15.  INTRAUTERINE TRANSFUION
Involves transfusion of the foetus which still in the womb
It is performed to save the foetus form intrauterine death
 It is a risky procedure and only those foetus who would not reach term
should be transfused
It is carried out at 32 – 36wks of pregnancy after analysis of the
amniotic fluid gives and indication that the foetus is in danger of death.
Packed cells are deposited in the foetal peritoneal sack where they are
absorbed intact. In most cases O –ve blood with low titre and about
100ml of blood is transfused
The transfusion is carried out to maintain the foetus up to 36 weeks for
induction of labour

16. EARLY LABOUR INDUCTION
Involves giving labour stimulants to the mother to induce labour so as
the baby to be born and managed.
 PHOTOTHERAPY
Bilirubin is photolabile therefore jaundiced infants are exposed to
direct light which will decompose the bilirubin and reduce the jaundice
 ALBUMIN INFUSION
The albumin will combine with the indirect bilirubin transport it to the
liver for conjugation

17. RH HDNB ABO HDNB
Occurrence in the first bornUnlikely Likely
Anaemia Moderate to severe Mild to moderate
Jaundice Very severe Mild to moderate
Hb concentration Low Normal to moderately low
Direct cooombs test Strongly +ve Weakly +ve or –ve
Eluate of infants cells Anti D Anti A or Anti B
Exchange transfusion Usually needed Frequently unnecessary
Reti’cs count Moderate to marked increaseMild to moderate increase
Incidence Less common More common
Prevention by antibody Yes No
Prediction Can be predicted Cannot be predicted

18. PREVENTION OF HDNB DUE TO ANTI – D
RHOGAM – Rho Gamma
Is a commercially prepared anti D. A Concentrated gamma G (Rh D
immunoglobin) prepared by alcohol fractionation to reduce the risk of
transmitting hepatitis
It is designed to suppress maternal antibody production as a result of
exposure to Rh +ve incompatible cells
It is given to a mother who has not yet formed anti D and has
delievered a Rh +ve baby
Rhogam prevents the mother form responding actively to the antigenic
stimulus of the incompatible foetal red cells that have entered her
circulation

19. CRITERIA FOR RHOGAM ADMINISTRATION
1.The mother must be Rh D –ve and Du – ve.
2.The Ab screening test must be –ve i.e. the mother serum must not
contain anti D.
3.The baby must be Rh D +ve or Du +ve.
4.DCT on the baby’s cells must be –ve.
 Rhogam is given to non-immunised rh –ve mother administered
intramuscularly within 72 hrs of delivery.

20. ANTENATAL SEROLOGY
All pregnant mothers should be grouped i.e. ABO Rh – usually done
early in pregnancy as a routine.
Perform Ab screening test on the mothers serum. If +ve identify the
antibody.
Titrate the antibody and note the titre of the antibody.
On the 2
nd
visit: repeat Ab screening test on the mother’s serum.
After delivery
Group the baby both ABO and Rh
Perform DCT. If +ve do Ab screening test on the mother. If the
mother is Rh –ve and the baby Rh +ve. No previous history of
immunization she should get rhogam

21. CAUSES OF NEONATAL JAUNDICE OTHER THAN HDNB
Physiologic
Hyperbilirubinaemia found in premature infants since their liver is not yet functioning
Cases of heredity spherocytosis
Congenital haemolytic anaemia
Metabolic
Maternal diabetes
Glucosaemia
Glucose 6 – phosphate deficiency
Pyruvate kinase deficiency
Infections
Congenital syphilis
Rubella (german measles)
Hepatitis
Drugs
Overdose of vit. K.
Naphthalene