1. UNIVERSIDAD AUTÓNOMA DE GUERRERO
UNIDAD ACÁDEMICA FACULTAD DE MEDICINA
ENGLISH CLASS: HEMOLYTIC DISEASE OF
NEWBORN
EQUIPO FISIOLOGÍA.
Mendoza McGinnis Gema Itzel
Villagómez Vélez Julio Andrés
Arzeta Serrano Laura Gabriela
Hernández Barrera Mario
2. Objectives
The student is expected to learn about clinical
symptoms, diagnosis, and treatment for hemolytic
newborn disease.
Reinforce everything learned in physiology class by
applying a case study.
Participate in a group dynamic to simplify the learning
experience.
8. 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
9. Antibodies
Five classes of antibodies
IgM
IgG
IgA
IgD
IgE
Blood groups specific antibodies are
IgG
IgM and rarely
IgA
10. Blood group antibodies
Blood group antibodies can be classified as
Naturally occurring and immune antibodies
Depending on presensitization
Complete and incomplete antibodies
Depends on agglutination of saline suspended
red cells
IgM is complete antibody; most naturally
occurring antibodies are complete and of IgM
class
IgG is incomplete antibody
12. Antibodies of Rh system
Naturally occurring
Anti- E
Occasionally anti-D and anti Cw
Immune antibodies
D antibodies are more immunogenic
Other are anti c, E, e, C.
Most common is anti- E
After anti- D, anti- c is the common cause of HDN
(The vast majority of Rh antibodies are IgG and do not fix complement)
13. Complement
Complements are series of proteins, present
in plasma as an inactive precursors
When activated and react sequentially with
each other they mediate destruction of cells
and bacteria
Complement activation involves two stages
Opsonization
Lytic stage
14. Complement
Antibodies can fix complement and cause rapid
destruction of red cells
Destruction depends on the amount of antibody
and complement
In ABO- incompatible transfusion no surviving A
or B red cells can be seen after 1 hour of
transfusion
Why?
Remember naturally occurring Abs. are IgM and fix
complement mediating the hemolysis
15. Disease mechanism - HDN
There is destruction of the RBCs of the
fetus by antibodies produced by mother
If the fetal red cells contains the corresponding
antigen, then binding of antibody will occur to red
cells
Coated RBCs are removed by
mononuclear phagocytic system
16. Neonatal
liver is immature and
unable to handle
bilirubin
Unconjugated
bilirubin
Conjugated
bilirubin
Coated red blood cell
are hemolysed in
spleen
17. Clinical features
Less severe form
Mild anemia
Severe forms
Icterus gravis neonatorum (Kernicterus)
Intrauterine death
Hydrops fetalis
Oedematous, ascites, bulky swollen & friable
placenta
Pathophysiology
Extravascular hemolysis with extramedullary
erythropoiesis
Hepatic and cardiac failure
18. Hemolytic disease of newborn HDN
BOFORE BIRTH
Anemia (destruction of red cells)
Heart failure
Fetal death
AFTER BIRTH
Anemia (destruction of red cells)
Heart failure
Build up of bilirubin
Kernicterus
Severe growth retardation
19. Rh HEMOLYTIC DISEASE OF
NEWBORN
Antibodies against
Anti-D and less commonly anti-c, anti-E
Mother is the case of anti-D is Rh -ve
(negative)
Firstborn infant is usually unaffected
Sensitization of mother occurs
During gestation
At the time of birth
All subsequent offspring inheriting D-antigen
will be affected in case of anti-D HDN
20. Pathogenesis
Fetomaternal Hemorrhage
Maternal Antibodies formed against Paternally derived
antigens
During subsequent pregnancy, placental passage of
maternal IgG antibodies
Maternal antibody attaches to fetal red blood cells
Fetal red blood cell hemolysis
21.
22. Factors affecting immunization and
severity
Antigenic exposure
Host factors
Antibody specificity
Influence of ABO group
ABO-incompatible Rh- positive cells will be hemolysed
before Rh antigen can be recognized by the mother’s
immune system
23. Diagnosis and Management
Cooperation between
Pregnant patient
Obstetrician
Her spouse
Clinical laboratory
24. Diagnosis and Management contd.
Intrauterine transfusion
Zone II or III
Cordocentesis blood sample Hb less than 10g/dl
Ultrasound evidence of hydrops
Early delivery
Phototherapy
Newborn transfusion
Exchange transfusion
Effects of transfusion
Removal of bilirubin
Removal of sensitized RBCs, and antibodies
Suppression of incompatible erythropoiesis
25. Mechanism of action
Administered antibodies will
bind the fetal Rh- positive cells
Spleen captured these cells by
Fc-receptors
Suppressor T cell response is
stimulated
Spleen remove anti-D coated
red cells prior to contact with
antigen presenting cells
“antigen deviation”
26. ABO HEMOLYTIC DISEASE OF
NEW BORN
For practical purpose, only group O
individuals make high titres IgG
Anti-A and anti-B are predominantly IgM
ABO antibodies are present in the sera of all
individuals whose RBCs lack the
corresponding antigens
27. 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
Laboratory findings
Differ from Rh- HDN; microspherocytes are characteristic of ABO-
HDN
Bilirubin peak is later; 1- 3 days after birth
Collection of cord blood and testing eluates form red cells will
reveal anti-A or anti-B
Treatment
Group O donor blood for exchange transfusion which is rarely
required