UNIVERSIDAD AUTÓNOMA DE GUERRERO

UNIDAD ACÁDEMICA FACULTAD DE MEDICINA

Mendoza McGinnis Gema Itzel

Villagómez Vélez Julio Andrés

Arzeta Serrano Laura Gabriela

Hernández Barrera Mario

ENGLISH CLASS: HEMOLYTIC DISEASE OF NEWBORN

EQUIPO FISIOLOGÍA.

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.

Antibodies - Anticuerpos Shortened - acortado Ocurring - ocurriendo Ag Glutination - Glutinacion antigenico Inmunogenic - Inmunogenico Involves - Involucrar

Phagocytic - Fagocitico Binding - Fristloorn - Microspheocytes - Microfeoscitos.

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

Antibodies

Five classes of antibodies IgM IgG IgA IgD IgE

Blood groups specific antibodies are IgG IgM and rarely IgA

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

Antibodies of ABO system

Anti- A

Anti- B

Anti- A1

Anti- H

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)

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

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

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

Conjugatedbilirubin

Unconjugatedbilirubin

Neonatalliver is immature and

unable to handle bilirubin

Coated red blood cellare hemolysed in

spleen

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

Hemolytic disease of newborn HDNBOFORE 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

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

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

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

Diagnosis and Management Cooperation between

Pregnant patient

Obstetrician

Her spouse

Clinical laboratory

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

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”

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

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