Acquired Hemolytic Anemia

Immune hemolytic anemia

None-immune hemolytic anemia

Immune hemolytic anemia

Allo -immune hemolytic anemia
Autoimmune hemolytic anemia

Drug induced immune hemolytic anemia

Allo-immune hemolytic anemia

1. Incompatible ABO blood transfusion
Donor Blood

Recipient

Goup A

Group O

(cells contain A antigen)

(cells contain neither A or B antigen)

Plasma contains Anti-A and Anti-B

(iso-antibody)

Agglutination

Hemolysis

Allo-immune hemolytic anemia

1. Incompatible ABO blood transfusion

Clinical and Pathological effects

Rigor : loin pain.
hemoglobinuria
jaudice (after 12 hours)
SHOCK maybe DEATH
Perhaps later
Hemostatic failure, Renal failure maybe DEATH

Allo-immune hemolytic anemia

2. Incompatibilities with in the Rh blood group system
Incompatible blood transfusion

DONOR

Rh +ve
(rbcs contain Rh antigen)

Later (months, years)

Transfusion
of Rh +ve blood

RECIPIENT
(not previously transfused or pregnant)
Rh-ve (i.e. rbcs do not contain Rh antigen)
Plasma contains no Rh antibodies
NO agglutination

to macrophage system for degradation

in usual way but Rh+ve cells
act as foreign antigens
Formation of
anti-Rh antibodies stimulated
Agglutination
and hemolysis

Allo-immune hemolytic anemia

2. Incompatibilities with in the Rh blood group system
Hemolytic Disease of the New born (HDN)
First Pregnancy Rh+ve fetus in Rh-ve mother-no antibodies present.
Healthy Baby

Fetal circulation

Rh+ve
fetal rbcs
into mother
(Rh-ve)

Gradual elimination
by macrophage system

Iso-immunisation
Placenta

Uterus

maternal
blood sinus
Maternal
circulation

Damaged
chorionic villus Trophoblast

Anti-Rh antibodies
formed (IgG type)

Allo-immune hemolytic anemia

2. Incompatibilities with in the Rh blood group system
Hemolytic Disease of the New born (HDN)
Subsequent pregnancies

Uterus
Placenta

Maternal anti-Rh antibodies IgG type

Pass placental barrier

Enter fetal circulation and destroy fetal red cells
(agglutination and hemolysis)

Allo-immune hemolytic anemia

2. Incompatibilities with in the Rh blood group system
Hemolytic Disease of the New born (HDN)
The effect are graded into 3 categories of severity:
1. Congenital hemolytic anemia

mild anemia and jaundice

2. Icterus gravis neonatorum
severe anemia and jaudice,
brain damage due to Kernicterus
3. Hydrops fetalis
severe anoxia in utero with cardiac failure and edema.

Autoimmune Hemolytic Anemia (AIHA)

1. Warm autoimmune hemolytic anemia (WAIHA)
2. Cold autoimmune hemolytic anemia (cold AIHA)

Autoimmune hemolytic anemia : Warm antibody type (WAIHA)

Reaction at normal temperature (37 C)
= Antibody usually IgG type
Cell membrane
modified

= Antigenic determinant

Cell becomes
microspherocytes

With consequences similar to

hereditary spherocytosisearly sequestration in spleen (RE)

Autoimmune hemolytic anemia : Cold antibody type

Reaction at temperatures usually below 30 C
they occur in peripheral circulation and in cold weather.
usually of IgM type

Antibody

= Antigenic determinant

combines
with RBC
Agglutination

Reactions

Amboceptor effect

Clinically present as painful

hand and feet

Ag/Ab activates complement

Acute intravascular hemolysis

Raynauds phenomenon
manifested by marked pallor
of the fingers, in the cold type

Peripheral blood film showing

a neutrophil/red cell rosette

Drug-Induced Immune Hemolytic Anemia

1. Drug Adsorption Mechanism
Penicillins, Cephalosporin and Streptomycins
mechanism
First the drug is nonspecifically adsorbed to the patients red cell
Second the drug must be able to elicit an antibody response
B-Lymphocyte

RBC + Drug (Ag)

Antibody

Drug-Induced Immune Hemolytic Anemia

2. Immune Complex Mechanism : Innocent bystander
Quinidine and Phenacetin
B-Lymphocyte

Drug (Ag)

Extravascular
hemolysis

Antibody

RE

Complement

(IgG and/or IgM)

Intravascular
hemolysis

Drug-Induced Immune Hemolytic Anemia

3. Methyldopa-Induced (Autoimmune) Mechanism
methyldopa and related drugs (Aldomet, L-dopa):
treatment of hypertension

B-Lymphocyte

Drug (Ag)

Hemolysis

Antibody

Direct Coombs test

Indirect Coombs test

None-immune hemolytic anemia

Red cell fragment syndrome
Microangiopathic hemolytic anemia
Macroangiopathic hemolytic anemia
March hemoglobinuria

Hypersplenism
Paroxymal Nocturnal Hemoglobinuria
the bone marrow produces red cells with defective cell
membrane which are particular sensitive to lysis by complement

PNH : Acid lysis test. The affected red cells (on left) show
marked complement-dependent lysis in acidified fresh serum
at 37 C. Preheating the acidified serum inactivates complement,
preventing lysis of the affected cells