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 RECIPIENT
(not previously transfused or pregnant)
Rh +ve Rh-ve (i.e. rbc’s do not contain Rh antigen)
(rbc’s contain Rh antigen) Plasma contains no Rh antibodies
 NO agglutination
to macrophage system for degradation
in usual way but Rh+ve cells
Later (months, years) act as foreign antigens
Transfusion
of Rh +ve blood 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
Gradual elimination
Rh+ve
fetal rbc’s
by macrophage system
into mother
Fetal circulation (Rh-ve)
Iso-immunisation

Placenta maternal
blood sinus
Damaged
Anti-Rh antibodies
Uterus Maternal chorionic villus Trophoblast formed (IgG type)
circulation
 Allo-immune hemolytic anemia
2. Incompatibilities with in the Rh blood group system
Hemolytic Disease of the New born (HDN)
Subsequent pregnancies

Uterus Maternal anti-Rh antibodies IgG type

Placenta

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 becomes

microspherocytes
Cell membrane
modified

= Antigenic determinant With consequences similar to

hereditary spherocytosis-
early 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.

Antibody usually of IgM type

= Antigenic determinant
combines
with RBC

Agglutination Reactions

Amboceptor effect

Ag/Ab activates complement

Clinically present as painful Acute intravascular hemolysis
hand and feet
Raynaud’s 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 patient’s 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) Antibody

RE Complement
Extravascular Intravascular
hemolysis hemolysis
(IgG and/or IgM)
Drug-Induced Immune Hemolytic Anemia

3. Methyldopa-Induced (Autoimmune) Mechanism

methyldopa and related drugs (Aldomet, L-dopa):

treatment of hypertension

B-Lymphocyte
Drug (Ag) Antibody

Hemolysis
Direct Coomb’s test

Indirect Coomb’s 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