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 Goup A
(cells contain A antigen)

Recipient Group O
(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 (i.e. rbcs do not contain Rh antigen) Plasma contains no Rh antibodies NO agglutination

Rh +ve
(rbcs contain Rh antigen)

Later (months, years) Transfusion of Rh +ve blood

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

Gradual elimination by macrophage system

Fetal circulation

Iso-immunisation
Placenta Maternal circulation maternal blood sinus Damaged chorionic villus Trophoblast

Uterus

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

Cell becomes microspherocytes

= Antigenic determinant

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. Antibody combines with RBC Agglutination Reactions
usually of IgM type

= Antigenic determinant

Amboceptor effect
Ag/Ab activates complement Acute intravascular hemolysis

Clinically present as painful hand and feet

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)

Antibody

Extravascular hemolysis

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)

Antibody

Hemolysis

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