- Inherited hemolytic anemias – Generally due to abnormal hemoglobin molecules as seen in sickle cell anemia or thalassemia, or due to abnormalities of the RBC membranes resulting in excess splenic sequestration.
- Acquired hemolytic anemias – These can be due to exposure to certain drugs, certain infections (bacterial or viral), autoimmune etiologies, hematologic malignancies, mechanical destruction (due to mechanical heart valves, including potential leakage around the site of insertion), or sequestration in the setting of hypersplenism.
Intravascular hemolysis occurs within the vessel due to either mechanical trauma (from damaged endothelium) or complement fixation / activation on cell surface, or from an infectious agent. Extravascular hemolysis occurs outside of blood vessels in the spleen or liver when RBCs are removed or destroyed due to membrane surface defects or surface antibodies. Autoantibodies that lead to extravascular hemolysis may be categorized as "warm" (usually immunoglobulin G [IgG] antibodies), which bind to RBCs at body temperature, or "cold" (usually IgM antibodies), which bind to RBCs at below body temperature, producing cold agglutinins (ie, cold agglutinin disease).
Specific types of hemolytic anemia have their own incidence, demographics, and unique risk factors.
Types of hemolytic anemias include but are not limited to:
- Acute hemolytic transfusion reaction
- Disseminated intravascular coagulation
- Thrombotic microangiopathy
- RBC parasites (babesia, malaria)
- Drug-induced hemolysis (see drug-induced anemia)
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency
- Autoimmune hemolytic anemia
- Thalassemia (alpha and beta)
- Sickle cell disease
- Hereditary spherocytosis
- Hereditary elliptocytosis
- Mechanical hemolytic anemia due to mechanical aortic valves
- Spur cell hemolytic anemia (SCHA)