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Chapter 6
Hemolytic anemias
Overview
Hemolysis is the accelerated destruction, and hence decreased life span, of red blood cells (RBCs). The bone marrow's response to hemolysis is increased erythropoiesis, evidenced by reticulocytosis. If the rate of hemolysis is modest and the marrow is able to completely compensate for the decreased RBC life span, then hemoglobin concentration may be normal; this is called compensated hemolysis. If the bone marrow is unable to completely compensate for hemolysis, then anemia occurs. This is called incompletely compensated hemolysis.
Clinically, hemolytic anemia produces variable degrees of fatigue, pallor, and jaundice. Splenomegaly occurs in some conditions. The complete blood count shows
Hemolysis due to intrinsic abnormalities of the RBC
Abnormalities of hemoglobin Hb production Hb structure Hb function Disorders of Hb Thalassemia β Thalassemias Molecular basis Pathophysiology Clinical features Laboratory findings Management of the β thalassemias  ThalassemiasMolecular basis Pathophysiology Clinical features Laboratory features Management of the thalassemiasSickle cell disease Pathophysiology Laboratory features Clinical manifestations Treatment Preventive interventions Painful episodes RBC transfusion Acute chest syndrome Central nervous system disease Pregnancy Modifying the disease course Hemoglobin E Hemoglobin C Hemoglobin D Unstable Hb Oxygen affinity mutants Acquired hemoglobinopathies Carboxyhemoglobinemia Methemoglobinemia Sulfhemoglobinemia Hemoglobin H Abnormalities of the RBC membrane RBC membrane protein composition and assembly Hereditary spherocytosis Pathophysiology Clinical manifestations Laboratory evaluation Treatment Hereditary elliptocytosis and hereditary pyropoikilocytosis Pathophysiology Clinical manifestations, laboratory evaluation, and treatment Other RBC membrane disorders Acanthocytosis Stomatocytosis Rh deficiency (null) syndrome Abnormalities of RBC enzymes Abnormalities of the glycolytic pathway Abnormalities of the hexose-monophosphate shunt Abnormalities of nucleotide metabolism
Hemolysis due to extrinsic abnormalities of the RBC
Hemolytic anemia due to immune injury to RBCs Pathophysiology Warm AHA Cold AHA Mixed AHA Drug-induced immune hemolytic anemia Hapten or drug adsorption mechanism Ternary or immune complex mechanism: drug-antibody-target cell interaction Autoantibody mechanism Nonimmunologic protein adsorption Clinical manifestations and laboratory findings Treatment Paroxysmal nocturnal hemoglobinuria Pathophysiology Laboratory findings Laboratory diagnosis Clinical manifestations Treatment Prognosis Fragmentation hemolysis Pathophysiology Etiology Cardiac valve hemolysis Hemolytic-uremic syndrome–thrombotic thrombocytopenia purpura Disseminated intravascular coagulation HELLP syndrome Kasabach-Merritt syndrome Foot strike hemolysis Hemolytic anemia due to chemical or physical agents Hemolytic anemia due to infection RBC membrane injury caused by bacteria Clostridial sepsis Hemolytic anemias with gram-positive and gram-negative organisms Immune hemolysis associated with infections Hemolytic anemia associated with parasitic infestation of RBCs Malaria Babesiosis Bartonellosis   CiteULike  Connotea  Delicious  Digg  Facebook  Reddit  Technorati  Twitter What's this?
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