– Abnormal or premature destruction of red blood cells and the inability of the bone marrow to produce sufficient RBCs to compensate.
Causes and Incidence
The etiology is typically related to an extracorpuscular factor (e.g., trauma, burns, surgery, chemical agents, drugs, infectious organisms, systemic diseases). Less common are intracorpuscular causes, such as a glucose-6-phosphate dehydrogenase (G6PD) deficiency.
The precipitating factor results in a shortened life span for erythrocytes and an increase in erythrocyte destruction by the reticuloendothelial system. The bone marrow is unable to produce sufficient replacement cells to keep pace with the destruction, and anemia ensues.
Hemolysis can be acute or chronic. The symptoms of chronic hemolysis resemble those of other anemias: fatigue, weakness, dyspnea, and pallor. Individuals with chronic symptoms may suffer from a physiologic or emotional stressor that triggers a hemolytic crisis. Acute hemolytic crisis, which is rare, is characterized by chills; fever; headache; pain in the back, abdomen, and joints; splenomegaly; hepatomegaly; lymphadenopathy; and reduced urinary output.
Chronic symptoms can lead to jaundice, arthritis, renal failure, and other organ failure. Crisis can lead to paresthesia, paralysis, chills, vomiting, shock, and organ failure.
Sickle cell test
To rule out sickle cell anemia.
Decreased Hgb and hematocrit (Hct).
Elevated lactate dehydrogenase and bilirubin.
Bone marrow aspiration
Surgery – Splenectomy.
Corticosteroids to depress extracorpuscular factors and diminish inflammatory response; diuretics to prevent tubular necrosis; folic acid to increase RBC production.
Elimination of causative agent; erythrocytopheresis (RBC exchange); transfusion; oxygen therapy for hypoxemia; fluid and electrolyte management.