Hemolytic anemias are a group of disorders where red blood cell survival is reduced either continuously or episodically. Because a patient’s bone marrow has the ability to increase erythroid production up to eighteen times in response to reduced red blood cell survival, a patient will only present with anemia when the patient’s bone marrow production is outstripped. This will occur when red blood cell survival is extremely short or when the bone marrow’s ability to compensate is impaired. Hemolytic disorders are generally classified based on whether the defect is intrinsic to the red blood cell or due to some external factor. Certain laboratory features are common to all hemolytic anemias. To take just a few examples, Haptoglobin, a normal plasma protein that binds and clears free hemoglobin released into plasma, may be depressed in hemolytic disorders. Haptoglobin levels, though, are influenced by many factors and may not be a reliable indicator of hemolysis – particularly in end-stage liver disease. When intravascular hemolysis occurs, transient hemoglobinemia ensues. Here, hemoglobin is filtered through the renal glomerulus and is usually reabsorbed by tubular cells. Hemoglobinuria will be present only when the patient’s capacity for reabsorption of hemoglobin by renal tubular cells is exceeded, In the absence of hemoglobinuria, evidence for prior intravascular hemolysis is the presence of hemosiderin in shed tubular cells. With severe intravascular hemolysis, hemoglobinemia and methemsalbuminemia may be present. Hemolysis increases indirect bilirubin levels and the total bilirubin may rise to 4mg/dL or more. Bilirubin levels higher than this may indicate some degree of hepatic dysfunction.