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Hemolysis of red blood cells (RBCs) within the circulation or in the extravascular spaces of the spleen and liver can produce a spectrum of disease, from mild, asymptomatic illness to severe hemodynamic compromise leading to critical ED encounters. Acquired hemolytic anemia consists of hemolysis not due to congenital or inherited disorders of hemoglobin synthesis or of the RBC membrane.


Presenting symptoms and signs of hemolytic anemia include those common to anemia in general: weakness or fatigue; dizziness; shortness of breath with dyspnea on exertion; tachycardia, particularly at rest; palpitations; chest pain; new or accentuated cardiac murmur; and pallor. RBC destruction generates free hemoglobin that is then broken down into bilirubin. When bilirubin production exceeds the liver’s ability to conjugate it for biliary and fecal excretion, jaundice, abdominal pain (particularly from gallstones), and darkened urine may develop. Splenic enlargement may promote the storage and extravascular breakdown of RBCs.


The laboratory findings characteristic of acquired hemolytic anemia are those that demonstrate blood loss and hemolysis of RBCs, hemoglobin breakdown, and compensatory RBC production (Table 232-1). The complete blood count (CBC) serves as the diagnostic cornerstone, providing the anemic level hemoglobin and hematocrit and the increased reticulocyte count indicative of the bone marrow’s effort to replace lost RBCs. Findings on peripheral blood smear demonstrate the abnormal RBC morphology needed to verify the presence of hemolysis: schistocytes generated by intravascular shearing of RBCs and spherocytes produced by extravascular phagocytosis of RBCs within the liver and spleen.

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Table 232-1 Basic Tests and Findings in the Evaluation of Hemolytic Anemia

Intravascular hemolysis of RBCs releases hemoglobin into the bloodstream that then binds to haptoglobin and other serum proteins. The hemoglobin-haptoglobin complex travels to the liver for processing, thus decreasing the amount of free haptoglobin in the serum—an important laboratory finding when corroborating the existence of intravascular hemolysis. Breakdown of RBCs releases lactate dehydrogenase and potassium, leading to elevation of both in serum. With excessive hemoglobin breakdown comes increased bilirubin production that cannot be conjugated by the liver for biliary and fecal excretion. Laboratory findings associated with excess bilirubin production include elevated total bilirubin; elevated indirect or unconjugated bilirubin; and increased urinary urobilinogen, a by-product of bilirubin breakdown formed by the intestine and passed into the urine. Excess free hemoglobin ...

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