Anemias Caused By Excessive Hemolysis

Symptoms and Signs?

Systemic manifestations resemble those of other anemias. Hemolysis may be acute, chronic, or episodic. Hemolytic crisis (acute, severe hemolysis) is uncommon; it may be accompanied by chills, fever, pain in the back and abdomen, prostration, and shock. In severe cases, hemolysis increases (jaundice, splenomegaly, and, in certain types of hemolysis, hemoglobinuria and hemosiderinuria), and erythropoiesis increases (reticulocytosis, hyperactive bone marrow). In chronic hemolysis, anemia may be exacerbated by aplastic crisis (temporary failure of erythropoiesis); this is usually related to an infection, often parvovirus.

Laboratory Findings   

Jaundice occurs when the conversion of Hb to bilirubin exceeds the liver's capacity to form bilirubin glucuronide and excrete it into bile (see also Ch. 38). Thus, unconjugated (indirect) bilirubin accumulates. Increased pigment catabolism is also manifested by increased stercobilin in the stool and urobilinogen in the urine. Pigment gallstones frequently complicate chronic hemolysis.

Although hemolysis can usually be identified by the simple criteria described, the definitive criterion is a measure of RBC survival, preferably with a nonreutilizable label such as radiochromium (51Cr). The measured survival of radiolabeled RBCs establishes not only hemolysis but also, with body surface counting, sites of RBC sequestration, thereby providing diagnostic and therapeutic options. In general, a half-life (for 51Cr-labeled RBCs) of >= 18 days (normal, 28 to 32 days) indicates hemolysis mild enough for a normally responsive marrow to maintain normal RBC values. The term compensated hemolytic anemia refers to a marrow that responds appropriately, producing near-normal RBC values. Selective splenic sequestration with expected repair after splenectomy can be anticipated when surface count ratios reveal a spleen:liver ratio > 3:1 (normal, 1:1).

Other tests (eg, increased indirect hyperbilirubinemia, increased fecal urobilinogen or carbon monoxide production) or evidence of repair (reticulocytosis) supports but does not establish the likelihood of hemolysis. LDH is commonly increased in hemolysis.

Morphologic examination of the peripheral blood may show evidence of hemolysis (eg, fragmentation, spherocytes) or erythrophagocytosis, which helps establish the diagnosis and the mechanism (ie, intravascular hemolysis). Other tests for causes of hemolysis include Hb electrophoresis, RBC enzyme assays, osmotic fragility, direct antiglobulin (Coombs') test, cold agglutinins, and acid hemolysis or sucrose lysis tests

The Merck Manual of Diagnosis and Therapy   hyperlink to list of sections
Section 11. Hematology And Oncology   hyperlink to list of chapters in current section
Chapter 127. Anemias
Topics
[General]
Anemias Caused By Blood Loss
Anemias Caused By Deficient Erythropoiesis

reticulocyte: a young red cell (erythrocyte) released by the bone marrow that contains no nucleus but has residual RNA; normally composes about 1% of circulating blood cells. The reticulocyte count is increased in hemolytic anemia.

Can support there being anemia, but not a diagnosis in itself


2-butoxyethanol

Other definitions for those who may need to check your blood in particular ways.

What ways? (Now with links to definitions)

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