Anemia is a decrease in the number of red blood cells (RBCs), which leads to a decrease in the hematocrit and the red cell hemoglobin content. (See also Red Blood Cell Production.)
The RBC mass represents the balance between the production and destruction or loss of RBCs. Thus, anemia can result from one or more of 3 basic mechanisms (see table Classification of Anemia by Cause):
Blood loss
Excessive hemolysis (RBC destruction)
Classification of Anemia by Cause
Mechanism | Examples |
|---|---|
Blood loss | |
Acute | Childbirth Gastrointestinal (GI) bleeding Injuries Surgery |
Chronic | Cancer or polyps in GI tract Kidney tumors Ulcers in the stomach or small intestine |
Deficient or ineffective erythropoiesis* | |
Microcytic | Iron-transport deficiency (iron refractory iron deficiency anemia [IRIDA]) Iron utilization defect (inherited sideroblastic anemia) |
Normochromic-normocytic | Kidney disease Endocrine failure (thyroid, pituitary) Parvovirus B19 infection Undernutrition |
Macrocytic | Liver disease Malabsorption (eg, tropical sprue) Myelodysplasia |
Excessive hemolysis due to extrinsically induced red blood cell abnormalities | |
Reticuloendothelial hyperactivity with splenomegaly | |
Immunologic abnormalities | Drug-induced |
Infection | Ebstein Barr virus (EBV) infection |
Mechanical injury | Foot strike hemolysis Thrombotic microangiopathies (hemolytic uremic syndrome [HUS], atypical or complement-mediated HUS, and thrombotic thrombocytopenic purpura [TTP]) |
Drugs/toxins | Spider bites |
Excessive hemolysis due to intrinsic red blood cell defects | |
Membrane alterations, acquired | |
Membrane alterations, congenital | Hereditary stomatocytosis Hereditary xerocytosis Neuroacanthocytosis |
Metabolic disorders (inherited enzyme deficiencies) | Glycolytic pathway defects (Embden-Meyerhof pathway defects) |
Hemoglobinopathies | Sickle cell disease (Hb SS disease, Hb S-C disease, Hb S–beta-thalassemia disease) Thalassemias (beta, beta-delta, and alpha) |
* Classified according to red blood cell indices. | |
Blood loss can be
Acute
Chronic
Anemia may not develop until several hours after acute blood loss when interstitial fluid diffuses into the intravascular space and dilutes the remaining RBC mass. During the first few hours, however, levels of polymorphonuclear granulocytes, platelets, and, in severe hemorrhage, immature white blood cells and normoblasts may rise. Chronic blood loss results in anemia if loss is more rapid than can be replaced or, more commonly, if accelerated erythropoiesis depletes body iron stores (see Iron Deficiency Anemia).
Deficient or inefficient erythropoiesis has myriad causes. Complete cessation of erythropoiesis results in a decline in RBCs of about 7 to 10%/week (1%/day). Impaired erythropoiesis, even if not sufficient to decrease the numbers of RBCs, often causes abnormal RBC size and shape.
Excessive hemolysis can be caused by intrinsic abnormalities of RBCs or by extrinsic factors, such as the presence of antibodies or complement on their surface, that lead to their early destruction. An enlarged spleen sequesters and destroys RBCs more rapidly than normal. Some causes of hemolysis deform as well as destroy RBCs. Hemolysis normally causes increased reticulocyte production unless iron or other essential nutrients are depleted or there is erythropoietin deficiency.
