Anemia Treatment & Management
- Author: Joseph E Maakaron, MD; Chief Editor: Emmanuel C Besa, MD more...
Approach Considerations
The purpose of establishing the etiology of an anemia is to permit selection of a specific and effective therapy. For example, corticosteroids are useful in the treatment of autoimmune hemolytic anemia.
Therapy and medical care vary considerably in the group of hereditary disorders. Splenectomy has been advantageous in hereditary spherocytosis and hereditary elliptocytosis, in some of the unstable hemoglobinopathies, and in certain patients with pyruvic kinase deficiency. It has little value in most other hereditary hemolytic disorders.
Drugs and chemicals capable of producing aplasia or a maturation arrest of erythroid precursors should be discontinued or avoided. Similarly, diseases known to be associated with anemia should be appropriately treated. Guidelines related to the treatment of chemotherapy-associated anemia are available.
Surgery is useful to control bleeding in patients who are anemic. Most commonly, bleeding is from the GI tract, uterus, or bladder. Patients should be hemodynamically stable before and during surgery. A blood transfusion may be needed.
Management of beta-thalassemia major and major hemoglobinopathies
Patients with beta-thalassemia major and the major hemoglobinopathies associated with sickle Hb usually require medical attention at frequent intervals for the treatment of anemia, infection, pain, and leg ulcers because of the serious nature of these illnesses. Conversely, many of the other hereditary abnormalities have minimal or no clinical manifestations; the patient only requires reassurance.
Consultations
Surgical consultation is indicated to control bleeding, for splenectomy when necessary, and for biopsies to establish the presence of neoplasia. Consultation with gastroenterologists is frequently sought to identify a bleeding site in the gut. Urologic consultation may be needed to investigate hematuria.
Follow-up
Patients with chronic anemia can usually be cared for on an outpatient basis. Follow-up care is necessary to ensure that therapy is being continued and to assess the efficacy of treatment.
Transfusion
Transfusion of packed RBCs should be reserved for patients who are actively bleeding and for patients with a severe and symptomatic anemia.[13] Transfusion is palliative and should not be used as a substitute for specific therapy. In chronic diseases associated with anemia of chronic disorders, erythropoietin may be helpful in averting or reducing transfusions of packed RBCs.
Hemolytic transfusion reactions and transmission of infectious disease are risks of blood product transfusions. Patients with autoimmune antibodies against RBCs are at greater risk of a hemolytic transfusion reaction because of difficulty in cross-matching the blood. Occasionally, the blood of patients with autoimmune hemolytic anemia cannot be cross-matched in vitro. In these cases, the patients require in vivo cross-matching, in which incompatible blood is transfused slowly and periodic determinations are made to ensure that the patient is not developing hemoglobinemia. This method should be used only in patients with either significant hypoxia from the anemia or evidence of coronary insufficiency.
Ferrous Sulfate Therapy
The appropriate treatment of anemia due to blood loss is correction of the underlying condition and oral administration of ferrous sulfate until the anemia is corrected and for several months afterward to ensure that body stores are replete with iron. Relatively few indications exist for the use of parenteral iron therapy, and blood transfusions should be reserved for the treatment of shock or hypoxia.
A study in Iran demonstrated that once-weekly, low-dose iron supplementation can be effective in improving iron status and in treating iron deficiency anemia.[14] Mozaffari-Khosravi et al randomly selected and assigned 193 adolescent girls aged 14-16 years to receive either 150 mg ferrous sulfate once weekly for 16 weeks or no iron supplementation. Before and after intervention, the percentage of anemia, iron deficiency anemia, and iron deficiency were measured in both groups of girls.
Although the parameters measured before the intervention were not significantly different, at the end of 16 weeks, the group that received the ferrous sulfate had significant improvement in the same parameters.[14] In addition, all cases of iron deficiency anemia were resolved in the group receiving the low-dose iron supplementation.
Nutritional Therapy and Dietary Considerations
Nutritional therapy is used to treat deficiencies of iron, vitamin B-12, and folic acid. Pyridoxine may be useful in the treatment of certain patients with sideroblastic anemia, even though this is not a deficiency disorder. A strict vegetarian diet requires iron and vitamin B-12 supplementation.
Iron deficiency anemia is prevalent in geographic locations where little meat is in the diet. Many of these locations have sufficient dietary inorganic iron to equal the iron content in persons residing in countries in which meat is eaten. However, heme iron is more efficiently absorbed than inorganic food iron. Folic acid deficiency occurs among people who consume few leafy vegetables. Coexistence of iron and folic acid deficiency is common in developing nations.
Management of Aplastic Disorders
Treatment of aplastic disorders includes removal of the offending agent whenever it can be identified, supportive therapy for the anemia and thrombocytopenia, and prompt treatment of infection. Avoid transfusion in patients with a potential bone marrow donor, because transfusion worsens the probability of cure from transplantation. Certain patients seem to develop a salutary response with immunosuppressive therapy (ie, antithymocyte globulin, cyclosporin). Splenectomy may provide sufficient improvement for patients with hypoplastic, but not totally aplastic, marrow so that transfusion is not necessary and platelet and granulocyte counts increase to less dangerous levels (see Splenectomy).
Splenectomy
Splenectomy is useful in the treatment of autoimmune hemolytic anemias and in certain hereditary hemolytic disorders (ie, hereditary spherocytosis and elliptocytosis, certain unstable Hb disorders, pyruvic kinase deficiency). Improvement in survival rates has been reported in patients with aplastic anemia, but splenectomy is not the preferential therapy. Leg ulcers have shown improvement in some patients with thalassemia. Prior to splenectomy, patients should be immunized with polyvalent pneumococcal vaccine. Preferably, this should be administered more than 1 week prior to surgery.
Bone Marrow and Stem Cell Transplantation
Bone marrow and stem cell transplantation have been used in patients with leukemia, lymphoma, Hodgkin disease, multiple myeloma, myelofibrosis, and aplastic disease. Survival rates in these patients improved, and hematologic abnormalities were corrected. Allogeneic bone marrow transplantation successfully corrected phenotypic expression of sickle cell disease and thalassemia and provided enhanced survival in patients who survived transplantation.
Activity Restriction
The activity of patients with severe anemia should be curtailed until the anemia is partially corrected. Transfusion can often be avoided by ordering bed rest, while therapy is initiated for a patient with correctable anemia (eg, pernicious anemia).
March hemoglobinuria is a rare hemolytic disorder usually observed in young males. Individuals develop hemoglobinuria after marching or running on hard surfaces. Curtailing the precipitating exercise (ie, running on grass rather than concrete) and using shoes with reinforced soles are helpful in preventing hemoglobinuria.
Transfer Considerations
Patients with a benign etiology for anemia usually do not require transfer to another institution. Occasionally, transfer is necessary to establish the etiology of the anemia or to provide a treatment that is not locally available.
If patients are being transferred for diagnostic reasons, transferring them before transfusion is helpful. If the transfusion is necessary before transfer to achieve hematopoietic stability, consult with the receiving physician to determine laboratory tests that should be performed before transfusion. Patients who are hemodynamically unstable should not be transported.
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Valenzuela JE, Schubert T, Fogel MR, Strong RM, Levine J, Mills PR, et al. A multicenter, randomized, double-blind trial of somatostatin in the management of acute hemorrhage from esophageal varices. Hepatology. Dec 1989;10(6):958-61. [Medline].
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| Condition | Serum Iron | Total Iron-Binding Capacity (TIBC) | Bone Marrow Iron | Comment |
| Iron deficiency | ↓ | ↑ | 0 | Responsive to iron therapy |
| Chronic inflammation | ↓ | ↓ | ++ | Unresponsive to iron therapy |
| Thalassemia major | ↑ | N | ++++ | Reticulocytosis and indirect bilirubinemia |
| Thalassemia minor | N | N - ↓ | ++ | Elevation of fetal hemoglobin and Hb A2, target cells, and poikilocytosis |
| Lead poisoning | N | N | ++ | Basophilic stippling of RBCs |
| Sideroblastic | ↑ | N | ++++ | Ring sideroblasts in marrow |
| Hemoglobin | N | N | ++ | Hemoglobin electrophoresis |
| ↓ = decreased; ↑ = increased; 0 = absent; +'s indicate the amount of stainable iron in bone marrow specimens, on a scale of 0-4; N = normal. | ||||
| Megaloblastic bone marrow | Deficiency of vitamin B-12 |
| Deficiency of folic acid | |
| Drugs affecting deoxyribonucleic acid (DNA) synthesis | |
| Inherited disorders of DNA synthesis | |
| Nonmegaloblastic bone marrow | Liver disease |
| Hypothyroidism and hypopituitarism | |
| Accelerated erythropoiesis (reticulocytes) | |
| Hypoplastic and aplastic anemia | |
| Infiltrated bone marrow |
| Macrocyte | Larger than normal (>8.5 µm diameter). See Table 2. |
| Microcyte | Smaller than normal (< 7 µm diameter). See Table 1. |
| Hypochromic | Less hemoglobin in cell. Enlarged area of central pallor. See Table 1. |
| Spherocyte | Loss of central pallor, stains more densely, often microcytic. Hereditary spherocytosis and certain acquired hemolytic anemias |
| Target cell | Hypochromic with central "target" of hemoglobin. Liver disease, thalassemia, hemoglobin D, and postsplenectomy |
| Leptocyte | Hypochromic cell with a normal diameter and decreased MCV. Thalassemia |
| Elliptocyte | Oval to cigar shaped. Hereditary elliptocytosis, certain anemias (particularly vitamin B-12 and folate deficiency) |
| Schistocyte | Fragmented helmet- or triangular-shaped RBCs. Microangiopathic anemia, artificial heart valves, uremia, and malignant hypertension |
| Stomatocyte | Slitlike area of central pallor in erythrocyte. Liver disease, acute alcoholism, malignancies, hereditary stomatocytosis, and artifact |
| Tear-shaped RBCs | Drop-shaped erythrocyte, often microcytic. Myelofibrosis and infiltration of marrow with tumor. Thalassemia |
| Acanthocyte | Five to 10 spicules of various lengths and at irregular intervals on surface of RBCs |
| Echinocyte | Evenly distributed spicules on surface of RBCs, usually 10-30. Uremia, peptic ulcer, gastric carcinoma, pyruvic kinase deficiency, and preparative artifact |
| Sickle cell | Elongated cell with pointed ends. Hemoglobin S and certain types of hemoglobin C and l |
| Hereditary | Acquired | |
| Intracorpuscular defect | Hereditary spherocytosis Hereditary elliptocytosis Hemoglobinopathies Thalassemias Congenital dyserythropoietic anemias Hereditary RBC enzymatic deficiencies Rarer hereditary abnormalities | Vitamin B-12 and folic acid deficiency Paroxysmal nocturnal hemoglobinuria Severe iron deficiency |
| Extracorpuscular defect | Physical agents: Burns, cold exposure Traumatic: Prosthetic heart valves, march hemoglobinuria, disseminated intravascular coagulation (DIC), graft rejection Chemicals: Drugs and venoms Infectious agents: Malaria, toxoplasmosis, mononucleosis, hepatitis, primary atypical pneumonia, clostridial infections, bartonellosis, leishmaniasis Hepatic and renal disease Collagen vascular disease Malignancies: Particularly hematologic neoplasia Transfusion of incompatible blood Hemolytic disease of the newborn Cold hemagglutinin disease Autoimmune hemolytic anemia Thrombotic thrombocytopenic purpura (TTP) and hemolytic-uremic syndrome (HUS) |

