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Sedentary Work Exerting up to 10 pounds (4.5 kg) of force occasionally and/or a negligible amount of force frequently or constantly to lift, carry, push, pull, or otherwise move objects, including the human body. Sedentary work involves sitting most of the time, but may involve walking or standing for brief periods of time. Jobs are sedentary if walking and standing are required only occasionally and other sedentary criteria are met.

Light Work Exerting up to 20 pounds (9.1 kg) of force occasionally and/or up to 10 pounds (4.5 kg) of force frequently, and/or negligible amount of force constantly to move objects. Physical demand requirements are in excess of those for Sedentary Work. Light Work usually requires walking or standing to a significant degree. However, if the use of the arm and/or leg controls requires exertion of forces greater than that for Sedentary Work and the worker sits most the time, the job is rated Light Work.

Medium Work Exerting up to 50 (22.7 kg) pounds of force occasionally, and/or up to 25 pounds (11.3 kg) of force frequently, and/or up to 10 pounds (4.5 kg) of forces constantly to move objects.

Heavy Work Exerting up to 100 pounds (45.4 kg) of force occasionally, and/or up to 50 pounds (22.7 kg) of force frequently, and/or in excess of 20 pounds (9.1 kg) of force constantly to move objects.

Very Heavy Work Exerting in excess of 100 pounds (45.4 kg) of force occasionally, and/or in excess of 50 pounds (22.7 kg) of force frequently, and/or in excess of 20 pounds (9.1 kg) of force constantly to move objects.

Job Classification

In most duration tables, five job classifications are displayed. These job classifications are based on the amount of physical effort required to perform the work. The classifications correspond to the Strength Factor classifications described in the United States Department of Labor's Dictionary of Occupational Titles. The following definitions are quoted directly from that publication.

Sedentary Work Exerting up to 10 pounds (4.5 kg) of force occasionally and/or a negligible amount of force frequently or constantly to lift, carry, push, pull, or otherwise move objects, including the human body. Sedentary work involves sitting most of the time, but may involve walking or standing for brief periods of time. Jobs are sedentary if walking and standing are required only occasionally and other sedentary criteria are met.

Light Work Exerting up to 20 pounds (9.1 kg) of force occasionally and/or up to 10 pounds (4.5 kg) of force frequently, and/or negligible amount of force constantly to move objects. Physical demand requirements are in excess of those for Sedentary Work. Light Work usually requires walking or standing to a significant degree. However, if the use of the arm and/or leg controls requires exertion of forces greater than that for Sedentary Work and the worker sits most the time, the job is rated Light Work.

Medium Work Exerting up to 50 (22.7 kg) pounds of force occasionally, and/or up to 25 pounds (11.3 kg) of force frequently, and/or up to 10 pounds (4.5 kg) of forces constantly to move objects.

Heavy Work Exerting up to 100 pounds (45.4 kg) of force occasionally, and/or up to 50 pounds (22.7 kg) of force frequently, and/or in excess of 20 pounds (9.1 kg) of force constantly to move objects.

Very Heavy Work Exerting in excess of 100 pounds (45.4 kg) of force occasionally, and/or in excess of 50 pounds (22.7 kg) of force frequently, and/or in excess of 20 pounds (9.1 kg) of force constantly to move objects.


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Medical Codes

280.0 - Iron Deficiency Anemia Secondary to Blood Loss (Chronic); Normocytic Anemia Due to Blood Loss
280.1 - Iron Deficiency Anemia Secondary to Inadequate Dietary Iron Intake
280.8 - Iron Deficiency Anemias, Other Specified; Paterson-Kelly Syndrome; Plummer-Vinson Syndrome; Sideropenic Dysphagia
280.9 - Iron Deficiency Anemia, Unspecified; Anemia, Achlorhydric, Chlorotic, Idiopathic hypochromic, Iron Deficiency NOS
281.0 - Pernicious Anemia; Anemia, Addisons, Biermers, Congenital Pernicious, Congenital Pernicious
281.1 - Vitamin B12 Deficiency Anemia, Other; Anemia, Vegans, Vitamin B12 Deficiency (Dietary), Due to Selective vitamin B12 Malabsorption with Proteinuria; Syndrome, Imerslunds, Imerslund-Gräsbeck
281.2 - Folate-deficiency Anemia; Congenital Folate Malabsorption; Folate or Folic Acid Deficiency Anemia: NOS, Dietary, Drug-induced; Goats Milk Anemia; Nutritional Megaloblastic Anemia (of Infancy)
281.3 - Megaloblastic Anemias, Not Elsewhere Classified, Other Specified; Combined B12 and Folate-deficiency Anemia; Refractory Megaloblastic Anemia
281.4 - Protein-deficiency Anemia; Amino-Acid-Deficiency Anemia
281.8 - Anemia Associated with Other Specified Nutritional Deficiency; Scorbutic Anemia
281.9 - Deficiency Anemia, , Unspecified; Dimorphic, Macrocytic, Megaloblastic NOS, Nutritional NOS, Simple Chronic
282.0 - Hereditary Spherocytosis; Acholuric (Familial) Jaundice; Congenital Hemolytic Anemia (Spherocytic); Congenital Spherocytosis; Minkowski-Chauffard Syndrome; Spherocytosis (Familial)
282.3 - Hemolytic Anemias Due to Enzyme Deficiency, Other; Hemolytic Nonspherocytic (Hereditary), Type II, Hexokinase Deficiency, Pyruvate Kinase [PK] Deficiency, Triosephosphate Isomerase Deficiency
282.40 - Thalassemia, Unspecified
282.41 - Sickle-cell Thalassemia without Crisis; Microdrepanocytosis; Sickle-cell Thalassemia NOS; Thalassemia Hb-S Disease without Crisis
282.42 - Sickle-cell Thalassemia with Crisis; Sickle-cell Thalassemia with Vaso-occlusive Pain; Thalassemia Hb-S Disease with Crisis
282.43 - Alpha Thalassemia
282.44 - Beta Thalassemia
285.1 - Anemia, Posthemorrhagic, Acute; Anemia Due to Acute Blood Loss
285.9 - Anemia, Unspecified, NOS, Essential, Normocytic, Not Due to Blood Loss, Profound, Progressive, Secondary
776.5 - Congenital Anemia

Related Terms

  • Aplastic Anemia
  • Cooley Anemia
  • Essential Anemia
  • Fanconi Anemia
  • Hemolytic Anemia
  • Hereditary Spherocytosis
  • Idiopathic Anemia
  • Iron Deficiency Anemia
  • Megaloblastic Anemia
  • Pernicious Anemia
  • Profound Anemia
  • Sickle Cell Disease
  • Sideroblastic Anemia
  • Spur Cell Anemia
  • Thalassemia Alpha
  • Thalassemia Beta


Anemia is defined as an abnormally low number of red blood cells (RBCs), an abnormally low amount of oxygen-carrying protein (hemoglobin) inside each RBC, or an abnormally low measure of red cell mass compared to the volume of plasma (hematocrit). In all three of these deficiencies, the oxygen-carrying capacity of the blood is decreased, resulting in less oxygen supply to body tissues (hypoxia).

Anemia is not a disease but rather a sign of many conditions or diseases. Causes are grouped into three categories: blood loss, RBC destruction (hemolysis), and impaired or decreased RBC production.

Blood loss can be sudden and acute such as with a traumatic penetrating injury, ruptured aneurysm, or major surgery. Slow and chronic blood loss can occur in gastrointestinal bleeding or in parasitic diseases such as uncinariasis. Blood coagulation disorders such as hemophilia also may cause excessive bleeding resulting in anemia. Blood loss due to heavy and prolonged menstrual bleeding (menorrhagia) or frequent menstrual bleeding (polymenorrhea) is another cause of this type of anemia.

RBCs may be destroyed or removed from circulation faster than they can be replaced by new RBCs produced in the bone marrow. This occurs when there are defects within the RBC (e.g., in sickle cell disease, hereditary spherocytosis), when antibodies attack and destroy otherwise healthy RBCs (e.g., in a transfusion reaction, autoimmune hemolytic anemia, systemic lupus erythematosus), when there are inclusion bodies within the RBC such as malarial parasites, or as a result of viral diseases that affect liver function (e.g., infectious mononucleosis, hepatitis). A general term for this type of anemia is hemolytic anemia, referring to hemolysis of RBCs at a much higher rate than normal regardless of the underlying cause.

Impaired RBC production is a broad category that includes conditions and diseases affecting either the number of RBCs produced or how they are produced. RBCs are produced in the bone marrow in response to the action of the hormone erythropoietin (EPO), which is made in the kidney. Kidney disease, cancer, chronic infection, or inflammation can decrease the production of EPO or interfere with its activity. Without active EPO, the bone marrow does not produce an adequate number of RBCs.

Problems inside the bone marrow also interfere with blood cell production. Sometimes the marrow stops producing RBCs as in aplastic anemia, a condition with severely decreased production of RBCs and other blood cells (white blood cells [WBCs] and platelets) due to defective regeneration within the bone marrow. This can occur in response to exposure to a toxic drug or chemical, or infection caused by certain viruses. Often, however, there is no known etiology for the condition (idiopathic aplastic anemia). A decrease in RBC production (hypoplasia) is found in malnutrition, particularly in the eating disorder anorexia nervosa. Myelodysplasia refers to a condition in which early RBCs (reticulocytes) do not develop properly in the bone marrow and die before being released into the circulatory system.

RBC production is impaired when the required synthesis of deoxyribonucleic acid (DNA) within the cell is defective, resulting in megaloblastic anemia. Megaloblastic anemia is most often caused by a deficiency of either folate or vitamin B12 (pernicious anemia). Some cases of megaloblastic or aplastic anemia are caused by administration of certain chemotherapeutic cancer drugs or exposure to certain chemical solvents such as benzene.

A problem with the synthesis of hemoglobin also can interfere with normal RBC production within the marrow. Because hemoglobin is an iron-containing protein, a deficiency of iron creates a deficiency of functional hemoglobin. Iron deficiency anemia may result from an insufficient amount of iron in the diet or malabsorption of iron from the gastrointestinal tract. More often, however, it occurs because either blood loss or increased demand has triggered the marrow to increase production in an effort to replace lost RBCs beyond the supply of iron available.

Chronic disease also can cause iron deficiency anemia if the disease interferes with the normal integration of iron into the RBC. Sideroblastic anemia is a type of anemia in which iron cannot be properly utilized.

In other cases, anemia can result when the RBC membrane that surrounds hemoglobin is abnormal, when certain glycolytic enzymes reduce the lifespan of RBCs, or when the chemical composition of hemoglobin itself is abnormal. Thalassemia is an inherited blood disorder with anemia that involves abnormal production of the proteins (polypeptide chains of globin) needed to make normal hemoglobin.

Some forms of blood disorders with anemia are inherited (e.g., hereditary spherocytosis, thalassemia, sickle cell disease), as are most blood coagulation disorders that involve deficiencies of specific coagulation factors needed to form clots when the skin is penetrated and bleeding occurs. Coagulation disorders are not forms of anemia but often result in extended bleeding that leads to anemia.

Incidence and Prevalence: Iron deficiency anemia is the most common type of anemia. About 20% of children will have anemia at some point in their childhood (Janus). There are 2.4 million children with iron deficiency, and 490,000 with iron deficiency anemia (Brotanek). The frequency of iron deficiency anemia varies by age, with 14% of children aged 1 to 2 years, 4% aged 3 to 5 years, and 9% of females aged 12 to 49 years old affected (CDC). Hispanic children are twice as likely to be iron deficient as white children (Brotanek). High anemia rates (between 18% to 39%) have been reported for blacks.

Among the elderly the prevalence of anemia is 12.6% in women and 14.1% in men. Anemia and mild anemia dramatically increases with age: from 4.9 per 1000 person-years among 65 to 69 year olds to 72.4 per 1000 person-years among 80 to 84 year olds (Tettamanti).

Source: Medical Disability Advisor

Causation and Known Risk Factors

Anemia occurs in all age, racial, and ethnic groups. Both men and women can have anemia. However, women of childbearing age are at increased risk because of blood loss from menstruation. Anemia can also develop during pregnancy. Infants and young children are at increased risk especially if they do not get enough iron in their diets. Older adults also are at increased risk for anemia if they have other precipitating medical conditions as well. A diet that is low in iron, vitamins, or minerals; premature birth; blood loss from surgery or an injury; long-term or serious illnesses, such as kidney disease, cancer, diabetes, rheumatoid arthritis, HIV/AIDS, inflammatory bowel disease (including Crohn's disease), liver disease, heart failure, and thyroid disease; long-term infections; and a family history of inherited anemia, such as sickle cell disease or thalassemia, can all increase the risk of anemia (CDC; NIH; Janus).

Source: Medical Disability Advisor


History: Symptoms depend on the suddenness of onset, severity of the condition, and the individual's age and general state of health. Mild anemia and anemia with a gradual onset often cause no symptoms and are not always investigated. Sudden loss of blood (hemorrhage) resulting in rapid onset of anemia produces immediate, dramatic symptoms such as a significant drop in blood pressure and oxygen levels or unconsciousness (hypovolemic shock). In this case, no prior symptoms will likely be reported unless the individual was aware of a sudden, significant nosebleed, injury, hemorrhage from mouth or rectum, or vaginal bleeding. Symptoms develop slowly in other forms of anemia.

General symptoms of anemia include fatigue, weight loss, headache, ringing in the ears (tinnitus), inability to concentrate, heart palpitations, and light-headedness when standing up. Some individuals may have abdominal discomfort, loss of appetite, nausea, diarrhea, or constipation, related to a gastrointestinal cause of the anemia. Individuals with iron deficiency anemia also may complain of a tingling in the arms or legs (paresthesias) and a burning sensation of the tongue. In severe anemia, exertion may cause breathing difficulties, dizziness, and chest pain.

Pregnancy and abortion history should be obtained for women of childbearing age or older.

It is important to inquire about a family history of anemia, abnormal hemoglobin levels, bleeding disorders, splenectomy, or transfusions. A record of prior blood studies may be helpful, as may a history of transfusions or prior treatment for nutritional deficiencies. Dietary history of foods consumed regularly and those avoided may be obtained. Rejection of the individual as a blood donor may also provide useful information.

Physical exam: Physical findings may include paleness (pallor) of the skin, the nail beds, and the mucous membranes that line the eye (conjunctiva). The heart rate may be increased (tachycardia), and blood pressure may be low when standing up (orthostatic hypotension). If anemia is severe, a heart murmur may be detected. The breathing rate also may be increased (tachypnea). The liver or spleen may be enlarged (hepatomegaly or splenomegaly). In individuals with pernicious anemia, nerve function may be impaired (peripheral neuritis, neuropathy).

Psychiatric symptoms, such as depression or confusion, also may be present. Individuals with anemia due to chronic disease may have evidence of infection, inflammation, or abnormal tissue growth. Iron-deficiency anemia may cause inflammation of the lips (cheilitis) or tongue (glossitis). Fingernails may be fragile or spoon-shaped (koilonychia). Individuals with severe sudden onset of anemia due to blood loss often have decreased urinary output.

Weight loss may indicate wasting due to metabolic or infectious diseases or malignancy. A complete physical exam may be done to rule out or include underlying malignancy or cardiac, liver, kidney, endocrine, and infectious diseases as a possible cause of anemia.

Tests: A complete blood count (CBC) may reveal a low number of RBCs. A reduced average size of red cells (mean corpuscular volume [MCV]) and reduced amount of hemoglobin within the RBCs (mean corpuscular hemoglobin [MCH]) may be noted. Microscopic examination of a blood smear may reveal reduced or enlarged size of red cells (microcytic or macrocytic RBCs), deformed RBCs (such as the crescent shaped sickle cell), or RBC fragments (schistocytes). Other findings may include low hemoglobin concentration and/or a low hematocrit. CBC results and information related to the size and appearance of the RBCs provide clues as to the cause of anemia and what tests to perform next. Special hematology tests or consultation with a hematologist may be needed to confirm diagnosis of a specific type of anemia.

Urinalysis may reveal the presence of hemoglobin or RBCs in the urine. A test for occult blood may be performed on a stool sample (fecal occult blood test [FOBT]). These tests may indicate chronic gastrointestinal bleeding or another possible bleeding site (e.g., rectal bleeding due to hemorrhoids). Urine of an abnormal color may suggest hemolytic anemia, kidney disease, or liver disease. The stool may be examined for color, bulk, odor, and density, which can point to malabsorption of nutrients.

A reticulocyte count helps differentiate anemia caused by decreased RBC production from that caused by blood loss or increased RBC destruction. Reticulocytes are immature RBCs, newly released from the bone marrow. A normal number of reticulocytes in the blood indicates that the bone marrow is appropriately producing RBCs. A low number of reticulocytes indicates that the anemia may be due to a problem in the bone marrow.

An indirect bilirubin test may help to confirm hemolysis indicative of hemolytic anemia and increased destruction of RBCs. Individuals whose reticulocyte count is reduced and whose indirect bilirubin is elevated have a hemolytic disorder. A direct Coombs test also may be positive in acquired hemolytic anemia, underlying autoimmune lupus erythematosus, or certain viral infections (e.g., hepatitis, infectious mononucleosis).

Tests for iron include ferritin, serum iron, and total iron-binding capacity (TIBC). These tests differentiate iron deficiency anemia from other types of anemia involving iron, such as sideroblastic anemia and anemia due to chronic disease.

Blood tests for folate and vitamin B12 differentiate between folate deficiency anemia and vitamin B12 deficiency anemia (pernicious anemia). Levels of methylmalonic acid and homocysteine can confirm B12 deficiency. Disorders of hemoglobin (e.g., thalassemia, sickle cell disease) can be confirmed with hemoglobin electrophoresis. This blood test identifies and measures abnormal forms of hemoglobin.

Sometimes a nutritional deficiency that results in anemia can be diagnosed by a therapeutic trial. Iron replacement therapy is given for a suspected case of iron deficiency anemia. Vitamin B12 is given to detect vitamin B12 deficiency, and folate to detect folate deficiency anemia. The diagnosis is made if improvement is seen after therapy.

If the individual's symptoms and initial test results are indicative of a serious form of anemia, a bone marrow aspiration or biopsy, where a sample of bone marrow is removed for microscopic examination, may be necessary to see whether normal RBCs are being produced at a normal rate. In rare equivocal cases, bone marrow examination may also be necessary to confirm iron deficiency anemia or megaloblastic changes caused by folate or vitamin B12 deficiency.

Other potential underlying causes can be ruled out by additional tests, such as kidney function tests, blood coagulation tests, and liver function tests.

If acute or chronic bleeding is suspected as a cause of the anemia, a search for the site of bleeding is indicated. This may require imaging studies (x-ray, magnetic resonance imaging [MRI], computed tomography [CT] scanning), endoscopy, or exploratory surgery.

Source: Medical Disability Advisor


The underlying condition or disease causing the anemia should be identified before beginning any treatment except when an individual is unstable due to significant blood loss. In this case, a blood transfusion may be required in order to replace lost blood before a diagnosis can be made. However, blood transfusions usually are reserved for those who are actively bleeding or are displaying signs of shock or hypoxia. Whenever possible, blood transfusions should comprise packed RBCs rather than whole blood.

Treatment is directed toward the underlying cause of the anemia. Iron deficiency anemia due to low iron in the diet or increased iron demand (such as during pregnancy) may be treated with oral iron supplements accompanied by vitamin C to encourage the assimilation of iron. Iron deficiency anemia caused by chronic bleeding is treated by finding the cause of the bleeding and treating that condition. Gastrointestinal bleeding is a common cause of iron deficiency anemia and may be treated with proton pump inhibitor or histamine (H2) antagonist drugs to control bleeding.

Folate deficiency anemia is treated with oral folate supplements. Injections of the hormone EPO, which stimulates the bone marrow to produce RBCs are given to replace EPO deficiency caused by kidney disease. Autoimmune hemolytic anemia may be treated with steroids or other immunosuppressive drugs. More serious forms of anemia such as thalassemia may require regular transfusions of packed RBCs, exchange transfusions of whole blood, or a bone marrow transplant from a compatible donor.

Occasionally, ingestion of certain drugs (e.g., sulfonamides, anticonvulsants, antithyroid drugs and chemotherapeutic agents), exposure to chemical solvents such as benzene, exposure to heavy metals such as arsenic, or receiving radiation therapy can reduce production of RBCs in the bone marrow (aplastic or hypoplastic bone marrow), resulting in anemia. If this is suspected, the causative drug should be identified and dosage reduced or discontinued, or the causative chemical should be identified and removed. Heavy metals must be removed from the body using either chelation therapy or appropriate chemical means of removal.

Treatments are continued until the problem is corrected. Lifelong conditions require lifelong treatment. Most forms of pernicious anemia require lifelong vitamin B12 injections. Individuals with blood coagulation disorders will need lifelong periodic replacement of the missing coagulation factors.

Surgery may be required to control bleeding in some anemic individuals, including bleeding from the gastrointestinal tract, uterus, or bladder; transfusions may be required to maintain hemodynamic stability throughout the surgery. Some types of anemia, including autoimmune hemolytic anemia, hereditary spherocytosis, and elliptocytosis, may require removal of the spleen (splenectomy). Newer treatments to correct severe anemia in hematologic abnormalities such as leukemia, lymphoma, and aplastic disease, involve transplantation of bone marrow and stem cells, which has been shown to increase life expectancy in sickle cell disease and thalassemia (Maakaron).

Source: Medical Disability Advisor


In any anemia, the cause of the anemia, its severity, and the rapidity of its development determine the outcome. The age of the patient and the presence of comorbid conditions such as heart, lung, kidney, or liver disease may also significantly influence outcome.

Outcome of anemia due to blood loss depends on the source of the bleeding, severity of the loss, and response to treatment. If the source of bleeding is identified and corrected, acute anemia due to massive blood loss can be successfully treated with blood transfusion. Chronic anemia due to a small but ongoing blood loss, such as in gastrointestinal bleeding, responds to correction of the bleeding without the need for transfusion if the source of bleeding is identified before blood loss is significant.

Anemia caused by dietary deficiencies usually can be corrected by replacement therapy, and improvement may be seen within weeks or months. Neuropsychiatric symptoms caused by pernicious anemia may take up to a year or more to show improvement. The symptoms may not resolve completely, but with ongoing treatment they typically do not progress.

Individuals with severe lifelong, hereditary anemias (e.g., sickle cell anemia, thalassemia) have a shortened life expectancy. Without a bone marrow transplant, severe forms of these anemias often result in death in the second or third decade of life (Maakaron).

Source: Medical Disability Advisor

Differential Diagnosis

  • Cancer
  • Heart failure

Source: Medical Disability Advisor


  • Emergency Medicine Physician
  • Family Physician
  • General Surgeon
  • Hematologist
  • Internal Medicine Physician

Source: Medical Disability Advisor

Comorbid Conditions

Source: Medical Disability Advisor


The most serious complication associated with sudden severe anemia due to acute blood loss is hypovolemic shock with deprivation of oxygen supply to organ systems (tissue hypoxia), low blood pressure (hypotension), and associated organ failure such as heart failure, respiratory failure, renal failure, and possibly death. This is more likely in older individuals who may already have underlying heart, lung, or kidney disease. Blood transfusions carry the risk of hemolytic transfusion reactions and infectious disease transmission.

Source: Medical Disability Advisor

Factors Influencing Duration

Length of disability will be influenced by the type of anemia, rapidity of onset, severity of symptoms, the individual's age, health status, alcohol or illicit substance use, method of treatment, and individual's compliance with and response to treatment.

Source: Medical Disability Advisor

Ability to Work (Return to Work Considerations)

Individuals with mild anemia typically do not require work accommodations or restrictions. Individuals with moderate anemia may experience fatigue, breathlessness, or dizziness with exertion. These individuals require a reduction in the physical requirements of work. This reduction may be temporary or permanent depending on the availability of and response to treatment. Individuals with severe anemia will likely need time off for more intensive treatment such as regular blood transfusions or bone marrow transplant, or surgery such as splenectomy. If exposure to chemical solvents has played a role in the anemia, the individual may require new work responsibilities.

Risk: No job that follows OSHA standards would be expected to place an individual at risk for anemia, nor to place an anemic individual at increased risk. If the anemia persists despite treatment, avoiding work at unprotected heights or at high altitude is prudent. Ensuring adequate hydration is also needed.

Capacity: This often can be gauged by the level of hemoglobin. A more functional assessment may be performed with metabolic stress testing.

Tolerance: Encouragement, counseling, and flexible work hours may be used to assist individuals with being in a work environment if their anemia is persistent.

Source: Medical Disability Advisor

Maximum Medical Improvement

120 days.

Source: Medical Disability Advisor

Failure to Recover

If an individual fails to recover within the expected maximum duration period, the reader may wish to consider the following questions to better understand the specifics of an individual's medical case.

Regarding diagnosis:

  • Does individual have underlying conditions creating risk of developing anemia such as recent blood loss, malignancy, or renal failure?
  • Is there a history of anemia?
  • Is individual a woman of childbearing age?
  • Has individual received transfusions before or had abnormal blood tests?
  • Was individual rejected as a blood donor at any time?
  • Was a complete physical examination performed to identify signs of possible underlying illness?
  • Was diagnosis of anemia confirmed with a CBC, peripheral blood smear, hemoglobin, and hematocrit? Were special hematology tests performed such as a reticulocyte count and direct Coombs test?
  • Were additional serological tests (e.g., total iron binding capacity, ferritin and folate levels, or hemoglobin electrophoresis) performed to determine type of anemia present?
  • Was a diagnostic workup performed including urinalysis, stool examination, and indirect bilirubin?
  • Was the possibility of a source of chronic bleeding investigated using radiography or other diagnostic imaging?

Regarding treatment:

  • Has individual received the appropriate intervention to address the underlying cause of the anemia?
  • Is individual complying with prescribed treatment?
  • Is lifelong treatment necessary?
  • Will individual require a splenectomy, bone marrow transplant, or other surgery?

Regarding prognosis:

  • Has underlying cause of the anemia been identified and successfully treated?
  • Is success of treatment being monitored by subsequent blood tests?
  • Does individual have access to needed medical care?
  • Does individual have an adequate diet? Would individual benefit from nutrition counseling?
  • If anemia was caused by ingestion of drugs or exposure to chemicals, have these been reduced, discontinued, or removed?
  • If anemia is related to alcohol abuse, has individual stopped using alcohol?
  • Does individual have an underlying condition such as cardiac, pulmonary, kidney, or liver disease that may affect recovery? Is individual elderly?
  • Did individual experience shock or organ failure associated with severe anemia?

Source: Medical Disability Advisor



"Explore Anemia." National Heart, Blood, and Lung Institute. 18 May. 2012. National Institutes of Health (NIH). 6 Apr. 2014 <>.

"Fast Stats: Anemia or Iron Deficiency." Centers for Disease Control and Prevention (CDC). 30 May. 2013. National Center for Health Statistics. 6 Apr. 2014 <>.

Brotanek, J. M. , et al. "Iron Deficiency in Early Childhood in the United States: Risk Factors and Racial/Ethnic Disparities ." Pediatrics 120 (2007): 568-575.

Friel, Lara A. "Anemia in Pregnancy." The Merck Manual of Diagnosis and Therapy. Eds. Robert S. Porter, et al. 18th ed. Whitehouse Station, NJ: Merck and Company, Inc., 2008. The Merck Manuals. 20 Jun. 2013. Merck & Co., Inc. 6 Apr. 2014 <>.

Janus, J. , and S. K. Moerschel. "Evaluation of Anemia in Children." American Family Physician 81 (2010): 1462-1471.

Maakaron, Joseph E. "Anemia." eMedicine. Ed. Emmanuel C. Besa. 30 Jul. 2013. Medscape. 6 Apr. 2014 <>.

Schick, Paul. "Hemolytic Anemia." eMedicine. Eds. Emmanuel C. Besa, et al. 21 Feb. 2013. Medscape. 6 Apr. 2014 <>.

Tettamanti, M. , et al. "Prevalence, Incidence, and Types of Mild Anemia in the Elderly: The "Health and Anemia" Population-Based Study." Haematologica 95 (2010): 1849-1856.

Source: Medical Disability Advisor