|281 - ||Deficiency Anemias, Other|
|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-GrΣsbeck|
|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)|
|282 - ||Hemolytic Anemia, Hereditary|
|282.0 - ||Hereditary Spherocytosis; Acholuric (Familial) Jaundice; Congenital Hemolytic Anemia (Spherocytic); Congenital Spherocytosis; Minkowski-Chauffard Syndrome; Spherocytosis (Familial)|
|282.1 - ||Hereditary Elliptocytosis; Elliptocytosis (Congenital); Ovalocytosis (Congenital) (Hereditary)|
|282.2 - ||Anemias Due to Disorders of Glutathione Metabolism, 6-phosphogluconic Dehydrogenase Deficiency, Enzyme Deficiency, Drug-induced Erythrocytic Glutathione Deficiency, Glucose-6-Phosphate Dehydrogenase [G-6-PD] Deficiency, Glutathione-Reductase Deficiency, Hemolytic Nonspherocytic (Hereditary), Type I|
|282.3 - ||Hemolytic Anemias Due to Enzyme Deficiency, Other; Hemolytic Nonspherocytic (Hereditary), Type II, Hexokinase Deficiency, Pyruvate Kinase [PK] Deficiency, Triosephosphate Isomerase Deficiency|
|282.4 - ||Thalassemia|
|282.41 - ||Sickle-cell Thalassemia without Crisis; 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|
|282.49 - ||Thalassemia, Other; Cooleys Anemia; Hereditary Leptocytosis; Mediterranean Anemia (with Other Hemoglobinopathy); Microdrepanocytosis; Thalassemia (Alpha) (Beta) (Intermedia) (Major) (Minima) (Minor) (Mixed) (Trait) (with Other Hemoglobinopathy)|
|285 - ||Anemias, Other and Unspecified|
|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|
|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 for body tissues (hypoxia).|
Anemia is not a disease but rather a symptom 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 that following a traumatic penetrating injury, ruptured aneurysm, or major surgery, or it may be slow and chronic such as that occurring in chronic 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 prolonged, heavy, or frequent menstrual bleeding is another cause of anemia.
RBCs may be destroyed or removed from circulation faster than they can be replaced by new cells produced in the bone marrow. This occurs when there are defects within the RBC (e.g., in sickle cell anemia, hereditary spherocytosis), when antibodies attack and destroy otherwise healthy RBCs (e.g., in a transfusion reaction, autoimmune hemolytic anemia, systemic lupus erythematosus), the presence of 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 RBC 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 RBC and hemoglobin 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, often 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 within the body. 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 a membrane that surrounds hemoglobin inside the red cell 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 form of anemia that involves abnormal production of the proteins (polypeptide chains of globin) needed to make normal hemoglobin.
Some forms of anemia are inherited, (e.g., hereditary spherocytosis, thalassemia sickle cell anemia), 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.
Risk: Anemia is twice as common in women as it is in men. Based on an average hemoglobin of 13.5g/dl in men and 12.5g/dl in women (determined by World Health Organization criteria), lower than average hemoglobin concentration is found in 4% of men and 8% of women, with greater prevalence found in menstruating or pregnant women and individuals diagnosed with specific types of anemia (Conrad).
Increased risk for some anemias is associated with racial heritage, especially nutritional anemias, inherited anemias, and anemia resulting from chronic untreated illnesses. Pernicious anemia is more common in women, particularly black women. It is less common in other racial or ethnic groups. Folate deficiency is associated with pregnancy, malnutrition, and alcoholism. Sickle cell anemia is the most common anemia caused by a defect in hemoglobin (hemoglobinopathy) and is found primarily in blacks (Schick) Thalassemia is associated with individuals of Mediterranean, Middle Eastern, or African descent as well as some Asian groups (Schick).
Risk of anemia increases with age; it is most prevalent among the elderly (Balducci). Age is also a risk factor for inherited anemias such as sickle cell anemia, thalassemia, or Fanconi syndrome, because it is diagnosed in childhood and results in reduced survival to adulthood. Women of childbearing age are at greater risk of iron-deficiency anemia than younger females or older, post-menopausal women. Increased use of certain medications such as aspirin, nonsteroidal anti-inflammatory drugs (NSAIDS), and warfarin (Coumadin) by older adults increases risk of anemia associated with gastrointestinal bleeding (Conrad).
Low socioeconomic status is a risk factor for anemia in developed areas such as the US and EU; populations in developing countries are at greater risk for anemias associated with poor diet and increased exposure to infectious diseases (Conrad).
Exact incidence of anemia is not known, since many cases of mild anemia go unreported and untreated. Prevalence is highest in the population over age 65 (Balducci).
Incidence and Prevalence: Iron-deficiency anemia is the most common type of anemia, and is responsible for 95% of anemia associated with pregnancy (Lichtin). It is rare in men, but may occur in association with gastrointestinal bleeding.
International incidence parallels that of the US (Conrad). Iron-deficiency anemia is more prevalent in developing countries with low meat consumption, and anemia associated with chronic illnesses is commonly found in conjunction with higher incidence of infectious diseases such as malaria, tuberculosis, or AIDS (Conrad).
Source: Medical Disability Advisor
History: Symptoms depend on the suddenness of onset, severity of the condition, and 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. 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 with the primary cause of the anemia. Individuals with iron-deficiency anemia also may complain of a tingling in the arms or legs (paresthesia) 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, creases in the palm of the hand, and the mucous membrane (conjunctiva) that lines the eye. 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. 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 anemia 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 cardiac, liver, kidney, endocrine, and infectious diseases, or malignancy, 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 RBC (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 RBC), deformed RBC such as the elongated 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 RBCs in urine, and a test for occult blood may be performed on a stool sample. 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. 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 RBC. 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). In some cases, a Schilling's test is needed to further study vitamin B12 deficiency. Levels of methylmalonic acid and homocysteine can confirm B12 deficiency. Disorders of hemoglobin (e.g., thalassemia, sickle cell anemia) 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 for 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, liver function studies, and fecal occult blood.
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, MRI, 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 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 and are displaying signs of shock or hypoxia.|
Treatment is directed toward the underlying cause of the anemia. Iron-deficiency anemia due to low iron in the diet or increased 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 RBC in the bone marrow (aplastic or hypoplastic bone marrow), resulting in anemia. If this is suspected, the causative drug or chemical should be identified and dosage reduced or discontinued. 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 (Conrad).
Source: Medical Disability Advisor
|In any anemia, the cause of the anemia, its severity, and 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 transfused blood. 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 (Conrad).
Source: Medical Disability Advisor
|The most serious complication associated with severe anemia is deprivation of oxygen to organ systems (tissue hypoxia), which can rapidly result in shock, low blood pressure (hypotension), and associated organ damage 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.|
Source: Medical Disability Advisor
|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.|
Source: Medical Disability Advisor
|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.|
- 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 the 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 complete blood count, 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 work up performed including urinalysis, stool examination, and indirect bilirubin?
Was the possibility of a source of chronic bleeding investigated using radiography or other diagnostic imaging?
- 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
CitedBalducci, Lodovico. "Definition and Epidemiology of Anemia." Medscape Today. 4 Feb. 2004. Medscape. 8 Aug. 2009 <http://www.medscape.com/viewarticle/465312_2>.
Conrad, Marcel E. "Anemia." eMedicine. Eds. Jose A. Perez, et al. 11 Mar. 2008. Medscape. 18 Jul. 2009 <http://emedicine.medscape.com/article/198475-overview >.
Lichtin, Alan E. "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. Merck & Co., Inc. 18 Jul. 2009 <http://www.merck.com/mmpe/sec18/ch261/ch261b.html>.
Schick, Paul. "Hemolytic Anemia." eMedicine. Eds. Rodger L. Bick, et al. 27 Apr. 2009. Medscape. 18 Jul. 2009 <http://emedicine.medscape.com/article/201066-overview>.
Source: Medical Disability Advisor
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