Anemia

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For other uses, see Anemia (disambiguation).

Anemia
Classification and external resources

ICD-10

D50-D64

ICD-9

280-285

DiseasesDB

663

MedlinePlus

000560

eMedicine

med/132 emerg/808emerg/734

MeSH

D000740

Anemia (/nimi/; also spelled anaemia and anmia; from Greek: anaimia, meaning lack of blood) is a decrease in number ofred blood cells (RBCs) or less than the normal quantity of hemoglobin in the blood.[1][2] However, it can include decreased oxygen-binding ability of each hemoglobin molecule due to deformity or lack in numerical development as in some other types of hemoglobin deficiency. Because hemoglobin (found inside RBCs) normally carries oxygen from the lungs to the tissues, anemia leads to hypoxia (lack of oxygen) in organs. Since all human cells depend on oxygen for survival, varying degrees of anemia can have a wide range of clinical consequences. Anemia is the most common disorder of the blood. There are several kinds of anemia, produced by a variety of underlying causes. Anemia can be classified in a variety of ways, based on the morphology of RBCs, underlying etiologic mechanisms, and discernible clinical spectra, to mention a few. The three main classes of anemia include excessive blood loss (acutely such as a hemorrhage or chronically through lowvolume loss), excessive blood cell destruction (hemolysis) or deficient red blood cell production (ineffective hematopoiesis). There are two major approaches: the "kinetic" approach which involves evaluating production, destruction and loss,[3] and the "morphologic" approach which groups anemia by red blood cell size. The morphologic approach uses a quickly available and low cost lab test as its starting point (the MCV). On the other hand,

focusing early on the question of production may allow the clinician to expose cases more rapidly where multiple causes of anemia coexist.

Contents
[hide]

1 Signs and symptoms 2 Diagnosis 3 Classification

o o o o o

3.1 Red blood cell size 3.2 Production vs. destruction or loss 3.3 Hyperanemia 3.4 Refractory anemia 3.5 Grading

4 Causes
o o o o

4.1 Impaired production 4.2 Increased destruction 4.3 Blood loss 4.4 Fluid overload

5 Treatments
o o

5.1 Blood transfusions 5.2 Hyperbaric oxygen

6 References 7 External links

[edit]Signs

and symptoms

Main symptoms that may appear in anemia.[4]

Anemia goes undetermined in many people, and symptoms can be minor or vague. The signs and symptoms can be related to the anemia itself, or the underlying cause. Most commonly, people with anemia report non-specific symptoms of a feeling of weakness, or fatigue, general malaise and sometimes poor concentration. They may also report dyspnea (shortness of breath) on exertion. In very severe anemia, the body may compensate for the lack of oxygen-carrying capability of the blood by increasing cardiac output. The patient may have symptoms related to this, such as palpitations,angina (if preexisting heart disease is present), intermittent claudication of the legs, and symptoms of heart failure. On examination, the signs exhibited may include pallor (pale skin, mucosal linings and nail beds) but this is not a reliable sign. There may be signs of specific causes of anemia, e.g., koilonychia (in iron deficiency), jaundice (when anemia results from abnormal break down of red blood cells in hemolytic anemia), bone deformities (found in thalassemia major) or leg ulcers (seen in sickle-cell disease). In severe anemia, there may be signs of a hyperdynamic circulation: tachycardia (a fast heart rate), bounding pulse, flow murmurs, and cardiacventricular hypertrophy (enlargement). There may be signs of heart failure. Pica, the consumption of non-food based items such as dirt, paper, wax, grass, ice, and hair, may be a symptom of iron deficiency, although it occurs often in those who have normal levels of hemoglobin. Chronic anemia may result in behavioral disturbances in children as a direct result of impaired neurological development in infants, and reduced scholastic performance in children of school age. Restless legs syndrome is more common in those with iron-deficiency anemia. Less common symptoms may include swelling of the legs or arms, chronic heartburn, vague bruises, vomiting, increased sweating, and blood in stool.

[edit]Diagnosis

Peripheral blood smear microscopy of a patient with iron-deficiency anemia.

Anemia is typically diagnosed on a complete blood count. Apart from reporting the number of red blood cells and the hemoglobin level, theautomatic counters also measure the size of the red blood cells by flow cytometry, which is an important tool in distinguishing between the causes of anemia. Examination of a

stained blood smear using a microscope can also be helpful, and is sometimes a necessity in regions of the world where automated analysis is less accessible. In modern counters, four parameters (RBC count, hemoglobin concentration, MCV and RDW) are measured, allowing others (hematocrit, MCHand MCHC) to be calculated, and compared to values adjusted for age and sex. Some counters estimate hematocrit from direct measurements.

WHO's Hemoglobin thresholds used to define anemia[5](1 g/dL = 0.6206 mmol/L)

Age or gender group

Hb threshold (g/dl)

Hb threshold (mmol/l)

Children (0.55.0 yrs)

11.0

6.8

Children (512 yrs)

11.5

7.1

Teens (1215 yrs)

12.0

7.4

Women, non-pregnant (>15yrs)

12.0

7.4

Women, pregnant

11.0

6.8

Men (>15yrs)

13.0

8.1

Reticulocyte counts, and the "kinetic" approach to anemia, have become more common than in the past in the large medical centers of the United States and some other wealthy nations, in part because some automatic counters now have the capacity to include reticulocyte counts. A reticulocyte count is a quantitative measure of the bone marrow's production of new red blood cells. The reticulocyte production index is a calculation of the ratio between the level of anemia and the extent to which the reticulocyte count has risen in response. If the degree of anemia is significant, even a "normal" reticulocyte count actually may reflect an inadequate response. If an automated count is not available, a reticulocyte count can be done manually following special staining of the blood film. In manual examination, activity of the bone marrow can also be gauged qualitatively by subtle changes in the numbers and the morphology of young RBCs by examination under a microscope. Newly formed RBCs are usually slightly larger than older RBCs and show polychromasia. Even where the source of blood loss is obvious, evaluation of erythropoiesis can help assess whether the bone marrow will be able to compensate for the loss, and at what rate.

When the cause is not obvious, clinicians use other tests: ESR, ferritin, serum iron, transferrin, RBC folate level, serum vitamin B12, hemoglobin electrophoresis, renal function tests (e.g.serum creatinine). When the diagnosis remains difficult, a bone marrow examination allows direct examination of the precursors to red cells.

[edit]Classification [edit]Red

blood cell size

In the morphological approach, anemia is classified by the size of red blood cells; this is either done automatically or on microscopic examination of a peripheral blood smear. The size is reflected in the mean corpuscular volume (MCV). If the cells are smaller than normal (under 80 fl), the anemia is said to be microcytic; if they are normal size (80100 fl), normocytic; and if they are larger than normal (over 100 fl), the anemia is classified as macrocytic. This scheme quickly exposes some of the most common causes of anemia; for instance, a microcytic anemia is often the result of iron deficiency. In clinical workup, the MCV will be one of the first pieces of information available; so even among clinicians who consider the "kinetic" approach more useful philosophically, morphology will remain an important element of classification and diagnosis.

[edit]Production

vs. destruction or loss

The "kinetic" approach to anemia yields what many argue is the most clinically relevant classification of anemia. This classification depends on evaluation of several hematological parameters, particularly the blood reticulocyte (precursor of mature RBCs) count. This then yields the classification of defects by decreased RBC production versus increased RBC destruction and/or loss. Clinical signs of loss or destruction include abnormal peripheral blood smear with signs of hemolysis; elevated LDH suggesting cell destruction; or clinical signs of bleeding, such as guaiac-positive stool, radiographic findings, or frank bleeding. The following is a simplified schematic of this approach:

Anemia Reticulocyte production indexshows inadequate production response to anemia. Reticulocyte production index shows appropriate response to anemia =ongoing hemolysis or blood loss without RBC production problem. Clinical findings and normal MCV= acutehemolysis or loss without adequate time for bone marrow production to

No clinical findings consistent with hemolysis or blood loss: pure disorder of production.

Clinical findings and abnormal MCV: hemolysis or loss andchronic disorder of production*.

compensate**. Macrocytic anemia (MCV>100) Normocytic anemia (80<MCV<100) Microcytic anemia (MCV<80)

* For instance, sickle cell anemia with superimposed iron deficiency; chronic gastric bleeding with B 12 and folate deficiency; and other instances of anemia with more than one cause. ** Confirm by repeating reticulocyte count: ongoing combination of low reticulocyte production index, normal MCV and hemolysis or loss may be seen in bone marrow failure or anemia of chronic disease, with superimposed or related hemolysis or blood loss.

Here is a schematic representation of how to consider anemia with MCV as the starting point:

Anemia Macrocytic anemia (MCV>1 00) High reticulocyte c ount Normocytic anemia (M CV 80 100) Low reticulocyte c ount Microcytic anemia (MCV< 80)

Other characteristics visible on the peripheral smear may provide valuable clues about a more specific diagnosis; for example, abnormal white blood cells may point to a cause in thebone marrow.

[edit]Microcytic
Main article: Microcytic anemia Microcytic anemia is primarily a result of hemoglobin synthesis failure/insufficiency, which could be caused by several etiologies:

Heme synthesis defect

Iron deficiency anemia Anemia of chronic disease (more commonly presenting as normocytic anemia)

Globin synthesis defect

alpha-, and beta-thalassemia HbE syndrome HbC syndrome and various other unstable hemoglobin diseases

Sideroblastic defect

Hereditary sideroblastic anemia Acquired sideroblastic anemia, including lead toxicity

Reversible sideroblastic anemia

Iron deficiency anemia is the most common type of anemia overall and it has many causes. RBCs often appear hypochromic (paler than usual) and microcytic (smaller than usual) when viewed with a microscope.

Iron deficiency anemia is caused by insufficient dietary intake or absorption of iron to replace losses from menstruation or losses due to diseases.[6] Iron is an essential part of hemoglobin, and low iron levels result in decreased incorporation of hemoglobin into red blood cells. In the United States, 20% of all women of childbearing age have iron deficiency anemia, compared with only 2% of adult men. The principal cause of iron deficiency anemia in premenopausal women is blood lost during menses. Studies have shown that iron deficiency without anemia causes poor school performance and lower IQ in teenage girls, although this may be due to socioeconomic factors.[7][8] Iron deficiency is the most prevalent deficiency state on a worldwide basis. Iron deficiency is sometimes the cause of abnormal fissuring of the angular (corner) sections of the lips (angular stomatitis).

Iron deficiency anemia can also be due to bleeding lesions of the gastrointestinal tract. Fecal occult blood testing, upper endoscopy and lower endoscopy should be performed to identify bleeding lesions. In men and post-menopausal women the chances are higher that bleeding from the gastrointestinal tract could be due to colon polyp or colorectal cancer.

Worldwide, the most common cause of iron deficiency anemia is parasitic infestation (hookworm, amebiasis, schistosomiasis and whipworm).[9]

[edit]Macrocytic
Main article: Macrocytic anemia

Megaloblastic anemia, the most common cause of macrocytic anemia, is due to a deficiency of either vitamin B12, folic acid (or both). Deficiency in folate and/or vitamin B12 can be due either to inadequate intake or insufficient absorption. Folate deficiency normally does not produce neurological symptoms, while B12 deficiency does.

Pernicious anemia is caused by a lack of intrinsic factor. Intrinsic factor is required to absorb vitamin B12 from food. A lack of intrinsic factor may arise from an autoimmunecondition targeting the parietal cells (atrophic gastritis) that produce intrinsic factor or against intrinsic factor itself. These lead to poor absorption of vitamin B12.

Macrocytic anemia can also be caused by removal of the functional portion of the stomach, such as during gastric bypass surgery, leading to reduced vitamin B12/folate absorption. Therefore one must always be aware of anemia following this procedure.

Hypothyroidism Alcoholism commonly causes a macrocytosis, although not specifically anemia. Other types of liver disease can also cause macrocytosis.

Methotrexate, zidovudine, and other drugs that inhibit DNA replication.

Macrocytic anemia can be further divided into "megaloblastic anemia" or "non-megaloblastic macrocytic anemia". The cause of megaloblastic anemia is primarily a failure of DNA synthesis with preserved RNA synthesis, which result in restricted cell division of the progenitor cells. The megaloblastic anemias often present with neutrophil hypersegmentation (610 lobes). The non-megaloblastic macrocytic anemias have different etiologies (i.e. there is unimpaired DNA globin synthesis,) which occur, for example in alcoholism. In addition to the non-specific symptoms of anemia, specific features of vitamin B12 deficiency include peripheral neuropathy and subacute combined degeneration of the cord with resulting balance difficulties from posterior column spinal cord pathology.[10] Other features may include a smooth, red tongue and glossitis. The treatment for vitamin B12-deficient anemia was first devised by William Murphy who bled dogs to make them anemic and then fed them various substances to see what (if anything) would make them healthy again. He discovered that ingesting large amounts of liver seemed to cure the disease. George Minot and George Whipple then set about to isolate the curative substance chemically and ultimately were able to isolate the vitamin B12 from the liver. All three shared the 1934 Nobel Prize in Medicine.[11]

[edit]Normocytic
Main article: Normocytic anemia Normocytic anemia occurs when the overall hemoglobin levels are decreased, but the red blood cell size (mean corpuscular volume) remains normal. Causes include:

Acute blood loss Anemia of chronic disease Aplastic anemia (bone marrow failure) Hemolytic anemia

[edit]Dimorphic
When two or more causes of anemia act simultaneously, e.g., macrocytic hypochromic, due to hookworm infestation leading to deficiency of both iron and vitamin B12 or folic acid [12] or following a blood transfusion more than one abnormality of red cell indices may be seen. Evidence for multiple causes appears with an elevated RBC distribution width (RDW), which suggests a wider-than-normal range of red cell sizes.

[edit]Heinz body anemia

Heinz bodies form in the cytoplasm of RBCs and appear like small dark dots under the microscope. There are many causes of Heinz body anemia, and some forms can be drug induced. It is triggered in cats by eating onions[13] or acetaminophen (paracetamol). It can be triggered in dogs by ingesting onions or zinc, and in horses by ingesting dry red maple leaves.

[edit]Hyperanemia

Hyperanemia is a severe form of anemia, in which the hematocrit is below 10%.

[edit]Refractory

anemia

Refractory anemia is an anemia which does not respond to treatment.[14] It is often seen secondary to myelodysplastic syndromes.[15] Iron deficiency anemia may also be refractory as a clinical manifestation of gastrointestinal problems which disrupt iron metabolism. [16]

[edit]Grading
WHO Grading of anemia:[17][18]

Grade 1 (Mild Anemia): 10 g/dl - cutoff point for ages Grade 2 (Moderate Anemia): 7-10 g/dl Grade 3 (Severe Anemia): below 7 g/dl

National Cancer Institute Grading of Anemia:[19]

Grade 0 (within normal limits) 12.016.0 g/dl for women and 14.018.0 g/ dl for men Grade 1 (Mild) 10 g/dl to levels within normal limits Grade 2 (Moderate) 8.010.0 g/dl Grade 3 (Severe) 6.57.9 g/dl Grade 4 (Life threatening) <6.5 g/dl

[edit]Causes
Broadly, causes of anemia may be classified as impaired red blood cell (RBC) production, increased RBC destruction (hemolytic anemias), blood loss and fluid overload (hypervolemia). Several of these may interplay to cause anemia eventually. Indeed, the most common cause of anemia is blood loss, but this usually doesn't cause any lasting symptoms unless a relatively impaired RBC production develops, in turn most commonly by iron deficiency.[20] (See Iron deficiency anemia)

[edit]Impaired

production

Disturbance of proliferation and differentiation of stem cells.

Pure red cell aplasia[21] Aplastic anemia,[21] affecting all kinds of blood cells. Fanconi anemia is a hereditary disorder or defect featuring aplastic anemia and various other abnormalities.

Anemia of renal failure,[21] by insufficient erythropoietin production Anemia of endocrine disorders

Disturbance of proliferation and maturation of erythroblasts

Pernicious anemia[21] is a form of megaloblastic anemia due to vitamin B12 deficiency dependent on impaired absorption of vitamin B12.

Anemia of folic acid deficiency.[21] As with vitamin B12, it causes megaloblastic anemia Anemia of prematurity, by diminished erythropoietin response to declining hematocrit levels, combined with blood loss from laboratory testing. It generally occurs in premature infants at 2 to 6 weeks of age.

Iron deficiency anemia, resulting in deficient heme synthesis[21] thalassemias, causing deficient globin synthesis[21] Congenital dyserythropoietic anemias, causing ineffective erythropoiesis Anemia of renal failure[21] (also causing stem cell dysfunction)

Other mechanisms of impaired RBC production

Myelophthisic anemia[21] or myelophthisis is a severe type of anemia resulting from the replacement of bone marrow by other materials, such as malignant tumors or granulomas.

Myelodysplastic syndrome[21] anemia of chronic inflammation[21]

[edit]Increased

destruction

Further information: Hemolytic anemia Anemias of increased red blood cell destruction are generally classified as hemolytic anemias. These are generally featuring jaundice and elevated LDH levels.

Intrinsic (intracorpuscular) abnormalities,[21] where there the red blood cells have defects that cause premature destruction. All of these, except paroxysmal nocturnal hemoglobinuria, are hereditary genetic disorders.[22]

Hereditary spherocytosis[21] is a hereditary defect that results in defects in the RBC cell membrane, causing the erythrocytes to be sequestered and destroyed by the spleen.

Hereditary elliptocytosis,[21] another defect in membrane skeleton proteins Abetalipoproteinemia,[21] causing defects in membrane lipids Enzyme deficiencies

Pyruvate kinase and hexokinase deficiencies,[21] causing defect glycolysis Glucose-6-phosphate dehydrogenase deficiency and glutathione synthetase deficiency,[21] causing increased oxidative stress

Hemoglobinopathies

Sickle cell anemia[21] Hemoglobinopathies causing unstable hemoglobins[21]

Paroxysmal nocturnal hemoglobinuria[21]

Extrinsic (extracorpuscular) abnormalities

Antibody-mediated

Warm autoimmune hemolytic anemia is an anemia caused by autoimmune attack against red blood cells, primarily by IgG. It is the most common of the autoimmunehemolytic diseases.[23] It can be idiopathic, that is, without any known cause, drug-associated or secondary to another disease such as systemic lupus erythematosus, or a malignancy, such as chronic lymphocytic leukemia (CLL)[24][24]

Cold agglutinin hemolytic anemia is primarily mediated by IgM. It can be idiopathic[25] or result from an underlying condition.

Rh disease,[21] one of the causes of hemolytic disease of the newborn Transfusion reaction to blood transfusions[21]

Mechanical trauma to red cells

Microangiopathic hemolytic anemias, including thrombotic thrombocytopenic purpura and disseminated intravascular coagulation[21]

Infections, including malaria[21] heart surgery

[edit]Blood

loss

Anemia of prematurity from frequent blood sampling for laboratory testing, combined with insufficient RBC production.

Trauma[21] or surgery, causing acute blood loss Gastrointestinal tract lesions,[21] causing a rather chronic blood loss Gynecologic disturbances,[21] also generally causing chronic blood loss From menstruation, mostly among young women

[edit]Fluid

overload

Fluid overload (hypervolemia) causes decreased hemoglobin concentration and apparent anemia:

General causes of hypervolemia include excessive sodium or fluid intake, sodium or water retention and fluid shift into the intravascular space.[26]

Anemia of pregnancy is anemia that is induced by blood volume expansion experienced in pregnancy.

[edit]Treatments
Treatments for anemia depend on severity and cause. Iron deficiency from nutritional causes is rare in men and post-menopausal women. The diagnosis of iron deficiency mandates a search for potential sources of loss such as gastrointestinal bleeding from ulcers or colon cancer. Mild to moderate iron-deficiency anemia is treated by oral iron supplementation with ferrous sulfate, ferrous fumarate, or ferrous gluconate. When taking iron supplements, it is very common to

experience stomach upset and/or darkening of the feces. The stomach upset can be alleviated by taking the iron with food; however, this decreases the amount of iron absorbed. Vitamin C aids in the body's ability to absorb iron, so taking oral iron supplements with orange juice is of benefit. Vitamin supplements given orally (folic acid) or intramuscularly (vitamin B-12) will replace specific deficiencies. In anemia of chronic disease, anemia associated with chemotherapy, or anemia associated with renal disease, some clinicians prescribe recombinant erythropoietin, epoetin alfa, to stimulate red-cell production. In severe cases of anemia, or with ongoing blood loss, a blood transfusion may be necessary.

[edit]Blood

transfusions

Doctors attempt to avoid blood transfusion in general, since multiple lines of evidence point to increased adverse patient clinical outcomes with more intensive transfusion strategies. The physiological principle that reduction of oxygen delivery associated with anemia leads to adverse clinical outcomes is balanced by the finding that transfusion does not necessarily mitigate these adverse clinical outcomes. In severe, acute bleeding, transfusions of donated blood are often lifesaving. Improvements in battlefield casualty survival is attributable, at least in part, to the recent improvements in blood banking and transfusion techniques.[citation needed] Transfusion of the stable but anemic hospitalized patient has been the subject of numerous clinical trials. Four randomized controlled clinical trials have been conducted to evaluate aggressive versus conservative transfusion strategies in critically ill patients. All four of these studies failed to find a benefit with more aggressive transfusion strategies.[27][28][29][30] In addition, at least two retrospective studies have shown increases in adverse clinical outcomes in critically ill patients that underwent more aggressive transfusion strategies.[31][32]

[edit]Hyperbaric

oxygen

Treatment of exceptional blood loss (anemia) is recognized as an indication for hyperbaric oxygen (HBO) by the Undersea and Hyperbaric Medical Society.[33][34] The use of HBO is indicated when oxygen delivery to tissue is not sufficient in patients who cannot be transfused for medical or religious reasons. HBO may be used for medical reasons when threat ofblood product incompatibility or concern for transmissible disease are factors.[33] The beliefs of some religions (ex: Jehovah's Witnesses) may require they use the HBO method.[33] In 2002, Van Meter reviewed the publications surrounding the use of HBO in severe anemia and found that all publications report a positive result.[35]

Anemia
Last reviewed: February 28, 2011.

Anemia is a condition in which the body does not have enough healthy red blood cells. Red blood cells provide oxygen to body tissues. See also:

Anemia due to B12 deficiency Anemia due to folate deficiency Anemia due to iron deficiency Anemia of chronic disease Hemolytic anemia Idiopathic aplastic anemia Megaloblastic anemia Pernicious anemia Secondary aplastic anemia Sickle cell anemia Thalassemia

Causes, incidence, and risk factors

While many parts of the body help make red blood cells, most of the work is done in the bone marrow. Bone marrow is the soft tissue in the center of bones that helps form blood cells. Healthy red blood cells last between 90 and 120 days. Parts of your body then remove old blood cells. A hormone called erythropoietin made in your kidneys signals your bone marrow to make more red blood cells. Hemoglobin is the oxygen-carrying protein inside red blood cells. It gives red blood cells their red color. People with anemia do not have enough hemoglobin. Possible causes of anemia include:

Certain medications Chronic diseases such as cancer, ulcerative colitis, or rheumatoid arthritis Genetics: Some forms of anemia, such as thalassemia, can be inherited Kidney failure Blood loss (for example, from heavy menstrual periods or stomach ulcers) Poor diet Pregnancy Problems with bone marrow such as lymphoma, leukemia, or multiple myeloma Problems with the immune system that cause the destruction of blood cells (hemolytic anemia)

Surgery to the stomach or intestines that reduces the absorption of iron, vitamin B12, or folic acid Too little thyroid hormone (underactive thyroid, or hypothyroidism) Testosterone deficiency

Symptoms
Possible symptoms include:

Chest pain Dizziness or light-headedness (especially when standing up or with activity) Fatigue or lack of energy Headaches Problems concentrating Shortness of breath (especially during exercise)

Some types of anemia may have other symptoms, such as:

Constipation Problems thinking Tingling

Signs and tests

The doctor will perform a physical examination, and may find:

Pale skin Rapid heart rate Heart murmur

Some types of anemia may cause other findings on a physical exam. Blood tests used to diagnose some common types of anemia may include:

Blood levels of vitamin B12, folic acid, and other vitamins and minerals Red blood count and hemoglobin level Reticulocyte count Ferritin level Iron level

Other tests may be done to identify medical problems that can cause anemia.

Treatment
Treatment should be directed at the cause of the anemia, and may include:

Blood transfusions Corticosteroids or other medicines that suppress the immune system Erythropoietin, a medicine that helps your bone marrow make more blood cells Supplements of iron, vitamin B12, folic acid, or other vitamins and minerals

Expectations (prognosis)
The outlook depends on the cause.

Complications
Severe anemia can cause low oxygen levels in vital organs such as the heart, and can lead to a heart attack.

Calling your health care provider

Call your health provider if you have any symptoms of anemia, or any unusual bleeding.

Anemia
Posted on 01/12/2011

Tips for preventing anemia content provided by Healthwise Anemia occurs when there are too few red blood cells in the blood. A complete blood count (CBC) can determine whether anemia is present. Women who have heavy and prolonged periods may develop anemia, because the body cannot produce blood as fast as it is being lost. Your body needs iron to make new blood cells. The recommended dietary allowance (RDA) is 18 mg.

You may need to increase your iron intake to 20 mg a day if your periods are heavy or prolonged. Your diet is the best source of iron. It is better for you to eat a balanced diet than it is to take dietary supplements. Red meats, shellfish, eggs, beans, and green leafy vegetables are the best sources of iron. Other good sources of iron include:

Clams [canned drained, 3 oz (85.1 g)] Oysters [3.5 oz (99.2 g)] Shrimp [3.5 oz (99.2 g)] Beef liver [3 oz (85.1 g)] Lean beef [3 oz (85.1 g)] Lentils (uncooked, 1 cup) Green peas (uncooked, 1 cup) Spinach (uncooked, 1 cup) Raisins (1 cup) Prunes (10) Enriched wheat bread (1 slice) Egg (1) Iron-enriched cereals (1 cup, read label for exact amounts)

Cooking in iron cookware will add small amounts of iron to the food. Vitamin C improves the absorption of iron. Be sure your diet includes 250 mg of vitamin C a day. Consider using a nonprescription iron supplement (such as ferrous sulfate) or a multivitamin if you are unable to meet your need for iron through your diet. For more information about iron, see the topic Healthy Eating. You may become constipated when you are taking an iron supplement. To avoid constipation:

Increase dietary fiber. Eat plenty of fruits. Drink at least 2 to 4 extra glasses of water a day.

Read too : Anemia Symptoms

In a person with anemia, symptoms will include tiredness and weakness because the bodys tissues are being starved of oxygen. As a matter of fact, fatigue is the main symptom of most types of anemia and the severity of anemia symptoms is partly related to the severity of anemia.

In a person suffering from anemia, symptoms that usually manifest themselves include: (a) Fatigue (b) Weakness (c) Fainting (d) Breathlessness (e) Heart palpitations (rapid or irregular beating) (f) Dizziness (g) Headache (h) Ringing in the ears (tinnitus) (i) Difficulty sleeping (j) Difficulty concentrating Other signs and anemia symptoms may include : (a) Pale complexion (b) The normally red lining of the mouth and eyelids fades in color (c) Rapid heartbeat (tachycardia) usually defined as a rate greater than 100 beats per minute.

(d) Abnormal menstruation (either absence of periods or increased bleeding) (e) Spoon-shaped finger nails and toenails in iron-deficiency anemia (f) Mild Jaundice that may be caused by obstruction of bile passage-ways, excessive destruction of red blood cells or a disturbance in the liver in hemolytic anemia g) Leg ulcers in sickle cell anemia Iron Deficiency Anemia content provided by Healthwise
TOPIC OVERVIEW

What is iron deficiency anemia? Iron deficiency anemia occurs when your body doesnt have enough iron. Iron is important because it helps you get enough oxygen throughout your body. Your body uses iron to make hemoglobin. Hemoglobin is a part of your red blood cells. Hemoglobin carries oxygen through your body. If you do not have enough iron, your body makes fewer and smaller red blood cells. Then your body has less hemoglobin, and you cannot get enough oxygen. What causes iron deficiency anemia? Iron deficiency anemia is caused by low levels of iron in the body. You might have low iron levels because you:

Have heavy menstrual bleeding. Are not getting enough iron in food. This can happen in people who need a lot of iron, such as small children, teens, and pregnant women. Have bleeding inside your body. This bleeding may be caused by problems such as ulcers, hemorrhoids, or cancer. This bleeding can also happen with

regular aspirin use. Bleeding inside the body is the most common cause of iron deficiency anemia in men and in women after menopause.

Cannot absorb iron well in your body. This problem may occur if you have celiac disease or if you have had part of your stomach or small intestine removed.

What are the symptoms? You may not notice the symptoms of anemia, because it develops slowly and the symptoms may be mild. In fact, you may not notice them until your anemia gets worse. As anemia gets worse, you may:

Feel weak and tire out more easily. Feel dizzy. Be grumpy or cranky. Have headaches. Look very pale. Feel short of breath. Have trouble concentrating.

Babies and small children who have anemia may:

Be fussy. Have a short attention span. Grow more slowly than normal. Develop skills, such as walking and talking, later than normal.

Anemia in children must be treated so that mental and behavior problems do not last long. How is iron deficiency anemia diagnosed? If you think you have anemia, see your doctor. Your doctor will do a physical exam and ask you questions about your medical history and your symptoms. Your doctor will take some of your blood to run tests. These tests may include a

complete blood count to look at your red blood cells and an iron test that shows how much iron is in your blood. Your doctor may also do tests to find out what is causing your anemia. How is it treated? Your doctor will probably have you take iron supplement pills to treat your anemia. Most people begin to feel better after a few days of taking iron pills. But do not stop taking the pills even if you feel better. You will need to keep taking the pills for several months to build up the iron in your body. If your doctor finds an exact cause of your anemia, such as a bleeding ulcer, your doctor will also treat that problem. If you think you have anemia, do not try to treat yourself. Do not take iron pills on your own without seeing your doctor first. If you take iron pills without talking with your doctor first, the pills may cause you to have too much iron in your blood, or even iron poisoning. Your low iron level may be caused by a serious problem, such as a bleeding ulcer or colon cancer. These other problems need different treatment than iron pills. You can get the most benefit from iron pills if you take them with vitamin C or drink orange juice. Do not take your iron pills with milk, caffeine, foods with high fiber, or antacids. Can you prevent iron deficiency anemia? You can prevent anemia by eating the right amount of iron every day. Iron-rich foods include meats, eggs, and whole-grain or iron-fortified foods. You can also get iron from many other foods, including peas, beans, oatmeal, prunes, and figs. You can prevent anemia in babies and children by feeding them enough iron. To make sure they get enough iron:

Breast-feed your baby for at least a year or as long after as you and your child desire. Introduce iron-enriched solid foods at 6 months of age to complement the breast milk. Iron-fortified cereals are a good source of iron.

After 6 months of age, give your child 2 to 3 servings of iron-rich foods a day. For babies who were weaned from the breast or the bottle before 12 months of age, give iron-fortified formula, not cows milk or goats milk. Cow and goat milks are low in iron.

If you are pregnant, you can prevent anemia by taking prenatal vitamins. Your doctor will give you prenatal vitamins that include iron. Your doctor will also test your blood to see if you are anemic. If you are anemic, you will take a higher-dose iron pill.

Blood transfusions for sickle cell disease

TREATMENT OVERVIEW

During a blood transfusion, a person (the recipient) receives healthy blood from another person (the donor). The donated blood is carefully screened for diseases before it is used. Before receiving a blood transfusion, the recipients blood is analyzed closely (using blood type) to make sure the donor blood is a close match to the recipients. Blood is transfused into an arm vein slowly over 1 to 4 hours (except in an emergency when blood is transfused more quickly). Blood transfusions can:

Treat a sudden or short-term condition related to sickle cell disease.

Treat severe complications of sickle cell disease. Prevent complications of sickle cell disease. Lower the risk of stroke in infants and children.

Blood transfusions arent usually used to treat uncomplicated painful events or mild to moderate anemia.

WHAT TO EXPECT AFTE R TREATMENT

Following a blood transfusion, doctors keep a close watch on the person for any negative reactions.

A transfusion reaction, resulting from mismatched blood type, may occur immediately or days later (5 to 20 days after transfusion). An acute transfusion reaction ranges from mild (fever, chills, and rash) to severe (shock, severe anemia, painful event, and death).

A person receiving repeat blood transfusions may develop antibodies to the donor blood (called alloimmunization). Alloimmunization makes repeated transfusions more difficult. It occurs in about 1 out of 4 people with sickle cell disease who get frequent transfusions.1

Hospital staff will also check for iron buildup in the body (iron overload). This can develop when a person gets many transfusions.

WHY IT IS DONE

A blood transfusion lowers the amount of hemoglobin S red blood cells in the body. When there are fewer sickled hemoglobin S cells in the bloodstream, they are less likely to build up and block blood vessels. Blood transfusion also increases the number of normal red blood cells in the body, increasing the supply of oxygen to the body. Anemia

Some sudden complications of sickle cell disease cause the bodys red blood cell count to drop to life-threatening levels (severe anemia). When severe, these conditions (including splenic sequestration, acute chest syndrome, and aplastic crisis) can be fatal if not treated with blood transfusions. Chronic severe anemia from kidney failure may need treatment with periodic blood transfusions. Surgery After having general anesthesia and surgery, people with sickle cell disease are at risk for sickling-related problems and acute chest syndrome. Blood transfusions before surgery can prevent or treat these complications.

Red blood cell sickling-related complications (vasoocclusion) Blood transfusions can treat acute chest syndrome and leg ulcers. Frequent blood transfusions may help prevent strokes in children who already had a stroke or are at high risk for a first stroke.2
HOW WELL IT WORKS

Blood transfusion is currently the single most effective and proven treatment for some severe complications of sickle cell disease.3 Blood transfusions reduce the risk of some complications of sickle cell disease and improve symptoms of severe anemia. Using repeat blood transfusions for 3 to 5 years can reduce the number of repeat strokes in children who have had a stroke.

RISKS

A person receiving many blood transfusions will gradually collect too much iron in the body (iron overload). Very high levels of iron can lead to hemochromatosis, which can be fatal if untreated. After 10 to 20 blood transfusions, iron chelation treatment can help rid the body of excess iron. Donated blood is carefully screened for diseases before it is used. But its remotely possible that donor blood may be contaminated with an infectious disease (such as HIV or hepatitis).

WHAT TO THINK ABOUT

If you have repeated blood transfusions, youll have routine testing for iron buildup in your body. Though blood transfusions are an effective treatment for sickle cell disease complications, they are only used selectively. The risks of hemochromatosis and alloimmunization from repeat transfusions makes this procedure more suitable for severe and high-risk conditions. Doctors and researchers continue to weigh the benefits against the risks of preventive blood transfusions. Repeat blood transfusion treatment for 3 to 5 years can reduce the number of repeat strokes in children who have sickle cell disease. It helps prevent a second stroke in most children. But some children who get repeat transfusions will still have a second stroke.