Image result for information about anaemia


Anemia is a decrease in the total amount of red blood cells (RBCs) or hemoglobin in the blood,[3][4] or a lowered ability of the blood to carry oxygen.[5] When anemia comes on slowly, the symptoms are often vague and may include feeling tired, weakness, shortness of breath or a poor ability to exercise.[1] Anemia that comes on quickly often has greater symptoms, which may include confusion, feeling like one is going to pass out, loss of consciousness, or increased thirst.[1] Anemia must be significant before a person becomes noticeably pale.[1] Additional symptoms may occur depending on the underlying cause.[1]

The three main types of anemia are due to blood loss, decreased red blood cell production, and increased red blood cell breakdown.[1] Causes of blood loss include trauma and gastrointestinal bleeding, among others.[1] Causes of decreased production include iron deficiency, a lack of vitamin B12, thalassemia, and a number of neoplasms of the bone marrow.[1] Causes of increased breakdown include a number of genetic conditions such as sickle cell anemia, infections like malaria, and certain autoimmune diseases.[1] It can also be classified based on the size of red blood cells and amount of hemoglobin in each cell.[1] If the cells are small, it is microcytic anemia.[1] If they are large, it is macrocytic anemia while if they are normal sized, it is normocytic anemia.[1] Diagnosis in men is based on a hemoglobin of less than 130 to 140 g/L (13 to 14 g/dL), while in women, it must be less than 120 to 130 g/L (12 to 13 g/dL).[1][6] Further testing is then required to determine the cause.[1]

Certain groups of individuals, such as pregnant women, benefit from the use of iron pills for prevention.[1][7] Dietary supplementation, without determining the specific cause, is not recommended.[1] The use of blood transfusions is typically based on a person's signs and symptoms.[1] In those without symptoms, they are not recommended unless hemoglobin levels are less than 60 to 80 g/L (6 to 8 g/dL).[1][8] These recommendations may also apply to some people with acute bleeding.[1] Erythropoiesis-stimulating medications are only recommended in those with severe anemia.[8]

Anemia is the most common blood disorder, affecting about a third of the global population.[2][1] Iron-deficiency anemia affects nearly 1 billion people.[9] In 2013, anemia due to iron deficiency resulted in about 183,000 deaths – down from 213,000 deaths in 1990.[10] It is more common in women than men,[9] during pregnancy, and in children and the elderly.[1] Anemia increases costs of medical care and lowers a person's productivity through a decreased ability to work.[6] The name is derived from Ancient Greek: ἀναιμία anaimia, meaning "lack of blood", from ἀν- an-, "not" and αἷμα haima, "blood".[11]

Main symptoms that may appear in anemia[12]

The hand of a person with severe anemia (on the left) compared to one without (on the right)
Anemia goes undetected in many people and symptoms can be minor. The symptoms can be related to an underlying cause or the anemia itself. Most commonly, people with anemia report feelings of weakness or fatigue, and sometimes poor concentration. They may also report 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 pre-existing heart disease is present), intermittent claudication of the legs, and symptoms of heart failure. On examination, the signs exhibited may include pallor (pale skin, lining mucosa, conjunctiva 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 cardiac ventricular hypertrophy (enlargement). There may be signs of heart failure. Pica, the consumption of non-food items such as ice, but also paper, wax, or grass, and even hair or dirt, 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 academic performance in children of school age. Restless legs syndrome is more common in those with iron-deficiency anemia.[13]

Causes

Figure shows normal red blood cells flowing freely in a blood vessel. The inset image shows a cross-section of a normal red blood cell with normal hemoglobin.[14]
The 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 does not cause any lasting symptoms unless a relatively impaired RBC production develops, in turn most commonly by iron deficiency.[15] (See Iron deficiency anemia)

Impaired production
Disturbance of proliferation and differentiation of stem cells
Pure red cell aplasia[16]
Aplastic anemia[16] affects all kinds of blood cells. Fanconi anemia is a hereditary disorder or defect featuring aplastic anemia and various other abnormalities.
Anemia of renal failure[16] by insufficient erythropoietin production
Anemia of endocrine disorders[medical citation needed]
Disturbance of proliferation and maturation of erythroblasts
Pernicious anemia[16] is a form of megaloblastic anemia due to vitamin B12 deficiency dependent on impaired absorption of vitamin B12. Lack of dietary B12 causes non-pernicious megaloblastic anemia
Anemia of folic acid deficiency,[16] as with vitamin B12, causes megaloblastic anemia
Anemia of prematurity, by diminished erythropoietin response to declining hematocrit levels, combined with blood loss from laboratory testing, generally occurs in premature infants at two to six weeks of age.
Iron deficiency anemia, resulting in deficient heme synthesis[16]
Thalassemias, causing deficient globin synthesis[16]
Congenital dyserythropoietic anemias, causing ineffective erythropoiesis
Anemia of renal failure[16] (also causing stem cell dysfunction)
Other mechanisms of impaired RBC production
Myelophthisic anemia[16] 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[16]
anemia of chronic inflammation[16]
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 lactate dehydrogenase levels.[medical citation needed]

Intrinsic (intracorpuscular) abnormalities[16] cause premature destruction. All of these, except paroxysmal nocturnal hemoglobinuria, are hereditary genetic disorders.[17]
Hereditary spherocytosis[16] 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[16] is another defect in membrane skeleton proteins.
Abetalipoproteinemia,[16] causing defects in membrane lipids
Enzyme deficiencies
Pyruvate kinase and hexokinase deficiencies,[16] causing defect glycolysis
Glucose-6-phosphate dehydrogenase deficiency and glutathione synthetase deficiency,[16] causing increased oxidative stress
Hemoglobinopathies
Sickle cell anemia[16]
Hemoglobinopathies causing unstable hemoglobins[16]
Paroxysmal nocturnal hemoglobinuria[16]
Extrinsic (extracorpuscular) abnormalities
Antibody-mediated
Warm autoimmune hemolytic anemia is caused by autoimmune attack against red blood cells, primarily by IgG. It is the most common of the autoimmune hemolytic diseases.[18] 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.[19][19]
Cold agglutinin hemolytic anemia is primarily mediated by IgM. It can be idiopathic[20] or result from an underlying condition.
Rh disease,[16] one of the causes of hemolytic disease of the newborn
Transfusion reaction to blood transfusions[16]
Mechanical trauma to red blood cells
Microangiopathic hemolytic anemias, including thrombotic thrombocytopenic purpura and disseminated intravascular coagulation[16]
Infections, including malaria[16]
Heart surgery[medical citation needed]
Haemodialysis[medical citation needed]
Blood loss
Anemia of prematurity from frequent blood sampling for laboratory testing, combined with insufficient RBC production
Trauma[16] or surgery, causing acute blood loss
Gastrointestinal tract lesions,[16] causing either acute bleeds (e.g. variceal lesions, peptic ulcers) or chronic blood loss (e.g. angiodysplasia)
Gynecologic disturbances,[16] also generally causing chronic blood loss
From menstruation, mostly among young women or older women who have fibroids
Infection by intestinal nematodes feeding on blood, such as hookworms[21] and the whipworm Trichuris trichiura.[22]
The roots of the words anemia and ischemia both refer to the basic idea of "lack of blood", but anemia and ischemia are not the same thing in modern medical terminology. The word anemia used alone implies widespread effects from blood that either is too scarce (e.g., blood loss) or is dysfunctional in its oxygen-supplying ability (due to whatever type of hemoglobin or erythrocyte problem). In contrast, the word ischemia refers solely to the lack of blood (poor perfusion). Thus ischemia in a body part can cause localized anemic effects within those tissues.

Fluid overload
General causes of hypervolemia include excessive sodium or fluid intake, sodium or water retention and fluid shift into the intravascular space.[23]
Intestinal inflammation
Certain gastrointestinal disorders can cause anemia. The mechanisms involved are multifactorial and not limited to malabsorption but mainly related to chronic intestinal inflammation, which causes dysregulation of hepcidin that leads to decreased access of iron to the circulation.[24][25][26]

Helicobacter pylori infection.[27]
Gluten-related disorders: untreated celiac disease[27][26] and non-celiac gluten sensitivity.[28] Anemia can be the only manifestation of celiac disease, in absence of gastrointestinal or any other symptoms.[29]
Inflammatory bowel disease.[30][31]

Definitions
There are a number of definitions of anemia; reviews provide comparison and contrast of them.[32] A strict but broad definition is an absolute decrease in red blood cell mass,[33] however, a broader definition is a lowered ability of the blood to carry oxygen.[5] An operational definition is a decrease in whole-blood hemoglobin concentration of more than 2 standard deviations below the mean of an age- and sex-matched reference range.[34]

It is difficult to directly measure RBC mass,[35] so the hematocrit (amount of RBCs) or the hemoglobin (Hb) in the blood are often used instead to indirectly estimate the value.[36] Hemotocrit; however, is concentration dependent and is therefore not completely accurate. For example, during pregnancy a woman's RBC mass is normal but because of an increase in blood volume the hemoglobin and hematocrit are diluted and thus decreased. Another example would be bleeding where the RBC mass would decrease but the concentrations of hemoglobin and hematocrit initially remains normal until fluids shift from other areas of the body to the intravascular space.

The anemia is also classified by severity into mild (110 g/L to normal), moderate (80 g/L to 110 g/L), and severe anemia (less than 80 g/L) in adult males and adult non pregnant females.[37] Different values are used in pregnancy and children.[37]

Testing
Anemia is typically diagnosed on a complete blood count. Apart from reporting the number of red blood cells and the hemoglobin level, the automatic 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 it is sometimes a necessity in regions of the world where automated analysis is less accessible.[medical citation needed]

In modern counters, four parameters (RBC count, hemoglobin concentration, MCV and RDW) are measured, allowing others (hematocrit, MCH and MCHC) to be calculated, and compared to values adjusted for age and sex. Some counters estimate hematocrit from direct measurements.[medical citation needed]
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, such as: ESR, ferritin, serum iron, transferrin, RBC folate level, serum vitamin B12, hemoglobin electrophoresis, renal function tests (e.g. serum creatinine) although the tests will depend on the clinical hypothesis that is being investigated. When the diagnosis remains difficult, a bone marrow examination allows direct examination of the precursors to red cells, although is rarely used as is painful, invasive and is hence reserved for cases where severe pathology needs to be determined or excluded.

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 (80–100 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. Limitations of MCV include cases where the underlying cause is due to a combination of factors – such as iron deficiency (a cause of microcytosis) and vitamin B12 deficiency (a cause of macrocytosis) where the net result can be normocytic cells.

Production vs. destruction or loss
The "kinetic" approach to anemia yields arguably 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 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.[medical citation needed] The following is a simplified schematic of this approach.

* For instance, sickle cell anemia with superimposed iron deficiency; chronic gastric bleeding with B12 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.

Information about Anemia

  Image result for information about anaemia


Anemia is a decrease in the total amount of red blood cells (RBCs) or hemoglobin in the blood,[3][4] or a lowered ability of the blood to carry oxygen.[5] When anemia comes on slowly, the symptoms are often vague and may include feeling tired, weakness, shortness of breath or a poor ability to exercise.[1] Anemia that comes on quickly often has greater symptoms, which may include confusion, feeling like one is going to pass out, loss of consciousness, or increased thirst.[1] Anemia must be significant before a person becomes noticeably pale.[1] Additional symptoms may occur depending on the underlying cause.[1]

The three main types of anemia are due to blood loss, decreased red blood cell production, and increased red blood cell breakdown.[1] Causes of blood loss include trauma and gastrointestinal bleeding, among others.[1] Causes of decreased production include iron deficiency, a lack of vitamin B12, thalassemia, and a number of neoplasms of the bone marrow.[1] Causes of increased breakdown include a number of genetic conditions such as sickle cell anemia, infections like malaria, and certain autoimmune diseases.[1] It can also be classified based on the size of red blood cells and amount of hemoglobin in each cell.[1] If the cells are small, it is microcytic anemia.[1] If they are large, it is macrocytic anemia while if they are normal sized, it is normocytic anemia.[1] Diagnosis in men is based on a hemoglobin of less than 130 to 140 g/L (13 to 14 g/dL), while in women, it must be less than 120 to 130 g/L (12 to 13 g/dL).[1][6] Further testing is then required to determine the cause.[1]

Certain groups of individuals, such as pregnant women, benefit from the use of iron pills for prevention.[1][7] Dietary supplementation, without determining the specific cause, is not recommended.[1] The use of blood transfusions is typically based on a person's signs and symptoms.[1] In those without symptoms, they are not recommended unless hemoglobin levels are less than 60 to 80 g/L (6 to 8 g/dL).[1][8] These recommendations may also apply to some people with acute bleeding.[1] Erythropoiesis-stimulating medications are only recommended in those with severe anemia.[8]

Anemia is the most common blood disorder, affecting about a third of the global population.[2][1] Iron-deficiency anemia affects nearly 1 billion people.[9] In 2013, anemia due to iron deficiency resulted in about 183,000 deaths – down from 213,000 deaths in 1990.[10] It is more common in women than men,[9] during pregnancy, and in children and the elderly.[1] Anemia increases costs of medical care and lowers a person's productivity through a decreased ability to work.[6] The name is derived from Ancient Greek: ἀναιμία anaimia, meaning "lack of blood", from ἀν- an-, "not" and αἷμα haima, "blood".[11]

Main symptoms that may appear in anemia[12]

The hand of a person with severe anemia (on the left) compared to one without (on the right)
Anemia goes undetected in many people and symptoms can be minor. The symptoms can be related to an underlying cause or the anemia itself. Most commonly, people with anemia report feelings of weakness or fatigue, and sometimes poor concentration. They may also report 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 pre-existing heart disease is present), intermittent claudication of the legs, and symptoms of heart failure. On examination, the signs exhibited may include pallor (pale skin, lining mucosa, conjunctiva 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 cardiac ventricular hypertrophy (enlargement). There may be signs of heart failure. Pica, the consumption of non-food items such as ice, but also paper, wax, or grass, and even hair or dirt, 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 academic performance in children of school age. Restless legs syndrome is more common in those with iron-deficiency anemia.[13]

Causes

Figure shows normal red blood cells flowing freely in a blood vessel. The inset image shows a cross-section of a normal red blood cell with normal hemoglobin.[14]
The 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 does not cause any lasting symptoms unless a relatively impaired RBC production develops, in turn most commonly by iron deficiency.[15] (See Iron deficiency anemia)

Impaired production
Disturbance of proliferation and differentiation of stem cells
Pure red cell aplasia[16]
Aplastic anemia[16] affects all kinds of blood cells. Fanconi anemia is a hereditary disorder or defect featuring aplastic anemia and various other abnormalities.
Anemia of renal failure[16] by insufficient erythropoietin production
Anemia of endocrine disorders[medical citation needed]
Disturbance of proliferation and maturation of erythroblasts
Pernicious anemia[16] is a form of megaloblastic anemia due to vitamin B12 deficiency dependent on impaired absorption of vitamin B12. Lack of dietary B12 causes non-pernicious megaloblastic anemia
Anemia of folic acid deficiency,[16] as with vitamin B12, causes megaloblastic anemia
Anemia of prematurity, by diminished erythropoietin response to declining hematocrit levels, combined with blood loss from laboratory testing, generally occurs in premature infants at two to six weeks of age.
Iron deficiency anemia, resulting in deficient heme synthesis[16]
Thalassemias, causing deficient globin synthesis[16]
Congenital dyserythropoietic anemias, causing ineffective erythropoiesis
Anemia of renal failure[16] (also causing stem cell dysfunction)
Other mechanisms of impaired RBC production
Myelophthisic anemia[16] 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[16]
anemia of chronic inflammation[16]
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 lactate dehydrogenase levels.[medical citation needed]

Intrinsic (intracorpuscular) abnormalities[16] cause premature destruction. All of these, except paroxysmal nocturnal hemoglobinuria, are hereditary genetic disorders.[17]
Hereditary spherocytosis[16] 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[16] is another defect in membrane skeleton proteins.
Abetalipoproteinemia,[16] causing defects in membrane lipids
Enzyme deficiencies
Pyruvate kinase and hexokinase deficiencies,[16] causing defect glycolysis
Glucose-6-phosphate dehydrogenase deficiency and glutathione synthetase deficiency,[16] causing increased oxidative stress
Hemoglobinopathies
Sickle cell anemia[16]
Hemoglobinopathies causing unstable hemoglobins[16]
Paroxysmal nocturnal hemoglobinuria[16]
Extrinsic (extracorpuscular) abnormalities
Antibody-mediated
Warm autoimmune hemolytic anemia is caused by autoimmune attack against red blood cells, primarily by IgG. It is the most common of the autoimmune hemolytic diseases.[18] 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.[19][19]
Cold agglutinin hemolytic anemia is primarily mediated by IgM. It can be idiopathic[20] or result from an underlying condition.
Rh disease,[16] one of the causes of hemolytic disease of the newborn
Transfusion reaction to blood transfusions[16]
Mechanical trauma to red blood cells
Microangiopathic hemolytic anemias, including thrombotic thrombocytopenic purpura and disseminated intravascular coagulation[16]
Infections, including malaria[16]
Heart surgery[medical citation needed]
Haemodialysis[medical citation needed]
Blood loss
Anemia of prematurity from frequent blood sampling for laboratory testing, combined with insufficient RBC production
Trauma[16] or surgery, causing acute blood loss
Gastrointestinal tract lesions,[16] causing either acute bleeds (e.g. variceal lesions, peptic ulcers) or chronic blood loss (e.g. angiodysplasia)
Gynecologic disturbances,[16] also generally causing chronic blood loss
From menstruation, mostly among young women or older women who have fibroids
Infection by intestinal nematodes feeding on blood, such as hookworms[21] and the whipworm Trichuris trichiura.[22]
The roots of the words anemia and ischemia both refer to the basic idea of "lack of blood", but anemia and ischemia are not the same thing in modern medical terminology. The word anemia used alone implies widespread effects from blood that either is too scarce (e.g., blood loss) or is dysfunctional in its oxygen-supplying ability (due to whatever type of hemoglobin or erythrocyte problem). In contrast, the word ischemia refers solely to the lack of blood (poor perfusion). Thus ischemia in a body part can cause localized anemic effects within those tissues.

Fluid overload
General causes of hypervolemia include excessive sodium or fluid intake, sodium or water retention and fluid shift into the intravascular space.[23]
Intestinal inflammation
Certain gastrointestinal disorders can cause anemia. The mechanisms involved are multifactorial and not limited to malabsorption but mainly related to chronic intestinal inflammation, which causes dysregulation of hepcidin that leads to decreased access of iron to the circulation.[24][25][26]

Helicobacter pylori infection.[27]
Gluten-related disorders: untreated celiac disease[27][26] and non-celiac gluten sensitivity.[28] Anemia can be the only manifestation of celiac disease, in absence of gastrointestinal or any other symptoms.[29]
Inflammatory bowel disease.[30][31]

Definitions
There are a number of definitions of anemia; reviews provide comparison and contrast of them.[32] A strict but broad definition is an absolute decrease in red blood cell mass,[33] however, a broader definition is a lowered ability of the blood to carry oxygen.[5] An operational definition is a decrease in whole-blood hemoglobin concentration of more than 2 standard deviations below the mean of an age- and sex-matched reference range.[34]

It is difficult to directly measure RBC mass,[35] so the hematocrit (amount of RBCs) or the hemoglobin (Hb) in the blood are often used instead to indirectly estimate the value.[36] Hemotocrit; however, is concentration dependent and is therefore not completely accurate. For example, during pregnancy a woman's RBC mass is normal but because of an increase in blood volume the hemoglobin and hematocrit are diluted and thus decreased. Another example would be bleeding where the RBC mass would decrease but the concentrations of hemoglobin and hematocrit initially remains normal until fluids shift from other areas of the body to the intravascular space.

The anemia is also classified by severity into mild (110 g/L to normal), moderate (80 g/L to 110 g/L), and severe anemia (less than 80 g/L) in adult males and adult non pregnant females.[37] Different values are used in pregnancy and children.[37]

Testing
Anemia is typically diagnosed on a complete blood count. Apart from reporting the number of red blood cells and the hemoglobin level, the automatic 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 it is sometimes a necessity in regions of the world where automated analysis is less accessible.[medical citation needed]

In modern counters, four parameters (RBC count, hemoglobin concentration, MCV and RDW) are measured, allowing others (hematocrit, MCH and MCHC) to be calculated, and compared to values adjusted for age and sex. Some counters estimate hematocrit from direct measurements.[medical citation needed]
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, such as: ESR, ferritin, serum iron, transferrin, RBC folate level, serum vitamin B12, hemoglobin electrophoresis, renal function tests (e.g. serum creatinine) although the tests will depend on the clinical hypothesis that is being investigated. When the diagnosis remains difficult, a bone marrow examination allows direct examination of the precursors to red cells, although is rarely used as is painful, invasive and is hence reserved for cases where severe pathology needs to be determined or excluded.

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 (80–100 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. Limitations of MCV include cases where the underlying cause is due to a combination of factors – such as iron deficiency (a cause of microcytosis) and vitamin B12 deficiency (a cause of macrocytosis) where the net result can be normocytic cells.

Production vs. destruction or loss
The "kinetic" approach to anemia yields arguably 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 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.[medical citation needed] The following is a simplified schematic of this approach.

* For instance, sickle cell anemia with superimposed iron deficiency; chronic gastric bleeding with B12 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.

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