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ICD-10 D50-D64
ICD-9 280-285
OMIM [1]
DiseasesDB 663
MedlinePlus 000560
eMedicine med/132 emerg/808 emerg/734
MeSH {{{MeshNumber}}}

Anemia (AmE) or anæmia (BrE), from the Greek (Ἀναιμία) meaning "without blood", is a deficiency of red blood cells (RBCs) and/or hemoglobin. This results in a reduced ability of blood to transfer oxygen to the tissues, causing tissue hypoxia. Since all human cells depend on oxygen for survival, varying degrees of anemia can have a wide range of clinical consequences. Hemoglobin (the oxygen-carrying protein in the red blood cells) has to be present to ensure adequate oxygenation of all body tissues and organs. The three main classes of anemia include excessive blood loss (acutely such as a hemorrhage or chronically through low-volume loss), excessive blood cell destruction (hemolysis) or deficient red blood cell production (ineffective hematopoiesis). In menstruating women, dietary iron deficiency is a common cause of deficient red blood cell production.


There are two major approaches of classifying anemias, the "kinetic" approach which involves evaluating production, destruction and loss[2], and the "morphologic" approach which groups anemia by red blood cell size. The morphologic approach uses a quickly available and cheap lab test as its starting point (the MCV). On the other hand, focusing early on the question of production may allow the clinician more rapidly to expose cases where multiple causes of anemia coexist.

Signs and symptomsEdit

Anemia goes undetected in many people, and symptoms can be vague. Most commonly, people with anemia report a feeling of weakness or fatigue, general malaise and sometimes poor concentration. People with more severe anemia often report dyspnea (shortness of breath) on exertion. Very severe anemia prompts the body to compensate by increasing cardiac output, leading to palpitations and sweatiness, and to heart failure.


Pica is the consumption of non-food such as dirt, paper, wax, grass and hair. It is a rare but characteristic sign of iron deficiency anemia.



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. For adult men, a hemoglobin level less than 13.0 g/dl is diagnostic of anemia, and for adult women, the diagnostic threshold is below 12.0 g/dl.






Production vs. destruction or lossEdit

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 guiaic-positive stool, radiographic findings, or frank bleeding.

Here is a simplified schematic of this approach:

Reticulocyte production index shows inadequate production response to anemia.
No clinical findings consistent with hemolysis or blood loss: pure disorder of production.
Clinical findings and abnormal MCV: hemolysis or loss and chronic disorder of production*.
Macrocytic anemia (MCV>100)
Normocytic anemia (80<MCV<100)
Microcytic anemia (MCV<80)


Red blood cell sizeEdit



Macrocytic anemia (MCV>100)
Normocytic anemia (80<MCV<100)
Microcytic anemia (MCV<80)
High reticulocyte count
Low reticulocyte count


Microcytic anemiaEdit

    • Iron deficiency anemia is caused by insufficient dietary intake or absorption of iron to replace losses from menstruation or losses due to diseases.[3] 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. Iron deficiency is the most prevalent deficiency state on a worldwide basis. Iron found in animal meats are more easily absorbed by the body than iron found in non-meat sources. In countries where animal meats are only occasionally available in the diet, iron deficiency anemia is six to eight times more prevalent than in North America and Europe. Iron deficiency is sometimes the cause of abnormal fissuring of the angular (corner) sections of the lips (angular cheilitis).
    • Iron deficiency anemia can also 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).[4]
  • Hemoglobinopathies - much rarer (apart from communities where these conditions are prevalent)
    • Hb S Sickle-cell disease
    • Hb C
    • Hb E
    • Hb D-Punjab
    • Hb O-Arab
    • Hb G-Philadelphia
    • Hb Hasharon
    • Hb Korle-Bu
    • Hb Lepore
    • Hb M


  • Heme synthesis defect
    • Iron deficiency, which may in turn be due to menstrual blood loss, or gastro-intestinal bleeding from benign (ulcers, gastritis) or malignant (colorectal cancer) causes.
    • Anemia of Chronic Disorders (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

A mnemonic commonly used to remember causes of microcytic anemia is TAILS: T - Thalassemia, A - Anemia of chronic disease, I - Iron deficiency anemia, L - Lead toxicity associated anemia, S - Sideroblastic anemia.

Normocytic anemiaEdit

Normocytic anaemia occurs when the overall Hb levels are decreased, but the red blood cell size (MCV) remains normal. Causes include:

Macrocytic anemiaEdit

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 (6-10 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 symptoms of vitamin B12 deficiency include neuropathy, in particular balance difficulties from posterior column spinal cord pathology,[5] and having a smooth, red tongue, (glossitis). The treatment for vitamin B12-deficient macrocytic and pernicious anemias 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 chemically isolate the curative substance and ultimately were able to isolate the vitamin B12 from the liver. All three shared the 1934 Nobel Prize in Medicine. [6]

Dimorphic anemiaEdit

When two 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 [7] 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.

Heinz body anemiaEdit

Heinz bodies are an abnormality that form on the cells in this condition. This form of anemia may be brought on by taking certain medications; it is also triggered in cats by eating onions.[8] or acetaminophen (Tylenol). It can be triggered in dogs by ingesting onions or zinc, and in horses by ingesting dry Red Maple leaves.

Specific anemiasEdit

Possible complicationsEdit

Anemia diminishes the capability of individuals who are affected to perform physical activities. This is a result of one's muscles being forced to depend on anaerobic metabolism. The lack of iron associated with anemia can cause many complications, including hypoxemia, brittle or rigid fingernails, cold intolerance, impaired immune function, and possible behavioral disturbances in children.

Hypoxemia resulting from anemia can worsen the cardio-pulmonary status of patients with pre-existing chronic pulmonary disease. Brittle or rigid fingernails may be a result of abnormal thinness of nails due to insufficient iron supply. Cold intolerance occurs in one in five patients with iron deficiency anemia, and becomes visible through numbness and tingling. Impaired immune functioning leading to increased likelihood of sickness is another possible complication.

Anemia during pregnancyEdit

Anemia affects 20% of all females of childbearing age in the United States. Because of the subtlety of the symptoms, women are often unaware that they have this disorder, as they attribute the symptoms to the stresses of their daily lives. Possible problems for the fetus include increased risk of growth retardation, prematurity, intrauterine death, rupture of the amnion and infection.

During pregnancy, women should be especially aware of the symptoms of anemia, as an adult female loses an average of two milligrams of iron daily. Therefore, she must intake a similar quantity of iron in order to make up for this loss. Additionally, a woman loses approximately 500 milligrams of iron with each pregnancy, compared to a loss of 4-100 milligrams of iron with each period. Possible consequences for the mother include cardiovascular symptoms, reduced physical and mental performance, reduced immune function, tiredness, reduced peripartal blood reserves and increased need for blood transfusion in the postpartum period.

Diet and anemiaEdit

Consumption of food rich in iron is essential to prevention of iron deficiency anemia.

The twenty richest sources of iron in descending order: Canned clams; Fortified dry cereals; Cooked oysters; Organ meats (liver, giblets); *Fortified instant cooked cereals; Soybeans, mature, cooked; Pumpkin and squash seed kernels, roasted; White beans; Blackstrap molasses, 1 Tbsp; Lentils, cooked; Spinach, cooked from fresh; Beef (chuck); Kidney beans; Sardines; Beef(rib); Chickpeas; Duck, meat only; Lamb shoulder; Prune juice.[9]

Certain foods have been found to interfere with iron absorption in the gastrointestinal tract, and these foods should be avoided in persons with established iron deficiency. They include tea, coffee, wheat bran, rhubarb, chocolate, chewing gum, red wine, and dairy products.[10]

Treatments for anemiaEdit


Iron deficiency from nutritional causes is rare in non-menstruating adults (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 iron supplementation with ferrous sulfate or ferrous gluconate. Vitamin C may aid in the body's ability to absorb iron.

Vitamin supplements given orally (folic acid) or subcutaneously vitamin b-12 will replace specific deficiencies.



Blood transfusions for anemiaEdit

Doctors attempt to avoid blood transfusion in general, but there are several instances where doctors are now more aggressive than in the past. For instance, the currently accepted Rivers protocol for early goal directed therapy for sepsis requires keeping the hematocrit above 30; this is based on evidence that even moderate anemia reduces survival [11]. The presumed physiological principle is that the reduction in oxygen delivery associated with anemia is especially dangerous to people who are already at risk for organ damage from lack of perfusion. There is controversy about what hematocrit or hemoglobin levels should be used as "triggers" for transfusion in other settings. Anemia also may be especially risky for people with acute coronary syndromes, again because anemia hampers already impaired oxygen delivery to the heart.[12] However, the point at which this danger emerges in other settings is controversial and awaits further study. [13]

Finally, 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. Behavioral disturbances may even surface as an attention deficit disorder.


See alsoEdit


External linksEdit


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