Anemia is a blood disorder characterized by abnormally low levels of
healthy red blood cells (RBCs) or reduced hemoglobin (Hgb), the
iron-bearing protein in red blood cells that delivers oxygen to tissues
throughout the body. Reduced blood cell volume (hematocrit) is also
considered anemia. The reduction of any or all of the three blood
parameters reduces the oxygen-carrying capability of the blood, causing
reduced oxygenation of body tissues, a condition called hypoxia.
All tissues in the human body need a regular supply of oxygen to stay
healthy and perform their functions. RBCs contain Hgb, a protein pigment
that allows the cells to carry oxygen (oxygenate) tissues throughout the
body. RBCs live about 120 days and are normally replaced in an orderly way
by the bone marrow, spleen, and liver. As RBCs break down, they release
Hgb into the blood stream, which is normally filtered out by the kidneys
and excreted. The iron released from the RBCs is returned to the bone
marrow to help create new cells. Anemia develops when either blood loss, a
slow-down in the production of new RBCs (erythropoiesis), or an increase
in red cell destruction (hemolysis) causes significant reductions in RBCs,
Hgb, iron levels, and the essential delivery of oxygen to body tissues.
Anemia can be mild, moderate, or severe enough to lead to life-threatening
complications. More than 400 different types of anemia have been
identified. Many of them are rare. Most are caused by ongoing or sudden
blood loss. Other causes include vitamin and mineral deficiencies,
inherited conditions, and certain diseases that affect red cell production
Anemia in newborn infants is noted when hemoglobin levels are lower than
expected for the birth weight and postnatal age. Premature or low
birth-weight infants may have lower hemoglobin levels. The normal newborn
Hgb is 16.8 dL, which may be 1 to 2 dL lower if birth weight is abnormally
low. Anemia may be the first sign of certain disorders in the newborn,
such as blood loss that has occurred from transplacental hemorrhage, a
condition in which the infant's blood bleeds back into the
mother's circulation; bleeding from ruptures in the liver, spleen,
adrenals, or kidneys; or hemorrhage within the brain (intracranial
hemorrhage). Anemia can also be caused by the destruction of red blood
cells or reduced red blood cell production. Newborns may also have low red
blood cell volume (hematocrit or Hct) if they were born by
. It must be noted, however, that hemoglobin decreases naturally
(physiologic decrease) in infants by eight to 12 weeks of age, leveling at
a normal value of 11 g/dL or better.
Iron deficiency anemia
is the most common form of anemia worldwide. In the United States, it
affects thousands of toddlers between one and two years of age and more
than 3 million women of childbearing age. This condition is less common in
older children and in adults over 50 and rarely occurs in teenage boys and
The onset of iron deficiency anemia is gradual and may not have early
symptoms. The deficiency begins when the body loses more iron than it
derives from food and other sources. Because depleted iron stores cannot
meet the red blood cell's needs, fewer red blood cells develop. In
this early stage of anemia, the red blood cells look normal, but they are
reduced in number. Then the body tries to compensate for the iron
deficiency by producing more red blood cells, which are characteristically
small in size (spherocytosis). Symptoms of anemia, especially weakness and
fatigue, develop at this stage. Individuals may be given iron preparations
by injection or advised to take oral iron supplements. It sometimes helps
to take vitamin C along with oral iron supplementation to encourage better
absorption of the iron. Taking iron supplements can result in
, cramps, or
deficiency anemia is the most common type of megaloblastic anemia,
arising from a problem with the synthesis of deoxyribonucleic acid (DNA)
within the cells of the body. It is characterized by RBCs that are larger
than normal and is caused by a deficiency of folic acid, a vitamin that
the body needs to produce normal cells and normal DNA.
Folic acid anemia is especially common in infants and teenagers. This
condition usually results from a dietary deficiency but may also be due to
an inability to absorb (malabsorption) folic acid. Folic acid is available
in many foods, such as cheese, eggs, fish, green vegetables, meat, milk,
mushrooms, and yeast.
raises the risk of developing this condition by interfering with the
absorption of vitamin C, which the body needs to absorb folic acid. Folic
acid anemia can be a complication of pregnancy, when a woman's body
needs eight times more folic acid than it does otherwise. Folic acid
deficiency in pregnant women may lead to birth defects in their children.
Supplementation of folic acid is recommended during pregnancy.
Less common in the United States than folic acid anemia, vitamin B
deficiency anemia is another type of megaloblastic anemia that develops
when the body does not absorb enough of this nutrient. Necessary for the
creation of healthy RBCs, B
is found in meat, eggs, whole grains, and most vegetables. Large amounts
are stored in the body, so this condition may not become apparent until
up to four years after B
absorption stops or slows down. The resulting drop in RBC production can
cause loss of muscle control; loss of sensation in the legs, hands, and
feet; soreness, slickness, or burning of the tongue; weight loss; or
. Confusion, depression, and memory loss may also be associated with the
Pernicious anemia is the most common form of B
deficiency. Since most people who eat meat or eggs get enough B
in their diets, a deficiency of this vitamin usually means that the body
is not absorbing it properly. This condition can be found in those who do
not produce adequate amounts of a chemical secreted by the stomach lining
that combines with B
to help its absorption in the small intestine. Pernicious anemia is
diagnosed more often in adults between ages 50 and 60 than in children or
young people, although there is the possibility of inheriting the
condition, with symptoms not appearing until later in life.
Anemia due to vitamin C deficiency is a rare disorder that causes the bone
marrow to manufacture abnormally small red blood cells. Vitamin C
deficiency anemia results from a severe, long-standing dietary deficiency
or malabsorption of this essential vitamin. It is usually easily corrected
Hemolytic anemia can be present at birth (congenital hemolytic anemia or
spherocytosis) or acquired later in life. It is the result of either
infection or the presence of antibodies that destroy RBCs more rapidly
than bone marrow can replace them. Hemolytic anemia can enlarge the
spleen, an organ that also produces red blood cells when necessary.
Production of cells by the spleen will increase to meet the demands of
accelerated RBC destruction (hemolysis). Complications of hemolytic anemia
in older children or adults include
, gallstones, and other serious health problems.
Hemolytic disease of the newborn is a specific variation of hemolytic
anemia in which an incompatibility exists between antigens on the cells of
the mother and baby, causing antibodies to develop in the mother's
circulation. The antibodies are produced as an immune response to what the
body views as foreign antigens on the surface of the infant's RBCs.
Several specific antigens
are responsible for the incompatibilities: Rh type incompatibility, ABO
blood group incompatibility, and other incompatibilities involving
antigens known as Kell, Duffy, M, N, and P, among many others. Hemolytic
disease of the newborn and the anemia that results is detectable within
the first few days after birth. Depending on the strength of the antibody,
the anemia may clear up on its own or exchange transfusions may be
necessary to replace the newborn's blood.
An inherited form of hemolytic anemia,
comes from the production of abnormal hemoglobin. It is characterized by
low hemoglobin and unusually small and fragile RBCs (microcytosis),
although the RBC count may be normal. Thalassemia has several types that
involve imbalances in the four chains of amino acids that comprise
hemoglobin (alpha- and beta-globins). In thalassemia minor or thalassemia
trait (heterozygous thalassemia), also called alpha-thalassemia, there is
an imbalance in the production of the alpha chain of amino acids. In
thalassemia minor, fetal hemoglobin (HbF), the hemoglobin form that
circulates in the fetus, does not decrease normally after birth and may
remain high in later life. A child may inherit thalassemia trait when only
one parent has the genes responsible for it. It is usually not treated and
does not have serious consequences. Thalassemia major (homozygous
thalassemia or Cooley's anemia) occurs in children in whom both
parents pass on the genes responsible. It is known as beta-thalassemia,
because of an imbalance in the beta chain amino acids of hemoglobin. It
also involves the persistence of HbF with larger than normal amounts
appearing in the child's circulation. Alpha-thalassemias occur most
commonly in African Americans; beta-thalassemias most commonly affect
people of Mediterranean or middle-Eastern ancestry and Southeast Asians.
Hemoglobin H disease is another form of thalassemia in which three of the
four beta-globin genes are missing.
Sickle cell anemia
is an inherited, chronic, incurable blood disorder that causes the body
to produce defective hemoglobin, the abnormal HgbS, which occurs primarily
in African Americans. The condition is characterized by abnormal,
crescent-shaped RBCs. Unlike normal oval cells, fragile sickle cells
cannot hold enough hemoglobin to nourish body tissues. The deformed shape
makes it hard for sickle cells to pass through narrow blood vessels. When
capillaries become obstructed, a life-threatening condition called sickle
cell crisis is likely to occur. A child who inherits the sickle cell gene
from each parent will have the disease. A child who inherits the sickle
cell gene from only one parent carries the sickle cell trait but does not
have the disease.
Sometimes curable by bone marrow transplant, but potentially fatal,
aplastic anemia is characterized by decreased production of red and white
blood cells and platelets (disc-shaped cells that are a key component of
blood coagulation). This disorder may be inherited or acquired as a result
of the following:
, chronic infection or inflammation, and kidney and liver disease often
cause mild or moderate anemia. Chronic liver failure generally produces
the most severe symptoms because the production of RBCs is directly
Causes and symptoms
Anemias do not all stem from the same causes. Anemia can be the result of
injuries, chronic or acute illnesses, complications of surgery or
, metabolic disturbances or deficiencies, and adverse response to drug
therapy administered for other conditions. Causes may include sudden or
ongoing loss of blood, nutritional deficiencies, decreased red blood cell
production, or increased red blood cell destruction.
or malabsorption of nutrients can contribute to vitamin deficiency anemia
and iron deficiency anemias. Although red cell destruction and replacement
is an ongoing process in the body, hereditary disorders and certain
diseases can accelerate blood cell destruction, resulting in anemia.
However, excessive bleeding is the most common cause of severe anemia, and
the speed with which blood loss occurs has a significant effect on the
severity of symptoms. Chronic blood loss may be a consequence of the
Acute blood loss may occur as a result of injury, a ruptured blood vessel,
or a complication of surgery or childbirth. When a lot of blood is lost
within a short time, blood pressure and the amount of oxygen in the body
drop suddenly, sometimes leading to heart failure or death. Loss of even
one third of the body's blood volume in the space of several hours
can be fatal. Gradual blood loss is less threatening, because the body has
time to replace RBCs and blood volume.
Weakness, fatigue, and a run-down feeling may be the first signs of
anemia. Pasty or sallow skin color, or the absence of color in the gums,
nail beds, creases of the palm, or lining of the eyelids are other signs
of anemia. Individuals who appear to be weak, easily tired, often out of
breath, and who may feel faint or dizzy on movement may be severely
Other symptoms of anemia may include the following:
Acquired anemias affect about 4 million individuals in the United States,
and over 50 percent of these are under age 45, although less than 10
percent of cases occur in children and adolescents. In the United States,
iron deficiency anemia is the most prevalent type of anemia, affecting
about 240,000 toddlers between one and two years of age and 3.3 million
women of childbearing age. Anemia due to gradual blood loss is more common
in women than in men, particularly pregnant women or women of menstruating
age. Pernicious anemia is more common in women and in African Americans
and is less common in other racial groups. Folate deficiency is not common
in young people who eat an adequate diet and is usually associated with
malnutrition, pregnancy, and
. Sickle cell anemia is more frequently diagnosed than thalassemias and
occurs most often among African Americans. Thalassemia occurs in four out
of 100,000 individuals in the United States, particularly among those of
Mediterranean, Asian, or middle Eastern descent.
When a child exhibits weakness,
, listlessness, or fatigue, it may be the first sign of anemia. The
pediatrician should be consulted if the child is also extremely pale or
has little or no color in the gums, nail beds, creases of the palm, or
lining of the eyelids. Any prolonged bleeding or sudden blood loss
requires examination by a physician and testing for anemia.
The child's medical history will be taken, including the
child's age, symptoms, illnesses, and general state of health, and
history of ancestry and known inherited anemias will be noted. Symptoms
noticed in children by their parents may include fatigue, weight loss,
inability to concentrate, loss of appetite, and light-headedness when
standing up. The physical examination may reveal paleness, lack of color
in the creases of the palm, gums, and the linings of the eyelids. The
child's breathing rate may be increased and, in advanced cases, the
spleen or liver may be enlarged when palpated. If anemia is due to chronic
disease, there may be evidence of infection or inflammation. Urine output
may be reduced in severe anemia.
Diagnostic testing begins with a complete blood count (CBC) and
differential to reveal the RBC count, white blood cell (WBC) count,
hemoglobin (Hgb), and hematocrit (Hct); any of these counts can be
altered, and in most anemias the RBC and hemoglobin will be reduced. The
mean corpuscular volume (MCV) will be measured to compare the size of RBCs
with normal RBCs. A reticulocyte (young RBCs) count will help determine if
anemia is caused by impaired RBC production or increased RBC destruction.
Iron, vitamin C, vitamin B
, and folate levels will be measured to evaluate
and identify possible deficiencies. Diagnosing thalassemia and sickle
cell anemia, both of which involve disorders of hemoglobin, will require
measuring the different types of hemoglobin through a laboratory testing
method called hemoglobin electrophoresis. In some anemias, a bone marrow
sample will be removed (bone marrow biopsy) for microscopic examination,
especially to confirm iron deficiency anemia or the megaloblastic anemias.
Kidney function tests, coagulation tests, and stool examinations for
occult blood may also be performed.
Surgery may be necessary to correct blood losses caused by injury or
hemorrhage (nose bleeds, aneurysm, cerebral hemorrhage, bleeding ulcer) or
childbirth. Transfusions of packed red blood cells or whole blood may also
be used to replace blood volume and to stimulate the body's own
production of red blood cells. Medication or surgery may also be necessary
to control heavy menstrual flow or to remove polyps (growths or nodules)
from the bowels.
Anemia due to nutritional deficiencies can usually be treated with iron
replacement therapy, specific vitamin supplements, or self-administered
injections of vitamin B
. People with folic acid anemia may be advised to take oral folic acid.
deficiency anemia requires a life-long regimen of B
shots to maintain vitamin levels and control symptoms of pernicious
anemia. The patient may be advised to limit physical activity until
treatment restores strength and balance.
Anemia resulting from chronic disease is typically corrected by treating
the underlying illness. This type of anemia rarely becomes severe. If it
does, transfusions or hormone treatments to stimulate red blood cell
production may be given.
Thalassemia minor is typically not treated. Thalassemia major may be
treated with regular transfusions, surgical resection of the spleen to
avoid its removal of RBCs from circulation, and sometimes iron chelation
therapy. Symptoms are treated as they occur. Children or young adults with
thalassemia major may require periodic
to receive blood transfusions or, in some cases, bone marrow transplants.
Sickle cell anemia will be monitored by regular eye examinations and
diagnostic blood work. Immunizations for
and infectious diseases are part of treatment along with prompt treatment
for sickle cell crises and infections of any kind. Psychotherapy or
counseling may help older children deal with the emotional symptoms
characteristic of this condition.
Children with aplastic anemia are especially susceptible to infection.
Treatment for aplastic anemia may involve blood transfusions and bone
marrow transplantation to replace malfunctioning cells with healthy ones.
Hemolytic anemia of the warm-antibody type may be treated with large doses
of intravenous and oral corticocosteroids (cortisone). Individuals who do
not respond to medical therapy, may undergo surgery to remove the spleen,
which controls the anemia in some individuals by helping to add more RBCs
to the circulation. Immune-system suppressants are prescribed when surgery
is not successful. There is no specific treatment for cold-anti-body
Treatment of newborn anemia depends on the severity of symptoms, the level
of Hgb, and the presence of any other diseases that may affect oxygen
delivery, such as lung or heart disease or hyaline membrane disease.
Transfusions may be given in certain situations or exchange transfusions
if hemolytic disease of the newborn is not quickly resolved. The risk of
transfusion (such as transfusion reactions, potential toxins, and
infections such as HIV or hepatitis) are carefully weighed against the
severity of the anemia in the infant.
Vitamin C is noted for helping to absorb iron and folate supplements.
Cooking in a cast iron skillet may leach small amounts of absorbable iron
into the diet. Folic acid can be readily absorbed from raw salad greens
such as lettuce, spinach, arugula, alfalfa sprouts, and others. Blackstrap
molasses is a good source of iron and B
. Herbal supplements that will benefit individuals who have anemia include
bilberry, dandelion, goldenseal, mullein, nettle, Oregon grape root, red
raspberry, and yellow dock. Herbs are available as tinctures and teas or
The diet is a ready source of nutrients that prevent and treat anemia.
Children with anemia can include more of these nutrients in their diet by
eating a broad variety of whole grains, fruits and vegetables, beans, lean
meat, poultry and fish, and supplementing the diet regularly with
, and iron (as recommended). Pediatricians should be consulted before iron
supplements are taken, however, because of the difficulty in absorbing
non-food sources of iron. Vitamin C can stimulate iron absorption. Good
food sources of iron
include: almonds, broccoli, dried beans, raisins, dried apricots, seaweed
(as soup stock), whole-grain breads and cereals, brown rice, lean red
meat, liver, potatoes, poultry, and shellfish.
Because light and heat destroy folic acid, fruits and vegetables should be
eaten raw or cooked as little as possible to help assimilation of folic
acid. Folic acid can also be taken as a supplement.
Most anemias can be treated or managed. The prognosis for anemias
generally depends upon the severity of the anemia, the type of anemia, and
the response to treatment. The hereditary anemias, such as the
thalassemias and sickle cell anemia, may require life-long treatment and
monitoring whereas other types of anemia, once treated, are apt not to
recur. Thalassemia major may cause deformities and may shorten life
expectancy. Severe anemia may lead to other serious conditions,
particularly if oxygen delivery is compromised for long periods of time or
RBC destruction is more rapid than can be controlled by normal RBC
replacement or specific treatment. Severe blood loss or prolonged anemia
can result in life-threatening complications.
is the primary preventive measure for blood loss by injury. A wholesome,
balanced diet rich in nutrients can help prevent dietary deficiencies that
lead to anemia. Hereditary anemias cannot be prevented; parents can seek
genetic testing and counseling if they are concerned about inherited
anemias noted in their families or ethnic background.
Sources of iron such as liver, red meat, whole grains, and poultry may
help maintain hemoglobin levels and reduce the likelihood of
deficiency-related anemias. Vitamin C is noted for helping to improve
assimilation of iron taken as supplements.
—The process through which new red blood cells are created; it
begins in the bone marrow.
—A measure of the percentage of red blood cells in the total
volume of blood in the human body.
—An iron-containing pigment of red blood cells composed of four
amino acid chains (alpha, beta, gamma, delta) that delivers oxygen from
the lungs to the cells of the body and carries carbon dioxide from the
cells to the lungs.
—The process of breaking down of red blood cells. As the cells
are destroyed, hemoglobin, the component of red blood cells which
carries the oxygen, is liberated.
—A condition characterized by insufficient oxygen in the cells of
—A large erythroblast (a red marrow cell that synthesizes
—An early, immature form of a red blood cell. Over time, the
reticulocyte develops to become a mature, oxygen-carrying red blood
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Everything You Need to Know about Anemia.
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