(ă-nē′mē-ă )

[¹an- + -emia]
A reduction in the mass of circulating red blood cells. Patients are considered anemic when their hemoglobin levels are more than two standard deviations below the mean level in their hospital's laboratory. The diagnosis of anemia is influenced by variables such as the patient's age (neonates are anemic at levels of hemoglobin that would be considered polycythemic in some adults), gender (men have higher hemoglobin levels than women), pregnancy (hemodilution in pregnancy lowers measured hemoglobin), residential altitude, and ethnic or racial background.
anemic (ă-nē′mik), adj.
anemically (ă-nē′mi-k(ă-)lē), adv.
Symptomatic anemia exists when hemoglobin content is less than meets the oxygen-carrying demands of the body. If anemia develops slowly, there may be no functional impairment even though the hemoglobin is less than 7 g/100/dL of blood.

Anemia is not a disease but a symptom of other illnesses. It is classified on the basis of mean corpuscular volume as microcytic (80), normocytic (80-94), and macrocytic (>94); on the basis of mean corpuscular hemoglobin as hypochromic (27), normochromic (27-32), and hyperchromic (>32); and on the basis of etiological factors.

ETIOLOGY
Anemia may be caused by bleeding, e.g., from the gastrointestinal tract or the uterus; vitamin or mineral deficiencies, esp. vitamin B₁₂, folate, or iron; decreases in red blood cell production, e.g., bone marrow suppression in kidney failure or bone marrow failure in myelodysplastic syndromes; increases in red blood cell destruction as in hemolysis due to sickle cell anemia; or increases in red blood cell sequestration by the spleen (as in portal hypertension), or administration of toxic drugs (as in cancer chemotherapy).

SYMPTOMS
Anemic patients may experience weakness, fatigue, lightheadedness, breathlessness, palpitations, angina pectoris, and headache. Signs of anemia include a rapid pulse or rapid breathing if blood loss occurs rapidly. The chronically anemic may have paleness of the skin, mucous membranes, or nail beds and fissures at the corners of the mouth.

TREATMENT
Treatment of anemia must be specific for the cause. The prognosis for recovery from anemia is excellent if the underlying cause is treatable.

Anemia due to excessive blood loss: For acute blood loss, immediate measures should be taken to stop the bleeding, to restore blood volume by transfusion, and to combat shock. Chronic blood loss usually produces iron-deficiency anemia.

Anemia due to excessive blood cell destruction: The specific hemolytic disorder should be treated.

Anemia due to decreased blood cell formation: For deficiency states, replacement therapy is used to combat the specific deficiency, e.g., iron, vitamin B₁₂, folic acid, ascorbic acid. For bone marrow disorders, if anemia is due to a toxic state, removal of the toxic agent may result in spontaneous recovery.

Anemia due to renal failure, cancer chemotherapy, HIV, and other chronic diseases: Erythropoietin injections are helpful.

PATIENT CARE
The patient is evaluated for signs and symptoms; the results of laboratory studies are reviewed for evidence of inadequate erythropoiesis or premature erythrocyte destruction. Prescribed diagnostic studies are scheduled and carried out. Rest: The patient is evaluated for fatigue; care and activities are planned and regular rest periods are scheduled. Mouth care: The patient's mouth is inspected daily for glossitis, mouth lesions, or ulcers. A sponge stick is recommended for oral care, and alkaline mouthwashes are suggested if mouth ulcers are present. A dental consultation may be required. Diet: The patient is encouraged to eat small portions at frequent intervals. Mouth care is provided before meals. The nurse or a nutritionist provides counseling based on type of anemia. Medications: Health care professionals teach the patient about medication actions, desired effects, adverse reactions, and correct dosing and administration. Patient education: The cause of the anemia and the rationale for prescribed treatment are explained to the patient and family. Teaching should cover the prescribed rest and activity regimen, diet, and prevention of infection, including the need for frequent temperature checks, and the continuing need for periodic blood testing and medical evaluation.

achlorhydric anemia

A hypochromic, microcytic anemia associated with a lack of free hydrochloric acid in gastric juice.

aplastic anemia

Anemia caused by a severe decrease in the number of stem cells and/or white blood cell ancestors.
SYN: SEE: hypoplastic annemia

autoimmune hemolytic anemia

ABBR: AIHA Any of several anemias caused by antibodies produced by the patient's own immune system that destroy red blood cells. They are classified by the thermal properties of the antibody involved; the warm form is most common and may be associated with viral infections. Drug-induced hemolytic anemias are clinically indistinguishable from AIHA and are therefore classified with this disorder.
SYN: SEE: immunohemolytic anemia

anemia of chronic inflammation

SEE: Inflammatory anemia.

congenital hemolytic anemia

Any of a group of inherited chronic anemias marked by disintegration of red blood cells, jaundice, splenomegaly, and gallstones. Hereditary spherocytosis is the most common of these hemolytic diseases. Other such anemias include congenital elliptocytosis, hereditary stomatocytosis, and hemolytic anemias caused by enzymatic defects of the red cell, of which glucose-6-phosphate dehydrogenase and pyruvate kinase deficiency are the most important.
SYN: SEE: hemolytic icterus; SEE: hemolytic jaundice
SEE: glucose-6-phosphate dehydrogenase

congenital hypoplastic anemia

SEE: Diamond-Blackfan anemia.

Cooley anemia

SEE: Cooley anemia

deficiency anemia

Anemia due to lack of an essential ingredient such as iron or vitamins in the diet or the inability of the intestine to absorb them.
SYN: SEE: nutritional anemia

Diamond-Blackfan anemia

SEE: Diamond-Blackfan anemia

erythroblastic anemia

Anemia due to inheritance of a recessive trait responsible for interference with hemoglobin synthesis.
SYN: SEE: thalassemia major

folic acid deficiency anemia

Anemia due to a deficiency of folic acid. It is one cause of megaloblastic anemia. It is common in patients with nutritional deficiencies (such as alcoholics), patients who take medications (such as methotrexate) that block the synthesis of purines, and patients with malabsorption, and during hemolysis or pregnancy. Folate deficiency during pregnancy increases the risk of thrombocytopenia, hemorrhage, infection, and fetal neural tube defects.

PATIENT CARE
Fluid and electrolyte balance is monitored, particularly if the patient has severe diarrhea. The patient can obtain daily folic acid requirements by including an item from each food group in every meal; a list of foods rich in folic acid (green leafy vegetables, asparagus, broccoli, liver and other organ meats, milk, eggs, yeast, wheat germ, kidney beans, beef, potatoes, dried peas and beans, whole-grain cereals, nuts, bananas, cantaloupe, lemons, and strawberries) is provided. The rationale for replacement therapy is explained, and the patient is advised not to stop treatment until test results return to normal. Periods of rest and correct oral hygiene are encouraged.

hemolytic anemia

Anemia due to the destruction of erythrocytes by drugs, artificial heart valves, toxins, snake venom, infections, and antibodies. Drugs may either destroy the erythrocyte membrane directly or stimulate production of autoantibodies that lyse the erythrocytes. Children may develop hemolytic anemia in response to destruction of erythrocytes by viral and bacterial organisms. Artificial valves cause physical damage to the erythrocyte membrane during the circulation of blood through the heart.
SEE: hemolytic uremic syndrome

hyperchromic anemia

Anemia in which mean corpuscular hemoglobin concentration is higher than normal. The red blood cells are darker staining than normal.

hypochromic anemia

Anemia in which hemoglobin is deficient and mean corpuscular hemoglobin concentration is lower than normal.

hypoplastic anemia

SEE: 1. Aplastic anemiaSEE: 2. Pure red cell aplasia.

immunohemolytic anemia

SEE: Autoimmune hemolytic anemia.

anemia of inflammation

SEE: Inflammatory anemia.

inflammatory anemia

Anemia due to chronic disease.
SYN: SEE: anemia of chronic inflammation; SEE: anemia of inflammation

iron-deficiency anemia

ABBR: IDA Anemia due to a greater demand on stored iron supplies than can be provided. The erythrocyte count may sometimes be normal, but there is insufficient hemoglobin. Erythrocytes are hypochromic and show poikilocytosis. IDA is present in about 8% of men and 14% of women ages 3 to 74 years in the U.S.

ETIOLOGY
IDA is caused by inadequate iron intake, malabsorption of iron, blood loss, pregnancy and lactation, intravascular hemolysis, or a combination of these factors.

SYMPTOMS
Chronically anemic patients often complain of fatigue and dyspnea on exertion. Iron deficiency resulting from rapid bleeding may produce palpitations, orthostatic dizziness, or syncope.

DIAGNOSIS
Laboratory studies reveal decreased iron levels in the blood, with elevated iron-binding capacity and a diminished transferrin saturation. Ferritin levels are low. The bone marrow does not show stainable iron.

Serum levels of zinc protoporphyrin (ZPP) can be used to screen infants and toddlers for iron deficiency anemia. ZPP levels are an early marker of iron deficiency and may begin to rise even before anemia or neurological complications of iron deficiency develop. Elevated levels of ZPP are suggestive of the disease.

ADDITIONAL DIAGNOSTIC STUDIES
Adult nonmenstruating patients with IDA should be evaluated to rule out a source of bleeding in the gastrointestinal tract.

TREATMENT
Dietary iron intake is supplemented with oral ferrous sulfate or ferrous gluconate (with vitamin C to increase iron absorption). Oral liquid iron supplements should be given through a straw to prevent staining of the teeth. Iron preparations cause constipation; laxatives or stool softeners should be considered as concomitant treatment. When underlying lesions are found in the gastrointestinal tract, e.g., ulcers, esophagitis, or cancer of the colon, they are treated with medications, endoscopy, or surgery.

Parents should be warned to keep iron preparations away from children because three or four tablets may cause serious poisoning.

macrocytic anemia

Anemia marked by abnormally large erythrocytes.

Mediterranean anemia

SEE: thalassemia

megaloblastic anemia

Anemia in which megaloblasts are found in the blood.
SYN: SEE: Zuelzer-Ogden syndrome

microcytic anemia

Anemia marked by abnormally small red blood cells.
SEE: iron-deficiency anemia; SEE: thalassemia

milk anemia

In a young child, iron-deficiency anemia caused by consistent drinking of more than 1 qt. of milk a day. This excessive milk intake displaces iron-rich foods in the diet.

anemia of the newborn

Anemia marked by hemoglobin levels less than 14 g/dL in term newborns. Common causes include peripartum bleeding, hemolytic disease of the newborn, twin-to-twin transfusion (15% to 30% of all monochorionic twins with abnormalities of placental blood vessels), and impaired red cell manufacture caused by glucose-6-phosphate dehydrogenase deficiency.

normochromic anemia

Anemia in which the red blood cells contain the normal amount of hemoglobin.

normocytic anemia

Anemia in which the size and hemoglobin content of red blood cells remain normal. The mean corpuscular volume is 80 to 100 fL.

nutritional anemia

SEE: Deficiency anemia.

pernicious anemia

A chronic macrocytic anemia marked by achlorhydria. It occurs most often in 40- to 80-year-old northern Europeans with fair skin, but it has been reported in other races and ethnic groups. It is rare in Africans and Asians.

ETIOLOGY
Pernicious anemia is an autoimmune disease. The parietal cells of the stomach lining fail to secrete enough intrinsic factor to ensure intestinal absorption of vitamin B₁₂, the extrinsic factor. This is the result of atrophy of the glandular mucosa of the fundus of the stomach and is associated with absence of hydrochloric acid.

SYMPTOMS
Symptoms include weakness, sore tongue, paresthesias (tingling and numbness) of the extremities, and gastrointestinal symptoms such as diarrhea, nausea, vomiting, and pain; in severe anemia, there may be signs of cardiac failure.

TREATMENT
Vitamin B₁₂ is given parenterally or, in patients who respond, intranasally or orally.

physiological anemia of pregnancy

Pseudoanemia of pregnancy due to an increase of plasma that exceeds the production of red blood cells.
SEE: pseudoanemia of pregnancy

anemia of prematurity

Anemia that gradually develops in the first months of life in an infant born before the 37th week of gestation. It is caused by insufficient production of erythropoietin. Treatment may include red blood cell transfusions to increase iron stores and/or recombinant human erythropoietin.

runner's anemia

Mild hemolysis with hematuria, hemoglobinemia, and hemoglobinuria produced by strenuous exercise such as running. The anemia may be caused by the destruction of red blood cells during repeated striking of the ground by the runner’s feet, by plasma volume expansion, and by intestinal blood loss. Blood may be lost in the feces, presumably due to transient ischemia of the gut during vigorous exercise.

septic anemia

Anemia due to severe infection.

severe anemia

Hemoglobin of less than 6 g/dL.

sickle cell anemia

An autosomal recessive disorder that causes an abnormality of the globin genes in hemoglobin.

INCIDENCE
The frequency of the genetic defect responsible for this chronic anemia disorder is highest among African American, native African, and Mediterranean populations. The disease also affects people from the Caribbean and Central and South America. Approximately 100,000 people in the U.S. have sickle cell anemia. The illness affects 1 of every 400 African American babies. Roughly 8% of the African American population carries the sickle cell trait. Sickle cell anemia during pregnancy increases the risk of crisis, preeclampsia, urinary tract infection, congestive heart failure, and pulmonary infarction. Use of supplemental oxygen during labor is recommended.
SEE: hemoglobin S disease

GENETICS
Most people with sickle cell anemia have two copies of the sickle cell hemoglobin gene and are designated as having genotype HbSS. A smaller number of people have one HbS gene, and one beta-thalassemia gene. Carriers of the sickle cell trait have one normal hemoglobin A gene and one sickle cell gene (designated HbAS).

ETIOLOGY
When both parental genes carry the same defect, the person is homozygous for hemoglobin S, i.e., HbSS, and manifests the disorder. When exposed to a decrease in oxygen, hemoglobin S becomes viscous. This causes the red cells to become crescent-shaped (sickled), rigid, sticky, and fragile, increasing red-cell destruction (hemolysis). When sickled red blood cells clump together, circulation through the capillaries is impeded, causing obstruction, tissue hypoxia, and further sickling. In infants younger than 5 months old, high levels of fetal hemoglobin inhibit the reaction of the hemoglobin S molecule to decreased oxygen.

SYMPTOMS
The shortened life span of the abnormal red cells (10 to 20 days) results in a chronic anemia; pallor, weakness, and fatigue are common. Jaundice may result from hemolysis of red cells. Crisis may occur as a result of sickling, thrombi formation, vascular occlusion, tissue hypoxia, and infarction. People with sickle cell anemia are at increased risk of bacterial infections relative to the general population. Specific risks include osteomyelitis, meningitis, pneumonia, and sepsis from agents such as Streptococcus pneumoniae, Mycoplasma, and Chlamydia. Sickle cell patients with fever, cough, and/or regional pain should begin antibiotic therapy immediately after cultures for blood and urine and diagnostic x-rays are obtained. Sickle cell anemia also increases the risk for ischemic organ and tissue damage. Intensely painful episodes (crises) affecting the extremities, back, chest, and abdomen can last from hours to weeks and are the most frequent cause of hospitalization. Crises can be triggered by hypoxemia, infection, dehydration, and worsening anemia. Sickle cell crisis should be suspected in the sickle cell patient with pale lips, tongue, palms, or nail beds; lethargy; listlessness; difficulty awakening; irritability; severe pain; or temperature over 104°F (37.8°C) lasting at least 2 days. Life-threatening complications may arise from damage to specific internal organs, including splenic infarcts, myocardial infarction, acute chest syndrome, liver injury, aplastic anemia, and multiorgan dysfunction syndrome.
SEE: sickle cell crisis

TREATMENT
Supportive therapy includes supplemental iron and blood transfusion. Administration of hydroxyurea stimulates the production of hemoglobin F and decreases the need for blood transfusions and painful crises. Prophylactic daily doses of penicillin have demonstrated effectiveness in reducing the incidence of acute bacterial infections in children. Life-threatening complications require aggressive transfusion therapy or exchange transfusion, hydration, oxygen therapy, and the administration of high doses of pain relievers. Bone marrow transplantation, when a matched donor is available, can cure sickle cell anemia.

PATIENT CARE
During a crisis, patients are often admitted to the hospital to treat pain and stop the sickling process. Adequate pain control is vital. Morphine is the opioid of choice to manage pain because it has flexible dosing forms, proven effectiveness, and predictable side effects. It should be administered using patient-controlled analgesia, continuous low-dose intravenous infusions, or sustained-release pain relievers to maintain consistent blood levels. Supplemental short-acting analgesics may be needed for breakthrough pain. Side effects of narcotic pain relievers should be treated with concurrent administration of antihistamines, antiemetics, stool softeners, or laxatives. When administering pain relievers, care providers should assess pain using a visual analog scale to evaluate the effectiveness of the treatment. Other standard pain-reduction techniques, such as keeping patients warm, applying warm compresses to painful areas, and keeping patients properly positioned, relaxed, or distracted may be helpful. Patients and families are to be advised never to use cold applications for pain relief because this treatment aggravates sickling. If transfusions are required, packed red blood cells (leukocyte-depleted and matched for minor antigens) are administered, and the patient is monitored for transfusion reactions. Scheduled deep breathing exercises or incentive spirometry helps to prevent atelectasis, pneumonia, and acute chest syndrome. During remission, the patient can prevent some exacerbations with regular medical checkups; the use of medications such as hydroxyurea; consideration of bone marrow transplantation; avoiding hypoxia (as in aircraft or at high altitudes); excessive exercise; dehydration; vasoconstricting drugs; and exposure to severe cold. The child must avoid restrictive clothing, strenuous exercise, and body-contact sports but can still enjoy most activities. Additional fluid should be consumed in hot weather to help prevent dehydration. Patients and families should be advised to seek care at the onset of fevers or symptoms suggestive of infectious diseases. Annual influenza vaccination and periodic pneumococcal vaccination may prevent these common infectious diseases. Affected families should be referred for genetic counseling regarding risks to future children and for psychological counseling related to feelings of guilt. Screening of asymptomatic family members may determine whether some are heterozygous carriers of the sickling gene. Families affected by sickle cell anemia may gain considerable support in their communities or from national associations such as the American Sickle Cell Anemia Association, www.ascaa.org.

splenic anemia

Enlargement of the spleen due to portal or splenic hypertension with accompanying anemia, leukopenia, thrombocytopenia, and gastric hemorrhage.
SEE: Banti syndrome; SEE: congestive splenomegaly

transfusion-dependent anemia

Anemia for which the only effective therapy is repeated blood transfusions.
Iron overload may be a complication of therapy, esp. after the transfusion of over 10 units of blood.

warm autoimmune hemolytic anemia

ABBR: WAHA Red blood cell destruction caused by immunoglobulin G antibodies that react against red cell membranes at body temperature (“warm agglutinins”).