Pathophysiology of Anemia and Nursing Care Implications

By Coyer, Sharon M Lash, Ayhan Aytekin

Anemia is a decrease in erythrocyte mass or amount of hemoglobin from impaired production of erythrocytes, blood loss, or increased erythocyte destruction. The pathophysiology, clinical manifestations, and selected pathologies of anemia and their implications for nursing practice are reviewed. As many as 4 million Americans have anemia; women younger than age 65 have six times more anemia than men. Anemia is increasingly a health problem for older adults, especially men over age 85 (Goddard, McIntyre, & Scott, 2000). Anemia occurs when there is a decrease in red blood cell numbers or a decrease in the amount of hemoglobin (Gaspad, 2005; Hodges, Rainey, Lappin, & Maxwell, 2007; Kumar, Cotran, & Robbins, 2003). It is recognized most often when laboratory screening tests are done because individuals often do not present with the signs and symptoms of advanced anemia. Acute anemia usually is due to blood loss or hemolysis (Adamson & Longo, 2001). Gastrointestinal bleeding or bleeding from colon cancer can cause chronic blood loss that also produces anemia (Goddard et al., 2000). In this article, the pathophysiology of anemia, clinical manifestations, and selected diseases that cause anemia will be reviewed, and the implications for nursing practice discussed.


All blood cells are produced by hematopoiesis in the bone marrow. The major raw material essentials for this process are proteins, vitamin B12, folic acid, and iron. Table 1 shows the substances needed for hematopoiesis in this well-orchestrated cell function. Pathophysiology of anemia differs according to its etiology. Acute or chronic red blood cell loss, inadequate production of red blood cells in the bone marrow, or an increased hemolysis can produce anemia (Gaspad, 2005; Hodges et al., 2007). When anemia develops because of hemorrhage, the reduction in red blood cell numbers causes a decrease in blood volume and the cardiovascular (CV) system becomes hypovolemic. Anemia becomes evident when the maximum level of hemodilution occurs, usually within 3 days after the acute blood loss. Hemodilution occurs in response to decreased blood volume when fluid moves from the interstitium into the intravascular space to expand the plasma volume. The decrease in blood viscosity from the lower number of red blood cells, along with increased intravascular fluid, causes the blood to flow faster through the CV system and the flow becomes more turbulent. This process causes pressure on the ventricles, the heart dilates, and heart valve dysfunction develops (Metivier, Marchais, Guerin, Pannier, & London, 2000).

Hypoxia contributes to the changes in the CV and respiratory systems in anemia by causing the blood vessels to dilate and the heart to contract more forcefully, which further increases the demand for oxygen. Tissue hypoxia causes the rate and depth of breathing to increase. Hemoglobin, the oxygen-carrying protein in the red blood cells (RBCs), releases that oxygen to the tissues more rapidly. When anemia becomes severe, the body directs blood to the vital organs, such as the heart and the brain, and renal blood flow decreases. Decreased renal blood flow in turn causes an activation of the renin-angiotensin system response, leading to salt and water retention. This process increases blood volume to improve kidney function without changing tissue hypoxia in other organs (Gaspad, 2005; Metivier et al., 2000).

Hemolytic Anemia

The pathophysiology of hemolytic anemia involves the destruction of erthythrocytes and the subsequent acceleration of erythropoesis. Hemolytic anemia may be inherited or acquired. The inherited form occurs from cellular abnormalities in the membrane or the enzymes that influence the production of hemoglobin. Acquired hemolytic anemia occurs as a result of infection, chemical agents, and abnormal immune response. Hemolytic anemia produces hemolyis within the blood vessels or lymphoid tissue that filters blood. Immunohemolytic anemias are caused by extravascular hemolysis and associated with autoimmune mechanisms or drug reactions (Hodges et al., 2007; Mansen & McCance, 2006).


Classification by Morphology

Anemia can be classified by cell morphology or by etiology. Morphology, the most common classification, includes cell size (cystic), color (chromic), and shape of the RBCs. Measurements of hemoglobin, hematocrit, and red cell indices provide information about the appearance of the RBC, which aids in the classification. Red cell indices include the mean corpuscular volume, mean hemoglobin, mean corpuscular hemoglobin concentration (MCHC), and red blood cell distribution width (Hoekelman, Adam, Nelson, Weitzman, & Wilson, 2001). In addition, serum ferritin concentration is used to measure iron storage. Measuring ferritin concentration is important in obtaining the diagnosis of iron deficiency anemia. Another test, transferrin saturation, measures dietary iron absorption and transport. Transferrin is the protein to which iron is bound for transport from within the body (Lemone & Burke, 2004; Rote & McCance, 2008; Uphold & Graham, 2003).

Classification by Etiology

Anemia can be caused by impaired cell production, blood loss, and increased rate of destruction of the red cell. Blood loss occurs during acute conditions such as trauma, or chronic diseases and gastrointestinal bleeding. Increased rate of destruction of red cells occurs in hemolytic anemia resulting from conditions inside and outside the cell. Abnormalities within the red cell can result from hereditary or acquired disease. Sperocytosis and elliptocytosis are hereditary conditions causing anemia due to a disorder in the red cell membrane. Disorders in enzymes within the red cell, such as glucose-6-phosphate dehydrogenase and pyruvate synthesis diseases, also can cause anemia. Sickle cell anemia and thalessemia are genetically determined diseases in which RBCs have structural abnormalities (Kumar et. al., 2003).

Conditions existing outside the RBC include diseases of red cell destruction, such as blood transfusion reactions, hemolytic anemia, thrombocytopenia purpura, or disseminating intravascular coagulation. Cell production can become impaired when there is a disturbance in maturation and proliferation of red cells. Conditions in this category include reduced erythropoietin, aplastic anemia, bone marrow dysfunction, anemia from renal cell aplasia, and anemia from renal failure or endocrine disorders. Impaired cell production occurs when cells have defective DNA synthesis, such as in vitamin B12 and folic acid anemia. Defective hemoglobin synthesis is the pathologic process for iron deficiency anemia, thalessemia, and the anemia of chronic infections (Brill & Baumgardner, 2000; Kumar et al., 2003).


Macrocytic Anemias

Macrocytic anemia occurs when the bone marrow produces very large cells called macrocytes. These cells are large in size, thickness, and volume. In addition to being larger, they also have an altered pattern of chromatin deposits in the nucleus which helps distinguish them from normocytes. Hemoglobin increases in proportion to the size of the cell. The MCHC remains normal, producing normochromic cells (Dharmarajan, Adiga, & Norkus, 2003; Mansen & McCance, 2006). The premature death of these cells decreases their numbers in circulation, leading to the manifestations of anemia (Rote & McCance, 2008).

In terms of the etiology of macrocytic anemias, both folic acid and vitamin B12 are needed for normal hematopoiesis and maturation of all cells. Hence, vitamin B12 deficiencies, folate deficiencies, inborn errors of metabolism that inhibit folate absorption, and poor nutritional intake can cause malabsorption syndromes leading to macrocytic anemia (Dharmarajan et al., 2003; Hoekelman et al., 2001).

Pernicious anemia (vitamin B12 deficiency). Pernicious anemia is caused by vitamin B12 deficiency. The term pernicious (highly destructive) indicates the significant damage the disease produces and is a reminder that it most often was fatal in the past. Pernicious anemia occurs in 20%-30% of relatives of people with pernicious anemia. The disease usually is seen in individuals over age 30, but older adults also are at risk (Suzuki et al., 2004). Pernicious anemia develops when there is a lack of the intrinsic factor enzyme that is required for absorption of vitamin B12. Intrinsic factor and vitamin B12 complex are absorbed from the distal small intestines. Pernicious anemia can occur following surgical removal of parts of the stomach, or with gastric atrophy from chronic gastritis that causes decreased secretion of intrinsic factor. Autoimmune conditions, which are common in elders, also can produce pernicious anemia due to the production of antibodies against gastric parietal cells (Dharmarajan et al., 2003; Uphold & Graham, 2003).

Clinical manifestations of pernicious anemia are a result of the inflammation of the gastric submucosa and subsequent degeneration of parietal cells. The greater the loss of cells from the gastrointestinal tract, the greater will be the lack of vitamin B12. Pernicious anemia develops slowly over 20-30 years. Vague symptoms in the early stages of the disease include infections, mood swings, and gastrointestinal and kidney disease. The individual also may develop weakness and fatigue, parasthesias of feet and fingers, and difficulty walking when the anemia becomes severe. Damage to the posterior and lateral columns of the spinal cord cause neurologic symptoms, such as loss of position, loss of vibration sense, ataxia, spasticity, memory loss, and loss of appetite. Gastrointestinal symptoms in later stages of the disease include abdominal pain and a beefy red tongue. Individuals with pernicious anemia have yellow, pale skin and an enlarged liver that ultimately produces right-side heart failure. Their hemoglobin may be as low as 7 or 8 g/dL (Dharmarajan et al., 2003; Mansen & McCance, 2006; Uphold & Graham, 2003). Folate deficiency. Folate (folic acid) is a vitamin required for red cell production and maturation. Pregnant or lactating women require a higher folate level for possible prevention of neural tube defects in the fetus. Women capable of becoming pregnant should consume 400 ug from supplements or fortified foods. Folate is absorbed from the upper intestine and is stored in the liver. Alcoholism, dietary fads, and a lowvegetable diet can be precursors for folate deficiency. As may as 10% of Americans have folate deficiency (Fink, 2004; Uphold & Graham, 2003).

Clinical manifestations of folate deficiency are similar to pernicious anemia because malnourishment and anemia are the effects of this disease. Individuals with folate deficiency have stomatitis and ulcerations on the tongue. They may have dysphagia, flatulence, and watery diarrhea. The neurologic changes that are present with pernicious anemia are not evident with folate deficiency unless other vitamin deficiencies also exist in the diet (Gaspad, 2005; Mansen & McCance, 2006).

Microcytic Anemias

In microcytic hypochromic anemia, red cells are small and have a reduced amount of hemoglobin. Iron metabolism is essential for the development of the red cell.

Iron deficiency anemia, thalassemia, and sideroblastic anemia present with microcytic, hemochromic cells (Mansen & McCance, 2006; Uphold & Graham, 2003). Iron deficiency anemia. As the most common type of anemia in practice, iron deficiency occurs in 2%-5% of adult men and postmenopausal women. Most cases of iron deficiency anemia in adults result from failure to recapture iron in RBCs for hemoglobin synthesis (for example, chronic blood loss from gastrointestinal bleeding or colon cancer). Each milliliter of blood contains 0.5 mg of iron. Loss of 500 milliliters of blood creates a loss of 250 milliliters of iron, the equivalent of 25% of the body?s iron reserves. In iron deficiency anemia, the demands for iron may exceed iron intake. This occurs in rapid growth periods, such as pregnancy and adolescence, or during nutritional deprivation that may occur in older adults. Blood loss of 10-20 milliliters of red cells per day is greater than the amount of iron a person can absorb in the diet (Adamson & Longo, 2001).

Any increase in the demand for iron or decrease in iron intake can cause iron deficiency anemia. Clinical manifestations of iron deficiency anemia include fatigue, pallor, fissures at the corners of the mouth, spooning of fingernails, and reduced exercise tolerance. Diagnosis of iron deficiency anemia depends on laboratory evidence. Anemia is defined as hemoglobin less than 13 g/dL for men and less than 12 g/dL for women on at least one laboratory assessment (Ioannou, Spector, Scott, & Rockey, 2002).

Thalassemias and sideroblastic anemia. The thalassemias are a group of disorders caused by an imbalance between the beta-chain and alpha-chain of the hemoglobin molecule. When one beta-chain is reduced, a mild form of anemia called beta-thalassemia occurs. Defects in both beta-chains result in a severe anemia called thalassemia major or Cooley?s anemia. The clinical features of maxillary hyperplasia and prominence of the frontal bones of the face occur in this type of anemia. This expansion of the marrow of the facial bones and skull produces facial overgrowth known as bossing. Alpha thalassemia is caused by a defect in two of the alpha genes and produces a mild anemia similar to beta-thalassemia. Thalassemia is found most often in Black, Mediterranean, and Southeast Asian ethnic groups (Segal, 2004).

Sideroblastic anemia is either acquired or hereditary. The acquired form is most common; it usually has no known etiology but may be associated with other conditions, such as alcoholism, drug reactions, copper deficiency, or hypothermia. Hereditary sources of sideroblastic anemia that occur from an X-linked transmission pattern only affect males. Females have hereditary sideroblastic anemia from autosomal transmission. Sideroblastic anemia may be present in childhood but it is most common is midlife (Mansen & McCance, 2006).

Clinical manifestations of sideroblastic leukemia are similar to other anemias, but affected individuals also have signs of iron overload. Enlargement of the spleen and liver occur. Individuals with sideroblastic anemia occasionally have a bronze-colored skin tone. Neurologic impairment does not occur in this type of anemia, but the cardiopulmonary systems are taxed from heart rhythm disturbance and congestive heart failure (Mansen & McCance, 2006).

Normocytic Anemias

Normocytic anemias are characterized by cells of normal size with normal hemoglobin content. The anemia occurs because the number of red cells is low. Normocytic anemias are less common than macrocytic or microcytic anemia. Several diseases result in normocytic anemia, including aplastic anemia, acute blood loss, hemolytic anemia, and anemia of chronic disease (Gaspad, 2005; Young, Calado, & Scheinberg, 2006).

Aplastic anemia. Aplastic anemia, also known as hypoplastic anemia, produces a decline in blood cell production due to bone marrow depression. Panocytopenia also may occur in this type of anemia, resulting in the absence of all three types of blood cells. The rate of decline in the bone marrow production of blood cells is slower for red cells than other types of cells, so the appearance of this anemia in adults is similar to a chronic anemia pattern. Aplastic anemia occurs rarely, but it is increasing in developing countries. Aplastic anemia can be either hereditary or acquired after birth. The most common hereditary form of aplastic anemia is called Fanconi anemia. It results from defects in DNA repair. Acquired aplastic anemia also occurs secondary to another disease, such as reactions to benzene, arsenic, chloramphenicol (Chloromycetin?), phenytoin (Dilantin ?), and antimetabolite chemotherapeutic drugs (6-mercaptopurine, vincristine, and busulfan). Ionizing radiation can cause secondary aplastic anemia (Gaspad, 2005; Young et al., 2006).

The clinical manifestations of aplastic anemia may develop slowly depending on which cells in the bone marrow are damaged and how fast the damage occurs. If there is a rapid onset of aplastic anemia, clinical manifestations include hypoxia, pallor, weakness, fever, and dyspnea. The slower progression of the disease produces clinical manifestations of progressive weakness, susceptibility to infection, low-grade fever, cellulitis in the neck, and ulceration and hemorrhaging in the nose, mouth, and gastrointestinal tract. The individual may develop waxy and pale skin tones. An individual with aplastic anemia has an extremely low hemoglobin of approximately 7 g/ dL. White cell and platelet numbers will be low due to alterations of manufacturing and production in the bone marrow (Gaspad, 2005; Young et al., 2006).

Acute blood loss. Acute blood loss can result in normocytic, normochromic red cell appearance. As much as 1,500 to 2,000 milliliters of blood can be lost without causing symptoms when the individual is prone, but light headedness is experienced when standing. Chronic bleeding produces fewer, less intense symptoms. Acute and chronic blood loss are treated by restoring blood volume with saline, dextran, albumin, or plasma (Adamson & Longo, 2001; Mansen & McCance, 2006).

Hemolytic anemias.Warm antibody hemolytic anemia is the most common type of immunohemolytic anemia and affects females over age 40. The mediating antibody for this process is immunoglobulin that attacks the RBCs. Warm antibody hemolytic anemia usually is idiopathic but also may be due to other conditions, such as lymphomas, leukemias, and other neoplastic disorders in about 50% of affected individuals. Other conditions associated with warm antibody hemolytic anemia are systemic lupus erythematosis or exposure to one or more drugs, such as a- Methyldopa (Aldomet?), penicillin (Bicillin?), and quinidine (Novoquinidin ?) (Adamson & Longo, 2001; Gaspad, 2005).

Cold agglutin immune hemolytic anemia is a less common condition mediated by immunoglobulin. This type of anemia occurs in cooler temperatures, with clinical manifestations similar to Raynaud?s disease. Cold agglutin anemia results from vascular obstruction rather than hemolysis. Diseases associated with development of cold agglutin anemia are mycoplasma pneumonia, lymphoid malignancies, Epstein Barr virus, cytomegalovirus infection, mumps, and Legionnaires disease (Mansen & McCance, 2006). Cold hemolysis hemolytic anemia is a rare disorder that causes massive hemolyis after exposure to cold temperatures. It is associated with several diseases, such as mycoplasma pneumonia, measles, mumps, nonspecific flu, and other viral syndromes. Syphilis causes a chronic type of this disease (Mansen & McCance, 2006).

The clinical manifestations of hemolytic anemia vary widely. The severe form of the disease usually is diagnosed at birth or within the first year of life. Mild-tomoderate disease is more common. There may be no symptoms unless there are other complications. Jaundice is a frequent symptom. An aplastic crisis can occur when the bone marrow and cell production fail. Papavirus B19 infection is a common cause of aplastic crisis and splenomegaly frequently occurs because the spleen becomes markedly enlarged from the breakdown of cells. Enlarged spleens become fragile and vulnerable to trauma (Gaspad, 2005; Mansen & McCance, 2006). Anemia of chronic illness. Anemia can occur when individuals have a chronic disease, though the cause is uncertain (Uphold & Graham, 2003). Chronic anemia usually is mild to moderate. Diseases that produce a chronic form of anemia include acquired immunodeficiency disease, chronic inflammatory bowel conditions, chronic renal failure, rheumatoid arthritis, systemic lupus erythematosus, acute and chronic hepatitis, and malignancies. This type of anemia develops 1-2 months after the beginning of the chronic disease. It produces normocytic and normochromatic red cells, but they also may be microcytic and hypochromic if the chronic disease produces iron deficiency (Thomas, 2004; Uphold & Graham, 2003).

The anemia of chronic illness produces a red cell with a decreased life span. In addition, the bone marrow does not respond by increasing red cell production. Altered iron metabolism also is possible. Impaired iron metabolism is impacted by lactoferrin and apoferrritin, which are present in the blood in small amounts. When infection or inflammation is present, neutrophils release lactoferrin or apoferritin. When iron binds to lactoferrin and apoferritin, it is converted to intoferritin and stored rather than being available for hemoglobin development (Gaspad, 2005).

Anemia of chronic illness is mild and only may impact physical activity unless the decrease in hemoglobin is significant. The treatment for this form of anemia is to address the iron deficiency and eliminate the primary disorder. If there is no infection or inflammation but anemia is present, a malignancy should be suspected (Gaspad, 2005; Thomas, 2004).



The nursing assessment of the patient with a potential for anemia includes both subjective and objective data. The nurse should review the patient?s medical history to determine the occurrence of recent blood loss or trauma, chronic liver disease, endocrine or renal disease, gastrointestinal bleeding, malabsorption syndrome, ulcers, gastritis or hemorrhoids, and surgery or radiation therapy. Inflammatory disorders such as Crohn?s disease and exposure to radiation, arsenic, lead, benzenes, and copper should be investigated (Jones, 2004). The patient?s medications should be identified, including iron supplementations, aspirin, anticoagulants, oral contraceptives, phenobaribital (Luminal ?), nonsteroidal anti-inflammatory drugs, quinine, phenytoin, a- Methyldopa, penicillin and quinidine (Adamson & Longo, 2001; Broyles, Reiss, & Evans, 2007; Jones, 2004; Smeltzer, Bare, Hinkle, & Cheever, 2008).

Clinical manifestations of anemia are not evident until the patient?s hemoglobin is less than 6-7 g/dL. The patients with higher hemoglobin may have only palpitations and dyspnea on exertion as clinical manifestation of anemia. With severe anemia, the patient may have lymphadenopathy and fever. Table 2 shows the symptoms associated with hemoglobin below 6-7 g/dL (Jones, 2004; Smeltzer et al., 2008).

The patient with anemia will have a low red blood cell count, hemoglobin, and hematocrit. The serum iron may be low. Ferritin, folate, and serum erythropoietin may be altered. Other laboratory data that may be altered in anemia are the bilirubin, platelet count, and total serum binding capacity. Anemia sometimes is caused by destruction of RBCs producing an elevated bilirubin. High serum bilirubin can injure the lipid components of the plasma membrane. In addition, because plasma proteins bind to unconjugated bilirubin, high serum counts also can lead to structural injury to the cells due to the loss of cellular proteins (Rote, McCance, & Manson, 2008; Smeltzer et al., 2008). Patient history and laboratory data often point clearly to the etiology for the anemia as a process of RBC destruction or inadequate production (Smeltzer et al., 2008). Understanding laboratory examination of cell morphology is helpful in planning care for the patient and educating patient and family regarding symptoms of anemia (Jones, 2004).


Nursing interventions depend on the etiology of the anemia. The major nursing diagnoses applicable to many patients with anemia include activity intolerance related to weakness, fatigue, and general malaise; altered nutrition, less than body requirements, related to inadequate intake of essential nutrients; altered tissue perfusion related to inadequate blood volume or hematocrit; and noncompliance with prescribed therapy. Blood or blood products may be ordered if acute blood loss is the reason for the anemia. The nurse also should monitor vital signs and oxygen saturation. When hemoglobin is low, the heart compensates by increasing the workload, producing initial symptoms of tachycardia, palpitations, and dyspnea. Long-term effects would include cardiomegaly and hepatomegaly (Jones, 2004; Lemone & Burke, 2004; Smeltzer et al., 2008). Monitoring laboratory results will direct the nurse in understanding the etiology for the anemia. Fatigue is a distressing symptom for most individuals with anemia. Nursing interventions should be directed at establishing balance between activities in the day, planning rest periods, and establishing a physical activity program (Smeltzer et al., 2008).

If the patient has iron deficiency anemia or other anemia with dietary etiology, dietary education and lifestyle changes will be needed. Financial planning may be needed if poverty or sudden loss of family income is contributing to a low iron intake or other dietary deficiency. The patient and family should be involved in planning for dietary changes. Small frequent meals during the day may increase the patient?s ability to maintain a nutritious diet, especially if the patient is an older adult or living alone (Jones, 2004; Lemone & Burke, 2004).

The nurse should educate the patient about how to take iron supplements and additional vitamins. Iron is absorbed from the duodenum and proximal jejunum. Iron preparations are enteric coated and given three times a day, or once a day using a higher dose. Iron is best absorbed as ferrous sulfate in an acid environment, and it should be given about an hour before meals. Taking vitamin C with iron helps absorption. Because iron can stain teeth, elixirs should be diluted and ingested through a straw. Iron causes gastrointestinal side effects, such as heartburn, constipation, and diarrhea. To decrease these effects, the dose of iron may be reduced or ferrous gluconate may be used as a substitute. Parenteral iron is given when the anemia is severe and cannot be managed adequately by diet changes or medication. Iron-dextran is the most common parenteral form used in the United States (Jones, 2004; Smeltzer et al., 2008). The nurse should evaluate the patient?s understanding of dietary issues contributing to the anemia. A 24-hour food log will assist the nurse to evaluate the intake of protein, iron, calories, and other nutrients needed for hematopoiesis.

The nurse should monitor the patient for the expected outcomes of nursing interventions. Does the patient tolerate activities and follow a program of progressive activities and rest? Does he or she maintain an adequate, well-balanced diet and comply with the nutritional supplements suggested through the treatment plan? Ongoing monitoring of the patient?s laboratory data will determine the status of the anemia. Monitoring the vital signs at rest and during activity will demonstrate the patient?s activities of daily living (Lemone & Burke, 2004). Are the vital signs within the patient?s baseline? Are pulse oximetry readings (oxygen saturation) values within normal limits (Lemone & Burke, 2004; Smeltzer et al., 2008)? Is the patient free of complications from the anemia? Do the patient and family verbalize understanding of the rationale for the treatment program (Smeltzer et al., 2008)? Evaluation of the outcome of teaching and therapy will depend on the etiology of the anemia and treatment plan (Jones, 2004). The patient and family often are anxious and may need additional literature in the language of their choice to support the education component of the nurse?s role.

Summary and Conclusions

The nurse should be aware of the pathophysiology and etiology of anemia. Careful assessment and ongoing monitoring are essential, especially when anemia results from acute blood loss. Ongoing monitoring of laboratory data and physical signs of cardiovascular health will be necessary until the patient demonstrates vital signs within his or her baseline and pulse oximetry results within normal limits (Smeltzer et al., 2008). The nurse consistently monitors the patient?s tolerance for daily activities and the dietary intake and nutritional status. The nurse is responsible for educating the patient and family about the cause of anemia as well as diet and medications required to address a low hemoglobin and hematocrit. The patient and family should be involved in determining the necessary lifestyles changes (Jones, 2004). Understanding of the disease process of the anemia and assisting the patient and family to manage the treatment plan are valuable contributions the nurse can make to the patient?s welfare.

Table 2. Symptoms of Anemia at Hemoglobin Levels Below 8 g/dL


Pale, jaundice

Pale skin and mucous membranes

Poor skin turgor

Brittle, spoon-shaped nails



Nasal Pharyngeal

Bleeding from the nose

Bleeding from lesions in the mouth

Beefy, red tongue

Stomatitis, glossitis


Abdominal distention






Postural hypertension

Widened pulse pressure


Ankle edema

Intermittent claudication

Neurologic System


Impaired judgment


Musculoskeletal System


Unsteady gait



Adamson, J.W., & Longo, D.L. (2001). Hematologic alterations. In E. Braumwald, A.S. Fauci, D.L. Kasper, S.L. Hauser, D.L. Longo, & J.L. Jameson (Eds.), Harrison?s principles of internal medicine (pp. 348-365). New York: McGraw Hill. Brill, J.R., & Baumgardner, J. (2000). Normocytic anemia. American Family Physician, 62, 2255- 2261.

Broyles, B.E., Reiss, B.S., & Evan, M.E. (2007). Pharmacological aspects of nursing care (7th ed.). Clifton Park, NY. Delmar.

Crowley, L.V. (2007). An introduction to human diseases (7th ed.). Boston: Jones and Bartlett Publishers.

Dharmarajan, T.S., Adiga, G.U., & Norkus, E.P. (2003). Vitamin B12 deficiency: Recognizing subtle symptoms in older adults. Geriatrics, 58(3), 30-38.

Fink, M.P. (2004). Pathophysiology of intensive care unit- acquired anemia. Critical Care, 8(2), S9-10.

Gaspad, K.J. (2005). Red cell disorders. In C.M. Porth (Ed.), Pathophysiology: Concepts of altered health states (pp. 279-284). Philadelphia: Lippincott Williams & Wilkins.

Goddard, A.F., McIntyre, A.S., & Scott, B.B. (2000). Guidelines for the management of iron deficiency anaemia [Electronic version]. Gut, 46, 1-5.

Hodges, V.M., Rainey, S., Lappin, T.R., & Maxwell, P. (2007). Pathophysiology of anemia and erythrocytosis. Critical Reviews in Oncology/Hematology, 64(2), 139-158.

Hoekelman, R.A., Adam, H.M., Nelson, N.M, Weitzman, M.L., & Wilson, M.H. (2001). Primary pediatric care (4th ed.). St. Louis: Mosby.

Ioannou, G.N., Spector, J., Scott, K., & Rockey, D.C. (2002). Prospective evaluation of a clinical guideline for the diagnosis and management of iron deficiency anemia. The American Journal of Medicine, 113(4), 281-287.

Jones, K.J. (2004). Nursing management hematologic problems. In S.M. Lewis, M.M. Heitkemper, & S.R. Dirksen (Eds.), Medical- surgical nursing: Assessment and management of clinical problems (pp. 705-755). St. Louis: Mosby.

Kumar, V., Cotran, R.S., & Robbins, S.L. (2003). Robbins basic pathology. Philadelphia: Saunders.

Lemone, P., & Burke, K. (Eds.). (2004). Nursing care of clients with hematologic disorders. In Medical surgical nursing: Critical thinking in client care (pp. 931-979). Upper Saddle River, NJ: Prentice Hall.

Mansen, T.L., & McCance, K.L. (2006). Alterations of erthyrocyte function. In K.L. McCance & S.E. Huether (Eds.), Pathophysiology: The biologic basis for disease in adults and children (5th ed., pp. 927-948). St. Louis: Mosby.

Metivier, F., Marchais, S.J., Guerin, A.P., Pannier, B., & London, G.M. (2000). Pathophysiology of anemia: Focus of the heart and blood vessels. Nephrology Dialysis and Transplant, 15(Suppl. 3), 14- 18.

Rote, S.N., & McCance, K.L. (2008). Structure and function of the hematologic systems. In S.E. Huether & K.L. McCance (Eds.), Understanding pathophysiology (4th ed., pp. 481-504). St. Louis: Mosby.

Rote, S.N., McCance, K.L., & Manson, T.J. (2008). Alterations in hematological function. In S.E. Huether & K.L. McCance (Eds.), Understanding pathophysiology (4th ed., pp. 508-539). St. Louis: Mosby.

Segal, G.B.E. (2004). Definitions and classifications hemolytic anemias. In R.E. Behrman, R.M. Kliegman, & H.B. Jenson (Eds.), Nelson textbook of pediatrics (pp. 1617-1620). Philadelphia: Saunders.

Smeltzer, S.C., Bare, B.G., Hinkle, J.L., & Cheever, K.H. (Eds.). (2008). Assessment and management of patients with hematologic disorders. In Brunner & Suddarth?s textbook of medical surgical nursing (pp. 1035-1117). Philadelphia: Lippincott Williams & Wilkins.

Suzuki, C., Hirai, Y., Terui, K., Kohsaka, A., Akagi, T., Toshihir, S., et al. (2004). Slowly progressive Type I diabetes mellitus associated with vitiligo vulgaris, chronic thryoiditis, and pernicious anemia. Internal Medicine, 43, 1183-1185.

Thomas, L. (2004). Anemia of chronic disease pathophysiology and laboratory diagnosis. Laboratory Hematology, 10(3), 163-165.

Uphold, C.R., & Graham, M.V. (2003).Clinical guidelines in family health (3rd ed.). Gainesville, FL: Barmarae Books.

Young, N.S., Calado, T.C., & Scheinberg, P. (2006). Current concepts in the pathophysiology and treatment of aplastic anemia. Blood, 108, 2509-2519.

Sharon M. Coyer, PhD, RN, APN, CPNP, is an Associate Professor, Northern Illinois University School of Nursing, DeKalb, IL.

Ayhan Aytekin Lash, PhD, RN, FAAN, is a Professor, Northern Illinois University School of Nursing, DeKalb, IL, and a MEDSURG Nursing Editorial Board Member.

Note: The authors and all MEDSURG Nursing Editorial Board members reported no actual or potential conflict of interest in relation to this continuing nursing education article.

Copyright Anthony J. Jannetti, Inc. Apr 2008

(c) 2008 Medsurg Nursing. Provided by ProQuest Information and Learning. All rights Reserved.

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