adult nursing - anemia

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(Relates to Chapter 31, “Nursing Management: Hematologic Problems,” in the textbook)


A deficiency in the Number of erythrocytes (red blood cells [RBCs])

Quantity of hemoglobin Volume of packed RBCs (hematocrit)


Diverse causes such as Blood loss Impaired production of erythrocytes

Increased destruction of erythrocytes


RBC function Transport oxygen (O2) from lungs to systemic tissues

Carry carbon dioxide from the tissues to the lungs


Not a specific disease Manifestation of a pathologic

processIdentified and classified by

laboratory diagnosis


Classified as Morphologic

▪ Cellular characteristics▪ Descriptive, objective laboratory information

Etiologic▪ Underlying cause


Caused by the body’s response to tissue hypoxia

Hemoglobin (Hb) levels are used to determine the severity of anemia


Pallor ↓ Hemoglobin ↓ Blood flow to the skin

Jaundice ↑ Concentration of serum bilirubin

Pruritus ↑ Serum and skin bile salt concentrations


Additional attempts by the heart and lungs to provide adequate O2 to the tissues

Cardiac output maintained by increasing the heart rate and stroke volume


Mild = Hb 10 to 14 g/dl May exist without symptoms Possible symptoms

▪ Palpitations, dyspnea, diaphoresisModerate = Hb 6 to 10 g/dl

Increased cardiopulmonary symptoms

Experienced at rest or during activity


Severe = Hb <6 g/dl Involve multiple body systems

▪ Integument ▪ Eyes▪ Mouth▪ Cardiovascular


Severe = Hb <6 g/dl Manifestations (cont'd)

▪ Pulmonary ▪ Neurologic ▪ Gastrointestinal (GI)▪ Musculoskeletal


Subjective Data Important health information

▪ Past health history▪ Medications ▪ Surgery or other treatments


Subjective Data Functional health patterns

▪ Health perception–health management

▪ Nutritional-metabolic▪ Elimination▪ Activity-exercise▪ Cognitive-perceptual ▪ Sexuality-reproductive


Objective Data General Integumentary Respiratory Cardiovascular Gastrointestinal Neurologic


Activity intoleranceImbalanced nutrition: Less

than body requirementsIneffective therapeutic

regimen management Potential complication:

Hypoxemia


Goals Assume normal activities of daily living

Maintain adequate nutrition Develop no complications related to anemia


Dietary and lifestyle changesBlood or blood product

transfusionsDrug therapy


Oxygen therapyPatient teaching

Nutrition intake Compliance with drug therapy


Common in older adults Chronic disease Nutritional deficiencies

Signs and symptoms may go unrecognized or mistaken for normal aging changes


Erythropoietin (EPO) is a glycoprotein primarily produced in the kidneys (10% in the liver) ↑ Number of stem cells committed to RBC production

Shortens the time to mature RBCs


Life span of an RBC is 120 daysThree alterations in

erythropoiesis that decrease RBC production Decreased hemoglobin synthesis Defective DNA synthesis in RBCs Diminished availability of erythrocyte precursors


One of the most common chronic hematologic disorders

Iron is present in all RBCs as heme in hemoglobin and in a stored form

Heme accounts for two thirds of the body’s iron


Inadequate dietary intake 5% to 10% of ingested iron is absorbed

Malabsorption Blood lossHemolysis


General manifestations of anemia

Pallor is the most common finding

Glossitis is the second most common Inflammation of the tongue


Laboratory findings Hb, Hct, MCV, MCH, MCHC, reticulocytes, serum iron, TIBC, bilirubin, platelets

Stool guaiac testEndoscopy Colonoscopy


Goal is to treat the underlying disease Increased intake of iron Nutritional therapy Oral or occasional parenteral iron supplements

Transfusion of packed RBCs


Oral iron Inexpensive Convenient Factors to consider

▪ Enteric-coated or sustained-release capsules are counterproductive


Oral iron Factors to consider (cont’d)

▪ Best absorbed as ferrous sulfate in an acidic environment

▪ Liquid iron should be diluted and ingested through a straw

▪ Side effects▪ Heartburn, constipation, diarrhea


At-risk groups Premenopausal women Pregnant women Persons from low socioeconomic backgrounds

Older adults Individuals experiencing blood loss


Diet teachingSupplemental ironDiscuss diagnostic studiesEmphasize compliance Iron therapy for 2 to 3

months after the hemoglobin levels return to normal


An autosomal recessive genetic disorder of inadequate production of normal hemoglobin Common in ethnic groups near the Mediterranean Sea and equatorial regions of Asia and Africa


Hemolysis also occursProblem with globulin

protein Abnormal Hb synthesis

One thalassemic gene Thalassemia minor

Two thalassemic genes Thalassemia major


Thalassemia minor Asymptomatic frequently Moderate anemia

▪ Splenomegaly ▪ Mild jaundice


Thalassemia major Life-threatening Physical and mental growth often retarded

Pale Symptoms develop in childhood


Thalassemia major (cont’d) Splenomegaly Hepatomegaly Jaundice Chronic bone marrow hyperplasia ▪ Expansion of bone marrow space


No specific drug or diet is effective in treating thalassemia

Thalassemia minor Body adapts to decreased Hb

Thalassemia major Blood transfusions with IV deferoxamine


Group of disorders caused by impaired DNA synthesis

Characterized by the presence of large RBCs (megaloblasts)

Majority result from deficiency in Cobalamin (vitamin B12) Folic acid


Classification Cobalamin (vitamin B12) deficiency

Folic acid deficiency Drug-induced suppression of DNA synthesis

Inborn errors Erythroleukemia


Intrinsic factor (IF) Protein secreted by the parietal cells of the gastric mucosa

IF is required for cobalamin absorption in the small intestine


Causes Pernicious anemia

▪ Insidious onset Nutritional deficiencies Hereditary enzymatic defects


Absence of IFAcid environment required

for IF secretionGI surgery Long-term users of H2-

histamine receptor blockers


General symptoms of anemia

Sore tongueAnorexiaNauseaVomitingAbdominal pain


Neuromuscular manifestations Weakness Paresthesias of the feet and hands

↓ Vibratory and position senses Ataxia Muscle weakness Impaired thought process


RBCs appear largeAbnormal shapesStructure contributes to

erythrocyte destructionDecreased serum

cobalamin levels


Normal serum folate levels and decreased cobalamin levels suggest megaloblastic anemia due to cobalamin deficiency

Schilling test


Parenteral administration of cobalamin

Increase in dietary cobalamin does not correct the anemia Still important to emphasize adequate dietary intake


Familial disposition Early detection and treatment can lead to reversal of symptoms

Ensure that injuries are not sustained because of the patient’s diminished sensations to heat and pain


Ensure patient compliance with treatment

Evaluate patient for gastric carcinoma frequently


Also a cause of megaloblastic anemia

Folic acid is required for DNA synthesis RBC formation and maturation


Common causes Poor nutrition Malabsorption syndromes Drugs Alcohol abuse and anorexia Lost during hemodialysis


Clinical manifestations are similar to those of cobalamin deficiency

Insidious onsetAbsence of neurologic problemsTreated by replacement therapyEncourage patient to eat foods

with large amounts of folic acid


Underproduction of RBCsMild shortening of RBC

survival


Causes End-stage renal disease

▪ Primary factor: ↓ Erythropoietin Chronic liver disease Chronic inflammation Malignant tumors Chronic endocrine diseases


Anemia of chronic disease findings ↑ Serum ferritin ↑ Iron stores Normal folate and cobalamin levels


Treating underlying cause is best

Rarely blood transfusionsErythropoietin therapy


Pancytopenia Decrease of all blood cell types

▪ RBCs▪ White blood cells (WBCs)▪ Platelets

Hypocellular bone marrow


Low incidence Affecting 4 of every 1 million persons

Manageable with erythropoietin or blood transfusion

Can be a critical condition Hemorrhage Sepsis


Types Congenital

▪ Chromosomal alterations Acquired

▪ Results from exposure to ionizing radiation, chemical agents, viral and bacterial infections


Gradual developmentSymptoms caused by

suppression of any or all bone marrow elements

General manifestations of anemia Fatigue, dyspnea


Confirmed by laboratory studies

Normocytic, normochromic anemia


Preventing complications from infection and hemorrhage

Untreated prognosis is poor 75% fatal

Treatment options Bone marrow transplantation Immunosuppressive therapy


Result of sudden hemorrhage Trauma Complications of surgery Disruption of vascular integrity


Concerns Hypovolemic shock Reduced plasma volume

▪ Diminished O2 because fewer RBCs available


Cause Body’s attempt to maintain an adequate blood volume and O2

Pain Internal hemorrhage

▪ Tissue distention, organ displacement, nerve compression


Pain (cont'd) Retroperitoneal bleeding

▪ Numbness ▪ Pain in the lower extremities

Shock is the major complication


Laboratory data do not adequately assess RBC problems for 2 to 3 days


Replacing blood volume to prevent shock

Identifying the source of the hemorrhage

Stopping blood lossCorrecting RBC loss


May be impossible to prevent if caused by trauma

Postoperative patients Monitor blood loss

No need for long-term treatment


Reduced iron stores Bleeding ulcer Hemorrhoids Menstrual and postmenopausal blood loss


Management Identify source Stop bleeding Possible use of supplemental iron


Destruction or hemolysis of RBCs at a rate that exceeds production

Third major cause of anemia, such as Thalassemia

Intrinsic hemolytic anemia Abnormal hemoglobin Enzyme deficiencies RBC membrane abnormalities


Extrinsic hemolytic anemia Acquired

Sites of hemolysis Intravascular Extravascular


Jaundice Destroyed RBCs cause increased bilirubin

Enlarged spleen and liver Hyperactive with macrophage phagocytosis of the defective RBCs


Accumulation of hemoglobin molecules can obstruct renal tubules Tubular necrosis


Group of inherited, autosomal recessive disorders

Presence of an abnormal form of hemoglobin in the erythrocyte

Hemoglobin S (HbS), abnormal


HbS causes the RBC to stiffen and elongate Sickle shape in response to ↓ O2 levels

Substitution of valine for glutamic acid on the β-globin chain of hemoglobin

Genetic disorderIncurable disease, often fatal


Types of SCD Sickle cell anemia

▪ Most severe▪ Homozygous for hemoglobin S (HbSS)

Sickle cell thalassemia Sickle cell HbC disease Sickle cell trait (HbAS)


Typical patient is asymptomatic except during sickling episodes

Symptoms can be Pain and swelling Pallor of mucous membranes Fatigue


Gradual involvement of all body systems

Usually fatal by middle age from renal and pulmonary failure

Prone to infection Pneumonia, most common infection


Peripheral blood smearSickling testElectrophoresis of

hemoglobinDNA testingSkeletal x-raysMagnetic resonance imaging

(MRI)


Alleviate symptoms of disease complications

Minimize end-organ damageNo specific treatment for

SCDPatient teaching

Avoid high altitudes, maintain fluid intake, treat infections, control pain


O2 for hypoxia and to control sickling

Pain managementAcute chest syndrome

Antibiotics O2 therapy Fluid therapy


Folic acid daily supplementsBlood transfusions in crisis Hydroxyurea: Antisickling

agent Erythropoietin in patients unresponsive to hydroxyurea

Bone marrow transplant Can cure some patients with SCD


Excessive production of red blood cells

Unknown cause Hemorrhage of distended blood

vesselsReddish face with deep‑red

purplish lips, fatigue, weakness, dizziness, headache, enlarged spleen (splenomegaly), and congested liver


Treatment: Phlebotomy, antineoplastic agents, and radiation therapy

Increased fluid intake Secondary polycythemia


Platelet count less than 150,000/mm3

Immune thrombocytopenic purpura

Heparin therapy Safety


For a patient with a low platelet count, whenever a venipuncture is performed, an injection is administered, or an intravenous catheter or needle is discontinued, pressure over the site must be maintained for 10 minutes to prevent continuous oozing.


EtiologyPathophysiologySigns and symptomsDiagnosis and treatmentNursing management


Aspirin must never be taken by a patient with hemophilia as it increases the bleeding problems.

Patients must read labels on every over-the-counter preparation to be certain that it does not contain aspirin or acetylsalicylic acid.

adult nursing - anemia

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