Chapter 30
Hematologic Problems
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Anemia (1 of 4)

A deficiency in



Number of erythrocytes (RBCs)
Quantity or quality of hemoglobin (Hgb)
Volume of packed RBCs (hematocrit)
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2
Causes of Anemia
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3
Anemia (2 of 4)

RBC function


Transport oxygen (O2) from lungs to systemic tissues
Carry carbon dioxide from tissues to lungs
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4
Anemia (3 of 4)



Not a specific disease
Manifestation of a pathologic process
Diagnosed based on



Complete blood count (CBC)
Reticulocyte count
Peripheral blood smear
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5
Anemia (4 of 4)

Classified according to

Morphology
• Cellular characteristic
• RBC size and color

Etiology
• Cause
• Clinical condition causing anemia
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6
Anemia
Clinical Manifestations

Caused by body’s response to tissue hypoxia


Manifestations vary based on how fast anemia has
evolved, its severity, and any coexisting disease
Hgb levels are often used to determine severity of
anemia
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77
Anemia
Integumentary Manifestations

Pallor



Jaundice


Decreased Hgb
Decreased blood flow to the skin
Increased concentration of serum bilirubin
Pruritus

Increased serum and skin bile salt concentrations
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8
Anemia
Cardiopulmonary Manifestations


Result from heart and lungs trying to provide
adequate O2 to tissues
Cardiac output maintained by increasing heart
rate and stroke volume
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9
Anemia
Nursing Assessment (1 of 2)

Subjective data

Important health information
•
•
•
•

Past health history
Medications
Surgery or other treatments
Dietary history
Functional health patterns
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10
Anemia
Nursing Assessment (2 of 2)

Objective data







General
Integumentary
Respiratory
Cardiovascular
GI
Neurologic
Diagnostic findings
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11
Anemia
Nursing Diagnoses



Fatigue
Impaired nutritional status
Ineffective tissue perfusion
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12
Anemia
Nursing Interventions (1 of 2)

Nursing care varies


Numerous causes of anemia
Patient specific needs
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13
Anemia
Nursing Interventions (2 of 2)

Patients with fatigue


Alternate rest and activity
Prioritize activities
• Accommodate energy levels
• Maximize O2 supply for vital functions



Aid to minimize risk of injury from falls
Monitor cardiorespiratory response
Evaluate nutritional needs
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14
Case Study (1 of 29)




K.L. is a 24-year-old female with increasing
lethargy, inability to pay attention at work, and
headache.
She has a pale, beefy tongue and inflamed lip.
She tells you she is breastfeeding her 4 month
old.
What should you do?
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15
Anemia
Gerontologic Considerations

Anemia is not normal



More common in the 70s and beyond
Often related to an underlying cause
Signs and symptoms may be overlooked


Other health issues
May be mistaken for normal aging
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16
Anemia
Decreased Erythrocyte Production


RBC production (erythropoiesis) is in equilibrium
with RBC destruction/ loss
Balance ensures that adequate number of RBCs
is always available
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17
Erythrocyte Production


Life span of an RBC is 120 days
Three changes in erythropoiesis may decrease RBC
production:



Decreased Hgb synthesis
Defective DNA synthesis in RBCs
Diminished availability of erythrocyte precursors
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18
Iron-Deficiency Anemia


Most common nutritional disorder in the world
Most susceptible



Very young
Poor diet
Women in reproductive years
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19
Iron-Deficiency Anemia
Etiology (1 of 2)

Inadequate dietary intake



Normally dietary intake is enough
Need more with menstruation, pregnancy
Malabsorption


Iron absorption occurs in the duodenum
Diseases or surgery that alter, destroy, or remove
absorption surface of this area of intestine cause
anemia
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20
Iron-Deficiency Anemia
Etiology (2 of 2)

Blood loss


Major cause of iron deficiency in adults
Chronic blood loss most commonly through GI and
GU systems
• Bleeding often not apparent
• May take time to identify

Postmenopausal bleeding, chronic kidney disease,
and dialysis may contribute
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21
Iron-Deficiency Anemia
Clinical Manifestations

General manifestations of anemia


Pallor is most common
Glossitis is second
• Inflammation of tongue

Cheilitis is also found
• Inflammation of lips
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22
Iron-Deficiency Anemia
Diagnostic Studies

Laboratory findings




Hgb, Hct, MCV, MCH, MCHC, reticulocytes, serum
iron, TIBC, bilirubin, platelets
Stool occult blood test
Endoscopy and colonoscopy
Bone marrow biopsy
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23
Iron-Deficiency Anemia
Interprofessional and Nursing
Management

Goal


Treat underlying problem causing loss, reduced
intake or poor absorption of iron
Replace iron



Nutritional therapy
Oral iron supplements
Transfusion of packed RBCs
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24
Case Study (2 of 29)

K.L. has lab work done. Her results are back, and
her lab values show



Decreased: Hct, Hgb, MCV, iron, ferritin, and
transferrin
Increased: TIBC
What is the likely cause of her anemia?
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25
Iron-Deficiency Anemia
Drug Therapy (1 of 3)

Oral iron



Inexpensive
Convenient
Factors to consider
• Enteric-coated or sustained-release capsules are
counterproductive
• Daily dose is 150 to 200 mg
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26
Iron-Deficiency Anemia
Drug Therapy (2 of 3)

Oral iron

Factors to consider
• Best absorbed in an acidic environment
• Undiluted liquid iron may stain teeth

Should be diluted and drank through a straw
• Side effects

Heartburn, constipation, diarrhea
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27
Iron-Deficiency Anemia
Drug Therapy (3 of 3)

Parenteral iron

Indicated for malabsorption, oral iron intolerance,
need for iron beyond normal limits, poor patient
compliance
 Can be given IM or IV
 IM may stain skin
• Z-track
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28
Iron-Deficiency Anemia
Nursing and Interprofessional
Management


Reassess Hgb and RBC count to evaluate response
to therapy
Emphasize adherence to dietary and drug therapy

Need to take supplement for 2 to 3 months after Hgb
returns to normal
 Monitor for liver problems with lifelong therapy
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29
Case Study (3 of 29)

How should K.L.’s anemia be treated?
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30
Case Study (4 of 29)



K.L. tells you she can’t afford medicine.
She has three children and her husband is out of
work.
Her income is barely keeping the household
going.
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31
Case Study (5 of 29)


Anything that costs money is out of the question.
What can you teach K.L. about effects of anemia
if left untreated?
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32
Thalassemia
Etiology



A group of diseases involving inadequate production
of normal Hgb
Results in decreased RBC production
Due to absent or reduced globulin protein


Abnormal Hgb synthesis
Hemolysis occurs
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33
Thalassemia
Genetic Link


Autosomal recessive genetic basis
One thalassemic gene


Thalassemia minor
Two thalassemic genes

Thalassemia major
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34
Thalassemia
Clinical Manifestations (1 of 3)

Thalassemia minor


Often asymptomatic
Moderate anemia
• Microcytosis
• Hypochromia

Body adapts to reduction of Hgb—thus no treatment
is indicated
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35
Thalassemia
Clinical Manifestations (2 of 3)

Thalassemia major





Life-threatening
Physical and mental growth often slowed
Jaundice is prominent
Splenomegaly, hepatomegaly, and cardiomyopathy
Symptoms develop in childhood
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36
Thalassemia
Clinical Manifestations (3 of 3)

Thalassemia major

As the bone marrow responds to the reduced O2carrying capacity of the blood, RBC production is
stimulated, and marrow becomes packed with
immature erythroid precursors that die
 Chronic bone marrow hyperplasia
 Endocrine problems and thrombosis
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37
Thalassemia
Interprofessional Care


No specific drug or diet is effective in treating
thalassemia
Thalassemia major



Blood transfusions or exchange transfusions with
chelating agents that bind to iron to reduce iron
overloading
Drugs may increase urine excretion of iron
Splenectomy
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38
Megaloblastic Anemias

Group of disorders



Caused by impaired DNA synthesis
Presence of large RBCs (megaloblasts)
Majority result from deficiency in


Cobalamin (vitamin B12)
Folic acid
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39
Cobalamin Deficiency
Etiology

Most commonly caused by pernicious anemia




Caused by absence of intrinsic factor (IF)
Insidious onset
Begins in middle age or later
Predominant in Scandinavians and blacks
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40
Cobalamin Deficiency

Intrinsic factor (IF)


Protein secreted by parietal cells of gastric mucosa
IF is required for cobalamin (extrinsic factor)
absorption in the distal ileum

If IF is not secreted, cobalamin will not be absorbed
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41
Cobalamin Deficiency
Etiology

Can also occur:






Surgery or chronic diseases of the GI tract
Excess alcohol or hot tea ingestion
Smoking
Long-term users of H2 histamine receptor blockers
and proton pump inhibitors
Strict vegetarians
Familial predisposition
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42
Cobalamin Deficiency
Clinical Manifestations

General manifestations of anemia develop slowly
due to tissue hypoxia

GI problems:
• Sore , red, beefy, and shiny tongue, anorexia, nausea,
vomiting, and abdominal pain

Neuromuscular problems:
• Weakness, paresthesias of feet and hands, decreased
vibratory and position senses, ataxia, muscle
weakness, and impaired thought processes
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43
Cobalamin Deficiency
Diagnostic Studies




Macrocytic RBCs have abnormal shapes and
fragile cell membranes
Serum cobalamin levels are low
Normal serum folate levels and low cobalamin
levels suggest megaloblastic anemia is due to
cobalamin deficiency
Upper GI endoscopy with biopsy of gastric
mucosa to rule out gastric cancer
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44
Cobalamin Deficiency
Interprofessional and Nursing
Management

Parenteral or intranasal administration of cobalamin
is treatment of choice


Patients will die in 1 to 3 years without treatment
Anemia can be reversed with ongoing treatment but
long-standing neuromuscular complications may not
be reversible
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45
Megaloblastic Anemia
Nursing and Interprofessional
Management


Early detection and treatment
Ensure safety



Diminished sensations to heat and pain from
neurologic impairment
Protect from falling, burns, and trauma
Physical therapy may be needed
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46
Megaloblastic Anemia
Folic Acid Deficiency


Causes megaloblastic anemia
Folic acid is needed for DNA synthesis


RBC formation and maturation
Manifestations are similar to those of cobalamin
deficiency, but if neurologic symptoms present, may
be caused by thiamine deficiency
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47
Folic Acid Deficiency (1 of 2)

Common causes






Dietary deficiency
Malabsorption syndromes
Drugs
Increased requirement
Alcohol use and anorexia
Loss during hemodialysis
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48
Folic Acid Deficiency (2 of 2)

Serum folate level is low



Serum cobalamin level is normal
Treated with replacement therapy


Normal is 5 to 25 ng/mL (11 to 57 nmol/L)
Usual dose is 1 mg/day by mouth
Encourage patient to eat foods with large amounts
of folic acid
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49
Audience Response Question (1 of
2)
At an outpatient clinic, K.L.’s 78-year-old grandma is found
to have a Hgb of 8.7 g/dL (87 g/L) and a Hct of 35%. Based
on the most common cause of these findings in the older
adult, the nurse collects information about:
a. a history of jaundice and black tarry stools.
b. a 3-day diet recall of the foods the patient has eaten.
c. any drugs that have depressed the function of the bone
marrow.
d. a history of any chronic diseases, such as cancer or
renal disease.
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50
Audience Response Question (2 of
2)
Answer: D
a history of any chronic diseases, such as cancer
or renal disease.
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51
Anemia of Chronic Disease
Anemia of Inflammation (1 of 2)

Can be caused by


Cancer
Autoimmune and infectious disorders
• HIV, hepatitis, malaria



Chronic inflammation
Heart failure
Bleeding episodes
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52
Anemia of Chronic Disease
Anemia of Inflammation (2 of 2)

Associated with


Underproduction of RBCs
Mild shortening of RBC survival
• Normocytic, normochromic, and hypoproliferative RBCs

Usually a mild anemia but can become severe if the
underlying disorder is untreated
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53
Anemia of Chronic Disease

Anemia of chronic disease findings




Increased Serum ferritin
Increased Iron stores
Normal folate and cobalamin levels
Treating underlying cause is best


Blood transfusions for severe cases
Limited use of erythropoietin therapy
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54
Aplastic Anemia

Pancytopenia

Decrease in all blood cell types
• Red blood cells (RBCs)
• White blood cells (WBCs)
• Platelets


Hypocellular bone marrow
Ranges from moderate to very severe

Potentially fatal
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55
Aplastic Anemia
Etiology

Rare



Annual rate of 2 to 5 new cases/million/year
About 70% due to autoimmune activity by
autoreactive T-lymphocytes
May be acquired


Toxic injury to bone marrow stem cells
Result of inherited stem cell defect
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56
Aplastic Anemia
Clinical Manifestations



Abrupt or insidious development
Symptoms caused by suppression of any or all bone
marrow elements
General manifestations of anemia



Fatigue, dyspnea
Cardiovascular and cerebral responses
Neutropenia, thrombocytopenia
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57
Aplastic Anemia
Diagnostic Studies

Diagnosis confirmed by laboratory studies




Decreased Hgb, WBC, and platelet values
Decreased reticulocyte count
Elevated serum iron and TIBC
Hypocellular bone marrow with increased yellow
marrow (fat content)
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58
Aplastic Anemia: Nursing and
Interprofessional Management (1 of
2)



Identify and remove causative agent (when
possible)
Provide supportive care until pancytopenia
reverses
Prevent complications from infection and
hemorrhage
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59
Aplastic Anemia: Nursing and
Interprofessional Management (2 of
2)


Prognosis of severe untreated aplastic anemia is
poor
Advances in treatment options have significantly
improved outcomes

Immunosuppressive therapy and bone marrow
transplantation can be curative
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60
Anemia Caused by Blood Loss
Acute and Chronic

Anemia from blood loss may be caused by either
acute or chronic problems

Acute blood loss occurs because of sudden
hemorrhage
• Trauma, complications of surgery, conditions or
diseases that disrupt total blood volume
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61
Acute Blood Loss

Conditions or diseases that disrupt vascular integrity


Hypovolemic shock
Compensatory increased plasma volume with
diminished O2 -carrying RBCs
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62
Acute Blood Loss
Clinical Manifestations (1 of 2)


Caused by body’s attempts to maintain
adequate blood volume and meet oxygen
requirements
Clinical signs and symptoms are more important
than laboratory values
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63
Acute Blood Loss
Clinical Manifestations (2 of 2)

Pain

Internal hemorrhage
• Tissue distention, organ displacement, nerve
compression

Retroperitoneal bleeding
• Numbness
• Pain in lower extremities

Shock is major complication
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64
Acute Blood Loss
Diagnostic Studies


With sudden blood volume loss, values may seem
normal or high for 2 to 3 days
Once plasma volume is replaced, low RBC
concentrations become evident

Low RBC, Hgb, and Hct levels reflect actual blood
loss
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65
Acute Blood Loss: Interprofessional
and Nursing Management (1 of 2)




Replace blood volume to prevent shock
Identify source of hemorrhage and stopping
blood loss
Correct RBC loss
Provide supplemental iron
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66
Acute Blood Loss: Interprofessional
and Nursing Management (2 of 2)


May be impossible to prevent blood loss if caused
by trauma
Postoperative patients



Monitor blood loss
Give blood products for anemia
No need for long-term treatment
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67
Chronic Blood Loss

Sources of chronic blood loss:




Bleeding ulcer
Hemorrhoids
Menstrual and postmenopausal blood loss
Management involves


Identifying the source and stop bleeding
Providing supplemental iron as needed
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68
Hemolytic Anemia (1 of 2)

Destruction or hemolysis of RBCs at a rate that
exceeds production

Caused by problems intrinsic or extrinsic to the RBCs
• Intrinsic forms are usually hereditary and result from
defects in RBCs themselves
• RBCs are normal in acquired forms, but damage is
caused by external factors.
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69
Sequences of Events in Hemolysis
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70
Hemolytic Anemia (2 of 2)


General manifestations of anemia
Specific manifestations including



Jaundice
Enlargement of the spleen and liver
Maintenance of renal function is a major focus of
treatment
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71
Case Study (6 of 29)

C.P. is a black woman with reports of severe
joint and abdominal pain, frequent urination
during past two nights, and knee swelling.
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72
Case Study (7 of 29)


She reports a history of feeling fatigued but
attributed it to her active lifestyle.
What should you do?
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73
Sickle Cell Disease (SCD)

Group of inherited, autosomal recessive disorders



An abnormal form of Hgb in RBC
Genetic disorder usually identified during routine
neonatal screening
Incurable, significantly affects quality of life
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74
Sickle Cell Disease
Etiology and Pathophysiology (1 of
3)

Abnormal Hgb, Hgb S, causes the RBC to stiffen
and elongate


Substitution of valine for glutamic acid on the β-globin
chain of Hgb
Erythrocytes take on a sickle shape in response to
decreased O2 levels
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75
Sickle Cell Disease
Etiology and Pathophysiology (2 of
3)

Substitution of valine for glutamic acid on the βglobin chain of Hgb
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76
Sickle Cell Disease
Etiology and Pathophysiology (3 of
3)

Types of SCD

Sickle cell anemia
• Most severe
• Homozygous for hemoglobin S (Hgb SS)



Sickle cell thalassemia
Sickle cell Hgb C disease
Sickle cell trait (Hgb AS)
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77
Sickle Cell Hemoglobin Aggregates
and Alters Shape of RBC
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78
Sickle Cell Disease
Sickling Episodes

The major pathophysiologic event of this disease



Triggered by low O2 tension in blood
Infection is most common precipitating factor
At first, sickling is reversible with re-oxygenation
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79
Sickle Cell Disease
Sickle Cell Crisis



Severe, painful, acute exacerbation of RBC
sickling causes a vaso-occlusive crisis
Severe capillary hypoxia eventually leads to
tissue necrosis
Life-threatening shock is a possible result of
severe O2 depletion of the tissues and a
reduction of the circulating fluid volume
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80
Case Study (8 of 29)

In taking a more complete history, C.P. tells you
she had one similar episode of symptoms
(severe joint and abdominal pain, frequent
urination during past two nights, fatigue, and
knee swelling) when she had an acute attack of
pneumonia 2 months ago.
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81
Case Study (9 of 29)

What is unusual about her episode of
pneumonia?
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82
Sickle Cell Disease
Clinical Manifestations


Typical patient is asymptomatic except during
sickling episodes
Symptoms may include




Pain from tissue hypoxia and damage
Pallor of mucous membranes
Jaundice from hemolysis
Prone to gallstones (cholelithiasis)
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83
Clinical Manifestations of Sickle
Cell Disease
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84
Sickle Cell Disease
Complications (1 of 2)

Infection is a major cause of morbidity and mortality

Function of spleen becomes compromised from
sickled RBCs
• Autosplenectomy is a result of scarring

Pneumococcal pneumonia most common
 Severe infections can cause aplastic crisis
• Can lead to shutdown of RBC production
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85
Sickle Cell Disease
Complications (2 of 2)

Acute chest syndrome

Lung complications include pneumonia, tissue
infarction, and fat embolism
 Characterized by fever, chest pain, cough, lung
infiltrates, and dyspnea
 Leads to multiple serious complications
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86
Sickle Cell Disease
Diagnostic Studies






Peripheral blood smear
Hemoglobin electrophoresis
Skeletal x-rays
Magnetic resonance imaging (MRI)
Doppler studies
Chest x-ray
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87
Case Study (10 of 29)




C.P. tells you that 2 days ago she went hiking in
the mountains.
She is sure her swollen knee is from the hike.
Physical examination showed an enlarged
spleen and an enlarged, inflamed knee joint.
What should be done next?
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88
Sickle Cell Disease: Nursing and
Interprofessional Management (1 of
5)

Care is directed toward




Preventing sequelae from disease
Alleviating manifestations from complications
Minimizing end-organ damage
Continuously assessing for and promptly treating
serious sequelae
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89
Sickle Cell Disease: Nursing and
Interprofessional Management (2 of
5)

Hospitalized patients in sickle cell crisis

O2 treats hypoxia and controls sickling
 Assess for changes in respiratory status
 Rest with VTE prophylaxis
 Give fluids
 Transfusion therapy
• Chelation therapy with repeated transfusions
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90
Sickle Cell Disease: Nursing and
Interprofessional Management (3 of
5)


Under-treatment is a major problem
Pain management



May develop pain medication tolerance
Require continuous and breakthrough analgesia with
morphine and hydromorphone
Multimodal and interdisciplinary approach involving
emotional and adjunctive measures
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91
Sickle Cell Disease: Nursing and
Interprofessional Management (4 of
5)




Treat infections
Give folic acid
Hydrea is only antisickling agent shown to be
clinically beneficial
Hematopoietic stem cell transplantation (HSCT)
is only available cure
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92
Sickle Cell Disease: Nursing and
Interprofessional Management (5 of
5)

Patient and caregiver teaching and support are
important

Ways to avoid crises
 Ways to maintain adequate fluid intake
 Immunizations
 Importance of prompt medical attention
 Pain control
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93
Case Study (11 of 29)

C.P.’s lab values show







Hematocrit 30%
Hgb 10 g/dL
WBC count 20,000/µL
Bilirubin 2.8 mg/dL
Urinalysis normal
Ferritin normal
X-ray of her knee is normal
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94
Case Study (12 of 29)

What problem do C.P.’s history and symptoms
suggest?
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95
Acquired Hemolytic Anemia (1 of 4)

Results from hemolysis of RBCs from extrinsic
factors



Physical destruction
Antibody reactions
Infectious agents and toxins
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96
Acquired Hemolytic Anemia (2 of 4)

Physical destruction of RBCs results from exertion
of extreme force on cells

Hemodialysis
 Extracorporeal circulation used in cardiopulmonary
bypass
 Prosthetic heart valves
 Abnormal vessels
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97
Acquired Hemolytic Anemia (3 of 4)

RBCs can be fragmented and destroyed as they try
to pass through abnormal arterial or venous
microcirculation

Excessive platelet aggregation and/or fibrin polymer
formation
• Seen in thrombotic thrombocytopenic purpura (TTP)
and disseminated intravascular coagulopathy (DIC)
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98
Acquired Hemolytic Anemia (4 of 4)

Antibodies may destroy RBCs by mechanisms
involved in antigen-antibody reactions


Blood transfusion reaction
Autoimmune antibody reactions
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99
Acquired Hemolytic Anemia
Infectious Agents

Cause hemolysis in three ways:

Invade the RBC and destroy its contents
• Parasites, such as in malaria

Release hemolytic substances
• Clostridium perfringens

Generate an antigen-antibody reaction
• Mycoplasma pneumoniae
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100
Acquired Hemolytic Anemia
Treatment and Management

Supportive care until the causative agent can be
eliminated or made less injurious

Emergency preparedness is essential for potential
hemolytic crises
• Aggressive hydration and electrolyte replacement,
corticosteroids, blood products, splenectomy

Folic acid replacement and immunosuppressive
agents for chronic conditions
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101
Hemochromatosis

Iron overload disorder



Genetic defect most common cause
May occur with other diseases
Genetic link


Increased intestinal iron absorption
Increased tissue and organ iron deposition
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102
Case Study (13 of 29)

What patient teaching is essential for you to discuss with
C.P.?
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103
Thrombocytopenia
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104
Thrombocytopenia

Normal Hemostasis

Involves the vascular endothelium, platelets, and
coagulation factors
 Function together to stop hemorrhage and repair
vascular injury
 Disruption of any component may result in bleeding or
thrombotic disorders
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105
Etiology and Pathophysiology


Reduction of platelets
Results in abnormal hemostasis


Prolonged or spontaneous bleeding
Primarily an acquired disorder

Commonly from ingestion of certain drugs
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106
Case Study (14 of 29)


R.H. is a 46-year-old cancer survivor who
returns to your clinic for a regular check-up.
She is currently reporting an increase in fatigue
for the last 2 to 3 weeks.
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107
Case Study (15 of 29)


She is also unable to complete her normal
morning ADLs without intermittent rest periods.
What should you do first?
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108
Causes of Thrombocytopenia


Inherited
Acquired



Immune thrombocytopenia purpura (ITP)
Thrombotic thrombocytopenia purpura (TTP)
Heparin-induced thrombocytopenia (HIT)
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109
Immune Thrombocytopenia (ITP)



Most common acquired thrombocytopenia
Syndrome of abnormal destruction of circulating
platelets
Acquired autoimmune disorder
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110
Immune Thrombocytopenic
Purpura (ITP)

Clinical syndrome presents as



Acute condition in children
Chronic condition in adults
Treated with multiple therapies
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111
Thrombotic Thrombocytopenia
Purpura (TTP) (1 of 2)



An uncommon syndrome with a variety of
features that are not always present
Called TTP-HUS as it is almost always
associated with hemolytic-uremic syndrome
Associated with enhanced aggregation of
platelets that form into microthrombi
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112
Thrombotic Thrombocytopenic
Purpura (TTP) (2 of 2)

Caused by plasma enzyme deficiency



Primarily in previously healthy adults
May be idiopathic or from drug toxicities
Medical emergency

Bleeding and clotting occur at the same time
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113
Heparin-Induced
Thrombocytopenia (HIT) (1 of 2)



Associated with use of heparin
Life-threatening
Two major responses to an immune-mediated
response to heparin:


Platelet destruction
Vascular endothelial injury
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114
Heparin-Induced
Thrombocytopenia (HIT) (2 of 2)

Develops 5 to 10 days after heparin therapy is
started


Platelet count drops by more than 50%
VTE is major clinical problem
• Arterial thrombosis can also develop
• VTE and PE often result
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115
Thrombocytopenia (1 of 6)

Clinical manifestations


Patients are often asymptomatic
Most common symptom is mucosal or cutaneous
bleeding
• Petechiae—microhemorrhages
• Purpura—bruise from numerous petechiae
• Ecchymoses—larger lesions from hemorrhage
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116
Thrombocytopenia (2 of 6)
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117
Thrombocytopenia (3 of 6)

Manifestations

Hemorrhage may be insidious or acute
• Internal bleeding may manifest as weakness, fainting,
dizziness, tachycardia, abdominal pain, or hypotension
• Cerebral hemorrhage may be fatal
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118
Thrombocytopenia (4 of 6)

Diagnostic studies

Decreased Platelet count< 150,000/μL
• Prolonged bleeding < 50,000/μL
• Hemorrhage decreased 20,000/μL



Medical history
Clinical examination
Lab parameter comparisons
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119
Thrombocytopenia (5 of 6)

Diagnostic studies



Lab tests for hemostasis and coagulation can be
normal
Specific assays can assist
Bone marrow exam can rule out production problems
as the cause
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120
Case Study (16 of 29)

When taking her BP, you notice R.H. has small,
flat, pinpoint, reddish-brown microhemorrhages
all over her forearms.
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121
Case Study (17 of 29)


On further inspection, you notice that on her left
thigh, she has a very large, purple bruise which
she reports is tender to the touch.
What are these lesions?
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122
Thrombocytopenia (6 of 6)

Interprofessional care



Based on the cause
Removal or treatment of underlying cause or disorder
may be sufficient
Avoid aspirin and other drugs that affect platelet
function or production
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123
Immune Thrombocytopenia
Purpura (ITP) (1 of 6)

Interprofessional care


Therapy initiated if platelets ↓ 30,000/μL
Corticosteroids
• Suppress phagocytic response of splenic macrophages
resulting in increased life span of the platelets
• Depress antibody formation
• Reduce capillary leakage
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124
Immune Thrombocytopenia
Purpura (ITP) (2 of 6)

Interprofessional care

High doses of IV immunoglobulin (IVIG) and anti-Rho
(D)
• Compete with antiplatelet antibodies for macrophage
receptors in the spleen

Rituximab (Rituxan)
• Lyse activated B cells
• Reduce immune recognition of platelets
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125
Immune Thrombocytopenic
Purpura (ITP) (3 of 6)

Interprofessional care

Thrombopoietin receptor agonists
• Used with chronic ITP when insufficient response to
other treatments
• Romiplostim (Nplate)
• Eltrombopag (Promacta)
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126
Immune Thrombocytopenia
Purpura (ITP) (4 of 6)

Interprofessional care

Splenectomy
• May be needed if patient does not respond to other
treatments
• 2/3 of patients achieve sustained remission
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127
Immune Thrombocytopenic
Purpura (ITP) (5 of 6)

•
•
Effectiveness of splenectomy based on
Spleen has an abundance of macrophages that
sequester and destroy platelets
Structural features enhance interaction of antibodycoated platelets and macrophages
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128
Immune Thrombocytopenia
Purpura (ITP) (6 of 6)

•
•
Effectiveness of splenectomy based on
Some antibody synthesis occurs in spleen , so
antiplatelet antibodies decrease after splenectomy
Spleen normally sequesters around 1/3 of the
platelets, so its removal increases number of platelets
in circulation
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129
Thrombotic Thrombocytopenia
Purpura (TTP) (1 of 2)

Interprofessional care



First treat underlying disorder or remove cause
Untreated TTP usually results in irreversible renal
failure and death
Plasmapheresis can aggressively reverse platelet
consumption
• Continued daily until platelet counts normalize and
hemolysis has ceased
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130
Thrombotic Thrombocytopenia
Purpura (TTP) (2 of 2)

Interprofessional care

Rituximab
• Used for patients refractory to plasma exchange
• Decreases level of inhibitory ADAMTS13 IgG
antibodies


Other immunosuppressants may be used
Splenectomy may be considered
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131
Case Study (18 of 29)

R.H.’s lab results are back:






Platelet count 40,000/μL
Hgb 9.10 g/dL; Hct 29%
RBCs 3.26 × 106/μL
Prothrombin (PT) time 15 seconds
Activated partial thromboplastin time (APTT) <35
seconds
What type of thrombocytopenia does she probably
have?
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132
Heparin-Induced
Thrombocytopenia (HIT) (1 of 2)

Interprofessional care

Stop all heparin including heparin flushes
• Note clearly on medical record


Start patient on a direct thrombin inhibitor
Start warfarin (Coumadin) only when platelet count
reaches 150,000/μL
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133
Heparin-Induced
Thrombocytopenia (HIT) (2 of 2)

Interprofessional care

For severe clotting:
• Plasmapheresis to clear platelet-aggregating IgG from
the blood
• Protamine sulfate to interrupt circulating heparin
• Thrombolytic agents to treat thromboembolic events
• Surgery to remove clots
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134
Thrombocytopenia From
Decreased Platelet Production

Interprofessional care

Management is based on identifying cause and
treating disease or removing the causative agent
 Treat with corticosteroids if precipitating factor is
unknown
 Platelet transfusions for life-threatening hemorrhage
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135
Acquired Thrombocytopenia From
Decreased Platelet Production

Interprofessional care

Often caused by another underlying condition or
therapy used to treat another problem
• In acute leukemia, all blood cell types may be
depressed
• Chemotherapeutic drugs can cause bone marrow
suppression
• Thrombocytopenia will resolve if patient is adequately
supported during treatment
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136
Case Study (18 of 29)
1. What kind of treatment should R.H. expect?
2. What could happen if she does not follow
through with treatment?
3. How will her doctor know when to stop
treatment?
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137
Nursing Management
Thrombocytopenia (1 of 10)

Nursing assessment

Subjective data
• Past health history
• Medications
• Functional health patterns

Objective data
• Fever, lethargy, bleeding, splenomegaly, abdominal
distention
• Lab data
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138
Nursing Management
Thrombocytopenia (2 of 10)

Nursing diagnoses

The primary nursing diagnosis is risk for bleeding
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139
Nursing Management
Thrombocytopenia (3 of 10)

Planning

Overall goals are that the patient will
• Have no bleeding
• Maintain vascular integrity
• Manage home care to prevent any complications
related to an increased risk for bleeding
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140
Nursing Management
Thrombocytopenia (4 of 10)

Nursing implementation

Health promotion
• Discourage the use of OTC medications, especially
aspirin products
• Encourage patients to have a complete medical
evaluation if manifestations of bleeding tendencies
develop
• Observe for early signs in patients receiving cancer
chemotherapy drugs
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141
Nursing Management
Thrombocytopenia (5 of 10)

Nursing implementation

Acute care
• Prevent or control hemorrhage
• Bleeding usually begins superficially
• Deep bleeding occurs only when clotting factors are
diminished
• Any bleeding needs evaluation and treatment
• Watch for bleeding that can be difficult to detect
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142
Nursing Management
Thrombocytopenia (6 of 10)

Nursing implementation

Acute care
• If subcutaneous injection is unavoidable, use smallgauge needles and apply direct pressure or ice packs
after
• Avoid IM injections
• Teach importance of adhering to self-care measures to
reduce risk of bleeding
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143
Nursing Management
Thrombocytopenia (7 of 10)

Nursing implementation

Acute care
• Closely monitor platelet count, coagulation studies,
Hgb, and Hct
• Manage blood loss from excessive menstrual bleeding


Count sanitary napkins used
Use hormones to suppress menses
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144
Nursing Management
Thrombocytopenia (8 of 10)

Nursing implementation


Administer platelet transfusions
Blood component therapy is frequently used to
manage hematologic diseases
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145
Nursing Management
Thrombocytopenia (9 of 10)

Nursing implementation

Ambulatory care
• Monitor patients for response to therapy
• Teach avoidance of causative agents, trauma, and
injury
• Teach clinical signs and symptoms of bleeding
• Encourage planned, periodic medical exams
• Address quality of life issues
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146
Nursing Management
Thrombocytopenia (10 of 10)

Evaluation

Expected outcomes
• No evidence of bleeding or bruising
• State needed knowledge and skills to manage disease
process
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147
Case Study (20 of 29)
1. If R.H. does not respond to plasmapheresis,
what surgery might be done?
2. What is your role in preparing her for care after
surgery?
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148
Hemophilia and
von Willebrand Disease (1 of 5)


Hemophilia is X-linked recessive genetic disorder
caused by defective or deficient coagulation factor
Two major types


Hemophilia A
Hemophilia B
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149
Hemophilia and
von Willebrand Disease (2 of 5)

von Willebrand disease is a related disorder
involving deficiency of von Willebrand coagulation
factor (Factor VIII)

Made in the liver
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150
Hemophilia and
von Willebrand Disease (3 of 5)

Clinical manifestations/complications






Bleeding, which may be life-threatening
Slow, persistent, prolonged bleeding
Delayed bleeding after minor injuries
Uncontrollable hemorrhage after dental extractions or
irritation with toothbrush
Epistaxis
GI bleeding from ulcers and gastritis
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151
Hemophilia and
von Willebrand Disease (4 of 5)

Clinical manifestations/complications





Hematuria and potential renal failure
Ecchymoses and subcutaneous hematomas
Compartment syndrome
Neurologic signs
Hemarthrosis
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152
Hemophilia and
von Willebrand Disease (5 of 5)

Diagnostic studies


Factor deficiency within the intrinsic system (factor
VIII, IX, XI, XII , vWF)
Interprofessional care



Preventive care
Replacement therapy
Treatment of complications
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153
Disseminated Intravascular
Coagulation (DIC) (1 of 5)

Serious bleeding and thrombotic disorder



Results from abnormally initiated and accelerated
clotting
Decreases in clotting factors and platelets ensue
May lead to uncontrollable hemorrhage
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154
Disseminated Intravascular
Coagulation (DIC) (2 of 5)

Always caused by an underlying disease or
condition

Abnormal response to clotting cascade stimulated by
a disease process or disorder
• Acute, catastrophic condition
• Subacute, or chronic level
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155
Disseminated Intravascular
Coagulation (DIC) (3 of 5)

Clinical manifestations


Bleeding in the skin, respiratory and cardiovascular
systems, GI and urinary tracts, neurologic and
musculoskeletal systems
Thrombosis in the skin, respiratory and
cardiovascular systems, GI tract, kidneys
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156
Disseminated Intravascular
Coagulation (DIC) (4 of 5)

Diagnostic studies




D-dimer is a specific marker for the degree of
fibrinolysis
Decreased Platelets
Decreased Fibrinogen
Clotting times prolonged
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157
Disseminated Intravascular
Coagulation (DIC) (5 of 5)

Interprofessional care


Early diagnosis and treatment of underlying cause
Control ongoing thrombosis and bleeding
• If chronic DIC and not bleeding, no therapy needed
• When patient with DIC is bleeding, blood products are
given while treating underlying cause
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158
Leukemia
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159
Leukemia (1 of 2)

A group of cancers affecting the blood and bloodforming tissues of



Bone marrow
Lymph system
Spleen
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160
160
Leukemia (2 of 2)




Occurs in all age-groups
Accumulation of dysfunctional cells due to loss
of regulation in cell division
Fatal if untreated
Accounts for 29% of all childhood cancers
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161
161
Leukemia
Etiology and Pathophysiology

No single cause

Combination of genetic and environmental influences
• Oncogenes, or abnormal genes, can cause many types
of cancers
• Chemical agents, chemotherapeutic agents, viruses,
radiation, and immunologic deficiencies have been
associated with development of leukemia
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162
162
Pathophysiology of Leukemia
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163
Leukemia
Classification (1 of 2)

Acute versus chronic

Cell maturity and nature of disease onset
• Acute: Clonal proliferation of immature hematopoietic
cells
• Chronic: More mature forms of WBC and onset is more
gradual
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164
164
Leukemia
Classification (2 of 2)

Based on type of WBC




Acute lymphocytic leukemia (ALL)
Acute myelogenous leukemia (AML)
Chronic myelogenous leukemia (CML)
Chronic lymphocytic leukemia (CLL)
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165
165
Case Study (21 of 29)


W.C. is a 64-year-old man who reports general
fatigue and recent weight loss.
What specific information will you be sure to
obtain during your initial nursing assessment?
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166
166
Acute Myelogenous Leukemia
(AML)

25% of all leukemias


Abrupt, dramatic onset


80% of the acute leukemias in adults
Serious infection or abnormal bleeding
Characterized by uncontrolled proliferation of
myeloblasts

Hyperplasia of bone marrow
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167
167
Acute Lymphocytic Leukemia (ALL)
(1 of 2)



Most common type of leukemia in children
20% of acute leukemia in adults
Immature, small lymphocytes proliferate in the bone
marrow

Most are of B cell origin
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168
Acute Lymphocytic Leukemia (ALL)
(2 of 2)

Signs and symptoms may appear

Abruptly
• Fever at time of diagnosis
• Bleeding

Insidiously
• Progressive weakness, fatigue, bone and/or joint pain,
bleeding tendencies

CNS manifestations are common
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169
169
Chronic Myelogenous Leukemia
(CML) (1 of 2)

Excessive development of neoplastic granulocytes
in bone marrow


Move into peripheral blood in massive numbers
Infiltrate liver and spleen
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170
170
Chronic Myelogenous Leukemia
(CML) (2 of 2)

Philadelphia chromosome



Genetic marker
Present in 90% or more CML patients
Chronic, stable phase

Followed by acute, aggressive (blastic) phase
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171
171
Chronic Lymphocytic Leukemia
(CLL) (1 of 2)


Most common leukemia in adults
Production and accumulation of functionally inactive
but long-lived, mature-appearing lymphocytes



B cells involvement
Lymphocytes infiltrate bone marrow, spleen, liver
Lymphadenopathy throughout body
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172
172
Chronic Lymphocytic Leukemia
(CLL) (2 of 2)

Complications are rare in early stage




May develop as disease advances
Pain, paralysis from pressure caused by enlarged
lymph nodes
Mediastinal node enlargement leads to pulmonary
symptoms
Many patients in early stages may require no
treatment
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173
173
Leukemia

Subtype may be difficult to identify



May have lymphoid, myeloid, or mixed characteristics
Poor prognosis
Overlap with non-Hodgkin’s lymphoma

Both involve proliferation of lymphocytes or their
precursors
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174
174
Leukemia
Clinical Manifestations (1 of 5)

Varied but usually related to

Bone marrow failure
• Overcrowding by abnormal cells
• Inadequate production of normal marrow elements

Formation of leukemic infiltrates
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175
175
Leukemia
Clinical Manifestations (2 of 5)

Inadequate marrow elements predispose patient to



Anemia
Thrombocytopenia
Decreased number and function of WBCs
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176
176
Leukemia
Clinical Manifestations (3 of 5)


As leukemia progresses, fewer normal blood
cells are made
Abnormal WBCs continue to accumulate, do not
go through normal cell cycle to death (apoptosis)
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177
177
Leukemia
Clinical Manifestations (4 of 5)

Leukemic cells may cause







Splenomegaly
Hepatomegaly
Lymphadenopathy
Bone pain
Meningeal irritation
Oral lesions
Solid masses (chloromas)
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178
178
Leukemia
Clinical Manifestations (5 of 5)

Leukostasis


Life-threatening complication
Caused by a high leukemic WBC count in peripheral
blood
• Greater than 100,000/µL

Blood thickens and blocks circulatory pathways
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179
179
Leukemia
Diagnostic Studies (1 of 2)

To diagnose and classify types of leukemia



Peripheral blood evaluation
Bone marrow examination
To identify cell types and stage

Morphologic, histochemical, immunologic, and
cytogenic methods
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180
180
Leukemia
Diagnostic Studies (2 of 2)

To determine the presence of leukemic cells outside
of blood and bone marrow


Lumbar puncture
PET/CT scan
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181
181
Case Study (22 of 29)

The provider orders a CBC for W.C.




WBC 110,000/µL
Hgb 10.5 g/L
Platelets 120,000 /µL
What problem do his symptoms and lab values
suggest?
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182
182
Leukemia
Interprofessional Care (1 of 6)

Initial goal is to attain remission

Complete, partial, or molecular
• Prognosis is directly related to ability to maintain a
remission
• Prognosis becomes more unfavorable with each
relapse

Chemotherapy is the mainstay of treatment
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183
183
Leukemia
Interprofessional Care (2 of 6)

Stages of chemotherapy
• Induction
• Postinduction or postremission (consolidation)
• Maintenance
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184
184
Leukemia
Interprofessional Care (3 of 6)

Induction therapy



Attempt to induce remission
Seeks to destroy leukemic cells in tissues, peripheral
blood, and bone marrow
Patient may become critically ill
• Neutropenia, thrombocytopenia, anemia

70% of patients younger than 60 achieve complete
remission
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185
185
Leukemia
Interprofessional Care (4 of 6)

Postinduction or postremission chemotherapy

Intensification therapy
• High-dose therapy
• May be given after induction therapy
• Other drugs that target cell in a different way than
those administered during induction may be added
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186
186
Leukemia
Interprofessional Care (5 of 6)

Postinduction or postremission chemotherapy

Consolidation therapy
• Started after remission is achieved
• 1 or 3 more courses of induction drugs
• Eliminate remaining leukemic cells that may not be
clinically or pathologically evident
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187
187
Leukemia
Interprofessional Care (6 of 6)

Maintenance therapy


Lower doses of the same drugs used in induction
given every 3 to 4 weeks
Goal is to keep body free of leukemic cells
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188
188
Leukemia
Chemotherapy Regimens

Combination chemotherapy


Mainstay of treatment
Three purposes
• Decrease drug resistance
• Decrease drug toxicity by using multiple drugs
• Interrupt cell growth at multiple points in cell cycle
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189
189
Leukemia
Other Treatments


Corticosteroids
Radiation therapy



Total body radiation in preparation for bone marrow
transplantation
Organ- or field-specific such as liver or spleen
Immunotherapy and targeted therapy
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190
190
Leukemia
Hematopoietic Stem Cell
Transplant

Goal of HSCT


Eliminate all leukemic cells using combinations of
chemotherapy with or without total body irradiation
Eradicates patient’s hematopoietic stem cells
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191
191
Leukemia
Stem Cell Transplantation

Replaced with those of an HLA-matched

Sibling
 HLA-half-matched relative
 Volunteer donor (allogenic)
 Identical twin (syngeneic)
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192
192
Nursing Management
Assessment (1 of 4)

Subjective data

Past health history
• Exposure to toxins, chromosome abnormalities,
frequent infections

Medications
• Previous chemotherapy

Surgery or radiation treatments
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193
193
Nursing Management
Assessment (2 of 4)

Functional health patterns
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194
194
Nursing Management
Assessment (3 of 4)

Objective data






Fever, lymphadenopathy, lethargy
Pallor, jaundice, petechiae, ecchymoses
CV—tachycardia, systolic murmurs
GI—oral lesions or bleeding, herpes or infection,
hepatomegaly, splenomegaly
Seizures, disorientation, confusion
Muscle wasting, bone or joint pain
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195
195
Nursing Management
Assessment (4 of 4)

Diagnostic findings






WBC may be normal or abnormal
Anemia
Decreased Hct and Hgb
Thrombocytopenia
Philadelphia chromosome
Hypercellular bone marrow aspirate or biopsy
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196
196
Nursing Management
Planning

Overall goals



Understand and adhere to treatment plan
Have minimal side effects and complications of
disease and treatment
Establish realistic hope and goals, feeling supported
during periods of treatment, relapse, and remission
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197
197
Nursing Management
Acute Care (1 of 3)

Many physical and psychologic needs




Diagnosis evokes great fear
Equated with death
Family needs help adjusting to stress of sick role
May be viewed as hopeless, horrible
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198
198
Nursing Management
Acute Care (2 of 3)

Important nursing interventions



Maximizing patient’s physical functioning
Teaching patients that acute side effects of treatment
are usually temporary
Encouraging patients to discuss quality of life issues
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199
199
Nursing Management
Acute Care (3 of 3)

You will face special challenges when meeting the
treatment needs of a patient with leukemia

Review all drugs being given
 Be prepared to manage the sometimes lifethreatening side effects of treatment
 Assess lab data reflecting effects of drugs and
sequelae of the disease
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200
200
Case Study (23 of 29)


W.C.’s wife comes to his next appointment to
find out results of all of his tests. She is quite
worried.
What is the primary nursing management for
W.C. and his wife?
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201
201
Nursing Management
Ambulatory Care (1 of 3)


Ongoing care is necessary to monitor for signs and
symptoms of disease control or relapse
Teach patient and caregiver



Diligence in disease management
Need for follow-up care
When to seek medical attention
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202
202
Nursing Management
Ambulatory Care (2 of 3)

Goals of rehabilitation

Manage the consequences
•
•
•
•
Physical
Psychosocial
Social
Spiritual
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203
203
Nursing Management
Ambulatory Care (3 of 3)

Vigilant follow-up care


Assures that we recognize and treat cancer survivor’s
unique needs
Often may need referral or consultation
• Physical therapy
• Pneumococcal vaccine
• Annual influenza vaccine
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204
204
Nursing Management
Evaluation

Expected outcomes

Cope effectively with the diagnosis, treatment
regimen, and prognosis
 Have no complications related to the disease or its
treatment
 Feel supported throughout treatment
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205
205
Case Study (24 of 29)


W.C.’s results indicate he is in the early stages
of CLL.
What would you teach W.C. about follow-up care
and managing his condition?
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206
206
Audience Response Question (1 of
2)
A patient with acute myelogenous leukemia is starting
chemotherapy. When teaching the patient about the
induction stage of chemotherapy, what is an appropriate
statement?
a. “The drugs are started slowly to minimize side effects.”
b. “You will be at increased risk for bleeding and infection.”
c. “High doses will be administered every day for several
months.”
d. “Most patients have more energy and are resistant to
infection.”
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207
Audience Response Question (2 of
2)
Answer: B
“You will be at increased risk for bleeding and
infection.”
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208
Lymphoma
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209
Lymphoma (1 of 3)

Cancers originating in bone marrow and lymphatic
structures

Result in proliferation of lymphocytes
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210
Lymphoma (2 of 3)


Comprise 4% to 5% of all cancers in United States
Two major types


Hodgkin’s lymphoma
Non-Hodgkin’s lymphoma (NHL)
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211
Lymphoma (3 of 3)

See Table 30-27 in the textbook for a
Comparison of Hodgkin’s and Non-Hodgkin’s
Lymphoma
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212
Hodgkin’s Lymphoma (1 of 2)

Known as Hodgkin’s disease


Makes up about 10% of all lymphomas
Cancerous condition with

Proliferation of abnormal giant, multinucleated cells
• Reed-Sternberg cells
• Proliferate in the lymph nodes
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213
Hodgkin’s Lymphoma (2 of 2)

Bimodal age-specific incidence

15 to 30 years of age
 Greater than 55 years of age


About 8260 new cases each year
Long-term survival exceeds 80% for all stages
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214
Hodgkin’s Lymphoma
Etiology and Pathophysiology (1 of
2)


Cause remains unknown
Key factors




Infection with Epstein-Barr virus (EBV)
Genetic predisposition
Exposure to occupational toxins
Incidence increased in those with HIV infection
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215
Hodgkin’s Lymphoma
Etiology and Pathophysiology (2 of
2)


Starts in a single location then spreads to adjacent
lymphatics
Eventually infiltrates other organs


Disease above diaphragm stays confined to lymph
nodes for variable time
Disease below diaphragm often spreads to
extralymphoid sites, such as liver
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216
Hodgkin’s Lymphoma
Clinical Manifestations (1 of 5)

Usually gradual onset

Enlargement of cervical, axillary, or inguinal lymph
nodes
 Second most common location is a mediastinal node
mass
 Nodes are movable and nontender
 Not painful unless nodes exert pressure on adjacent
nerves
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217
Enlarged Cervical Lymph Nodes
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218
Hodgkin’s Lymphoma
Clinical Manifestations (2 of 5)

Patient may notice





Weight loss
Fatigue and weakness
Fever and chills
Tachycardia
Night sweats
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219
Hodgkin’s Lymphoma
Clinical Manifestations (3 of 5)

Initial findings that correlate with a worse prognosis

Called B symptoms
• Fever greater than 100.4° F (380° C)
• Drenching night sweats
• Weight loss exceeding 10% in 6 months
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220
Hodgkin’s Lymphoma
Clinical Manifestations (4 of 5)



Alcohol-induced pain at site of disease
Generalized pruritus without lesions
With mediastinal node involvement




Cough
Dyspnea
Stridor
Dysphagia
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221
Hodgkin’s Lymphoma
Clinical Manifestations (5 of 5)

Advanced cases




Hepatomegaly
Splenomegaly
Anemia
Other physical signs vary, depending on disease
location
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222
Case Study (25 of 29)

N.L. is a 74-year-old man who visits his primary care
provider with “GI issues”.


Blood work and a CT are ordered


Enlarged cervical lymph nodes are noted on
assessment.
Followed by a lymph node biopsy.
What is lymphoma?
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223
Hodgkin’s Lymphoma
Diagnostic Studies





Peripheral blood analysis
Increased ESR, high leukocyte alkaline
phosphatase, hypercalcemia, hyperalbuminemia
Excisional lymph node biopsy
Bone marrow examination
Radiologic evaluation
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224
Stages of Hodgkin’s Lymphoma
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225
Hodgkin’s Lymphoma: Nursing and
Interprofessional Management (1 of
8)

Nomenclature used in staging

A or B classification
• Presence of systemic symptoms when disease is found

Roman numeral (I to IV)
• Location and extent of disease
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226
Hodgkin’s Lymphoma: Nursing and
Interprofessional Management (2 of
8)

Management focuses on selecting a treatment plan


Least amount to achieve cure
Minimize short- and long-term complications
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227
Hodgkin’s Lymphoma: Nursing and
Interprofessional Management (3 of
8)

Combination chemotherapy



Favorable early-stage disease, receive 2 to 4 cycles
Unfavorable early stage, receive 4 to 6 cycles
Advanced stage, receive 6 to 8 cycles
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228
Hodgkin’s Lymphoma: Nursing and
Interprofessional Management (4 of
8)

Involved site radiation as a supplement to
chemotherapy varies depending on



Extent of disease
Presence of resistant disease after chemotherapy
Response to therapy determined by PET/CT scans,
other diagnostic tests
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229
Hodgkin’s Lymphoma: Nursing and
Interprofessional Management (5 of
8)


A variety of chemotherapy regimens and newer
agents used to treat patients who have relapsed
or refractory disease
Once remission is obtained, a curative option
may be intensive chemotherapy with the use of
autologous or allogeneic HSCT
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230
Hodgkin’s Lymphoma: Nursing and
Interprofessional Management (6 of
8)



Therapy must be aggressive
Potentially life-threatening problems are
encountered in an attempt to achieve remission
Maintenance chemotherapy does not contribute
to increased survival after achieving complete
remission
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231
Hodgkin’s Lymphoma: Nursing and
Interprofessional Management (7 of
8)

Secondary cancers


Occur 10 years after treatment for Hodgkin’s
lymphoma
Most common secondary solid tumor cancers
• Lung cancer
• Breast cancer
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232
Hodgkin’s Lymphoma: Nursing and
Interprofessional Management (8 of
8)

Nursing care based on managing problems related
to disease



Pancytopenia
Other side effects of therapy
Address physical and spiritual consequences,
fertility issues, long-term effects of therapy
Copyright © 2020 by Elsevier, Inc. All rights reserved.
233
Case Study (26 of 29)

What is staging and what does it mean?
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234
Non-Hodgkin’s Lymphoma (1 of 3)

Broad group of cancers of immune system affecting
all ages


Primarily B-, T-, or NK- , histocytic and dendritic cells
Over 75 types
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235
Non-Hodgkin’s Lymphoma (2 of 3)

Categorized by





Level of differentiation (maturity)
Cell of origin
Rate of cellular proliferation
Immunophenotype (cell surface markers)
Clinical features
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236
Non-Hodgkin’s Lymphoma (3 of 3)

Most common subtypes in the United States are





Diffuse large B-cell lymphoma
Follicular lymphoma
Marginal zone lymphoma
Mantle cell lymphoma
Peripheral T-cell lymphoma
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237
Non-Hodgkin’s Lymphoma
Etiology and Pathophysiology (1 of
2)


Unknown cause
May result from




Chromosomal translocations
Infections
Environmental factors
Immunodeficiency states
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238
Non-Hodgkin’s Lymphoma
Etiology and Pathophysiology (2 of
2)

Most common in people who have




Inherited immunodeficiency syndromes
Have used immunosuppressive agents
Received chemotherapy or radiation
No hallmark feature

All NHLs involve lymphocytes arrested in various
stages of development
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239
Non-Hodgkin’s Lymphoma
Clinical Manifestations (1 of 2)


Widespread disease usually present at time of
diagnosis
Painless lymph node enlargement



Primary clinical manifestation
Lymphadenopathy can wax and wane
Other symptoms depending on where disease is
present
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240
Non-Hodgkin’s Lymphoma
Involving the Spleen
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241
Non-Hodgkin’s Lymphoma
Clinical Manifestations (2 of 2)

Patients with high-grade lymphomas


Lymphadenopathy
B symptoms
• Fever
• Night sweats
• Weight loss
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242
Non-Hodgkin’s Lymphoma
Diagnostic and Staging Studies (1
of 3)


Resemble those used for Hodgkin’s lymphoma
Since NHL is more often extranodal

MRI
 Lumbar puncture
 Bone marrow biopsy
 Barium enema or upper endoscopy
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243
Non-Hodgkin’s Lymphoma
Diagnostic and Staging Studies (2
of 3)

Staging guides therapy



Precise histologic subtype through biopsy is
extremely important
Classified based on morphologic, genetic,
immunophenotypic, and clinical features
In early NHL, CBC may be normal
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244
Non-Hodgkin’s Lymphoma
Diagnostic and Staging Studies (3
of 3)

Treatment guided by



Cell type
Cytogenetic studies
Clinical behavior
• Indolent (low grade)
• Aggressive (high grade)
• Highly aggressive (very high grade)
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245
Non-Hodgkin’s Lymphoma: Nursing
and Interprofessional Management
(1 of 5)

Treatment

Chemotherapy
 Biotherapy
 Radiation therapy
 Sometimes phototherapy and topical therapy
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246
Non-Hodgkin’s Lymphoma: Nursing
and Interprofessional Management
(2 of 5)

More aggressive lymphomas (diffuse large Bcell) are generally more responsive to treatment

Indolent lymphomas are hard to effectively treat
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247
Case Study (27 of 29)


N.L. is diagnosed with intermediate-grade,
diffuse, large non-Hodgkin’s lymphoma.
What is his primary treatment option?
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248
Non-Hodgkin’s Lymphoma: Nursing
and Interprofessional Management
(3 of 5)


Hematopoietic stem cell transplant
Rituximab (Rituxan)

Monitor for symptoms of severe hypersensitivity
infusion reactions
• Especially with first infusion

Ibritumomab tiuxetan (Zevalin)
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249
Non-Hodgkin’s Lymphoma: Nursing
and Interprofessional Management
(4 of 5)


Use radiation precautions in caring for patients
Teach patients about safety issues and how to
minimize risk of radiation exposure to staff and
others
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250
Case Study (28 of 29)

What other treatments might N.L. receive?
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251
Non-Hodgkin’s Lymphoma: Nursing
and Interprofessional Management
(5 of 5)


Complete remission is uncommon
However, improvement in symptoms is expected
in the majority of patients
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252
Non-Hodgkin’s Lymphoma
Nursing Management (1 of 2)


Largely based on managing problems related to
disease, pancytopenia, and other side effects
Must know about subtype and extent of disease
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253
Non-Hodgkin’s Lymphoma
Nursing Management (2 of 2)



Skin in radiation field requires special attention
Psychosocial considerations
Fertility concerns
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254
Case Study (29 of 29)

What is the most important nursing care for
N.L.?
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255
Multiple Myeloma


Condition in which cancerous plasma cells
proliferate in bone marrow and destroy bone
Accounts for 1.8% of all cancers


1% of all hematologic cancers
Occurs between ages of 65 and 74
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256
Multiple Myeloma
Etiology and Pathophysiology (1 of
2)

Cause unknown

Possible exposure to chemicals, herbicides,
insecticides
 Viral infections
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257
Multiple Myeloma
Etiology and Pathophysiology (2 of
2)

Involves excess production of plasma cells


Normal plasma cells make immunoglobulins to
protect the body
In multiple myeloma, plasma cells make monoclonal
antibodies that are ineffective and even harmful
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258
Multiple Myeloma
Clinical Manifestations (1 of 2)


Develops slowly and insidiously
Skeletal pain is major manifestation


Pelvis, spine, and ribs
Diffuse osteoporosis develops


Osteolytic lesions seen in skull, vertebrae, long
bones, ribs
Compression of spinal cord, pathologic fractures
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259
Multiple Myeloma
Clinical Manifestations (2 of 2)

Calcium loss from bones causes hypercalcemia


Leads to renal, GI, neurologic manifestations
Serum hyperviscosity leads to cerebral, lung,
renal, and other organ dysfunction
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260
Multiple Myeloma
Diagnostic Studies

Laboratory




Radiologic


M protein found in blood
Pancytopenia
Hypercalcemia
MRI, PET, and CT scans
Bone marrow examination
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261
Multiple Myeloma: Nursing and
Interprofessional Management (1 of
4)





Corticosteroids
Chemotherapy
Immunotherapy
Targeted therapy
HSCT
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262
Multiple Myeloma: Nursing and
Interprofessional Management (2 of
4)


Seldom cured, but treatment can relieve symptoms,
produce remission, and prolong life
Goals of management


Control pain
Prevent pathologic fractures
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263
Multiple Myeloma: Nursing and
Interprofessional Management (3 of
4)



Bisphosphonates
Kyphoplasty
Chemotherapy



Corticosteroids
Bortezomib and lenalidomide
Bortezomib and cyclophosphamide
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264
Multiple Myeloma: Nursing and
Interprofessional Management (4 of
4)






Immunotherapy and targeted therapy
Ambulation and adequate hydration
Pain management
Braces
Assessment/ treatment of infections
Psychosocial needs
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265