30
Lower Respiratory Problems
Eugene E. Mondor
http://evolve.elsevier.com/Lewis/medsurg/
CONCEPTUAL FOCUS
Cellular Regulation
Clotting
Functional Ability
Gas Exchange
Infection
LEARNING OUTCOMES
1.Compare and contrast the clinical manifestations and
nursing and interprofessional management of patients
with acute bronchitis and pertussis.
2.Distinguish among the types of pneumonia and their
etiology.
3.Describe the pathophysiology, clinical manifestations,
diagnostic studies, and interprofessional and nursing
management of patients with pneumonia.
4.Explain the pathophysiology, classification, clinical
manifestations, complications, diagnostic abnormalities,
and interprofessional and nursing management of patients
with tuberculosis.
5.Describe the pathophysiology, clinical manifestations, and
nursing and interprofessional management of a patient
with a lung abscess.
6.Identify the etiology, clinical manifestations, and nursing
and interprofessional management of a patient with a
pleural effusion.
7.Compare and contrast the pathophysiology, clinical
manifestations, and nursing and interprofessional
management of fractured ribs, flail chest, and
pneumothorax.
8.Describe the pathophysiology, clinical manifestations,
and nursing and interprofessional management of
pulmonary embolism, pulmonary hypertension, and
cor pulmonale.
9.Identify the causative factors, clinical manifestations, and
nursing and interprofessional management of patients
with environmental lung diseases.
10.State lung disorders in which lung transplantation
may be a treatment option, explaining the nursing and
interprofessional management of the transplant patient.
11.Describe the etiology, risk factors, pathophysiology,
clinical manifestations, and interprofessional and nursing
management of the patient with lung cancer.
KEY TERMS
acute bronchitis
community-acquired pneumonia (CAP)
cor pulmonale
empyema
flail chest
hemothorax
hospital-acquired pneumonia (HAP)
lung abscess
pertussis
pleural effusion
pleurisy (pleuritis)
pneumoconiosis
pneumonia
pneumothorax
pulmonary edema
pulmonary embolism (PE)
pulmonary hypertension
tension pneumothorax
tuberculosis (TB)
A variety of problems affect the lower respiratory system. This
chapter discusses lower respiratory tract diseases that influence gas exchange. We will focus on infectious, restrictive,
traumatic, vascular, environmental, and oncologic problems
that have the potential to impair gas exchange. Left untreated,
many of these conditions will have profound consequences for
the patient, as adequate oxygenation and ventilation are both
essential for life.
596
CHAPTER 30
Lower Respiratory Problems
597
LOWER RESPIRATORY TRACT INFECTIONS
PERTUSSIS
Lower respiratory tract infection is a common and serious
problem. It is the reason for thousands of clinic and emergency
department (ED) visits and hospital admissions each year. In
the United States, pneumonia and influenza cause around
50,000 deaths each year.1
Pertussis is a highly contagious respiratory tract infection. It is
caused by the gram-negative bacillus Bordetella pertussis. The
bacteria attach to the cilia of the respiratory tract and release
toxins that damage the cilia, causing inflammation and swelling.
Cases of pertussis have been steadily increasing in the United
States since the 1980s.2 The largest increase is in teens and
adults. We think that immunity from childhood tetanus, diphtheria, and pertussis vaccine (Tdap) vaccination may decrease
over time, allowing a milder (but still contagious) infection to
occur. The Centers for Disease Control and Prevention (CDC)
currently recommends that all adolescents (11 years and older)
and adults who have not received a dose of Tdap receive a onetime vaccination as soon as possible.3
Manifestations of pertussis occur in stages. The 1st stage,
lasting 1 to 2 weeks, manifests as a mild upper respiratory
tract infection (URI) with a low-grade or no fever, runny nose,
watery eyes, malaise, and mild, nonproductive cough. The 2nd
stage, from the 2nd to 10th weeks of infection, is characterized
by paroxysms of cough. The last stage lasts 2 to 3 weeks. The
cough is less severe. The patient may still be weak.
The hallmark characteristic of pertussis is uncontrollable, violent coughing. Inspiration after each cough produces the typical
“whooping” sound as the patient tries to breathe in air against an
obstructed glottis. The “whoop” is often not present in teens and
adults (especially those who are vaccinated). Coughing is more frequent at night. Vomiting may occur with coughing. Unlike acute
bronchitis, the cough with pertussis may last from 6 to 10 weeks.
In the community, diagnosis is mainly by history and
assessment. In the acute care setting, the CDC recommends
nasopharyngeal cultures, polymerase chain reaction (PCR) of
nasopharyngeal secretions, or serology testing.4 The treatment
is macrolide (erythromycin, azithromycin) antibiotics to minimize symptoms and prevent disease spread (see Table 15.8). For
the patient who cannot take macrolides, trimethoprim/sulfamethoxazole is used.
The patient is infectious from the beginning of the 1st stage
through the 3rd week after onset of symptoms or until 5 days
after starting antibiotic therapy. Place hospitalized patients on
droplet precautions. Patients should not use cough suppressants
and antihistamines as they are ineffective and may cause coughing. Corticosteroids and bronchodilators are also not helpful.
The CDC recommends antibiotic therapy for those who had
close contact with the patient.
ACUTE BRONCHITIS
Acute bronchitis is a self-limiting inflammation of the bronchi in the lower respiratory tract. It is the reason for 2.7 million
outpatient clinic visits and 4 million ED visits per year. Viruses
cause most acute bronchial infections. Air pollution, dust, inhalation of chemicals, smoking, chronic sinusitis, and asthma are
other triggers.
Cough is the most common symptom. It may last for up
to 3 weeks and is the main reason for seeking medical care.
Coughing is more frequent at night. When present, sputum
is often clear, although some patients have purulent sputum.
Other symptoms may include headache, fever, malaise, hoarseness, myalgias, dyspnea, and chest pain.
Diagnosis is based on the assessment. Assessment may reveal
normal breath sounds or crackles or wheezes, usually on expiration and with exertion. Consolidation (when fluid accumulates
in the lungs), suggestive of pneumonia, is absent with bronchitis. Chest x-rays are normal and not needed unless we suspect
pneumonia or some other lung problem.
The goal of treatment is to relieve symptoms and prevent
pneumonia. Treatment is supportive. It includes cough suppressants (e.g., dextromethorphan), encouraging oral fluid intake,
and using a humidifier. Throat lozenges, hot tea, and honey may
help relieve cough. β2-agonist (bronchodilator) inhalers are useful for patients with wheezes or underlying lung problems. We
do not prescribe antibiotics for viral infections because they are
not effective against viruses and giving them promotes antibiotic resistance. Antibiotics may be given to patients with underlying chronic conditions who are at risk for or have a prolonged
infection with systemic symptoms.
Encourage patients to not smoke, avoid secondhand smoke,
and wash their hands often (Box 30.1). If acute bronchitis is
due to influenza, we may start treatment with antiviral drugs.
If patients with acute bronchitis develop a fever, have trouble
breathing, or have symptoms last longer than 4 weeks, they
should see their HCP.
BOX 30.1
HEALTH
PROMOTING POPULATION
Preventing Respiratory Diseases
• Wash hands often to prevent and avoid spreading infections.
• Get a Tdap, pneumococcal, COVID, and flu vaccines as directed by the HCP.
• Avoid smoking and exposure to environmental smoke.
• Wear proper personal protective equipment (PPE) when working in an occupation with prolonged exposure to dust, fumes, or gases.
• Avoid exposure to allergens, indoor pollutants, and ambient air pollutants.
PNEUMONIA
Pneumonia is an acute infection of the lung parenchyma.
Despite progress in antibiotic therapy to treat pneumonia, pneumonia still has significant morbidity and mortality. Pneumonia
and lower respiratory tract infections were the 4th leading cause
of death worldwide in 2019.5
Etiology
Normally, various defense mechanisms protect the airway
distal to the larynx from infection. Mechanisms that create a
598
SECTION 6
Problems of Oxygenation: Ventilation
mechanical barrier to microorganisms entering the tracheobronchial tree include air filtration, epiglottis closure over the
trachea, cough reflex, mucociliary escalator mechanism, and
reflex bronchoconstriction. Immune defense mechanisms
include secretion of immunoglobulins A and G and alveolar
macrophages.
Pneumonia is more likely to occur when defense mechanisms become incompetent or are overwhelmed by the virulence or quantity of infectious agents. A weakened cough or
epiglottal reflex may allow aspiration of oropharyngeal contents
into the lungs. Tracheal intubation bypasses normal filtration
processes and interferes with the cough reflex and mucociliary
escalator mechanism. Air pollution, smoking, viral URIs, and
normal changes that occur with aging can impair the mucociliary mechanism. Chronic diseases can suppress the immune
system’s ability to inhibit bacterial growth. Risk factors for
pneumonia are listed in Table 30.1.
Pathogens that cause pneumonia reach the lung in 3 ways:
1.Aspiration of normal flora from the nasopharynx or oropharynx. Many organisms that cause pneumonia are normal
inhabitants of the mouth and pharynx in healthy adults.
2.Inhalation of microbes present in the air. Examples include
Mycoplasma pneumoniae and fungal pneumonias.
3.Hematogenous spread from a primary infection elsewhere in
the body. One example is Staphylococcus aureus from infective endocarditis.
Classifications of Pneumonia
There is no universally accepted classification system for pneumonia. Some classify pneumonia by the causative pathogens
(e.g., bacterial, viral, fungal), disease characteristics, or appearance on chest x-ray. The most widely recognized and effective
way to classify pneumonia is as either community-acquired or
hospital-acquired pneumonia. This classification helps the HCP
TABLE 30.1
Risk Factors for Pneumonia
• Abdominal or chest surgery
• Age >65 years
• Air pollution
• Altered level of consciousness (e.g., head injury, seizures, anesthesia,
drug overdose, stroke)
• Bed rest and prolonged immobility
• Chronic diseases: chronic lung and liver disease, diabetes, heart disease,
cancer, chronic kidney disease
• Debilitating illness
• Enteral feedings via naso- or orogastric or intestinal tubes
• Exposure to bats, birds, rabbits, and farm animal feces
• Immunosuppressive conditions and/or therapy (e.g., corticosteroids, cancer chemotherapy, HIV infection, immunosuppressive therapy after organ
transplant)
• Inhalation or aspiration of noxious substances
• IV drug use
• Malnutrition
• Resident of a long-term care facility
• Smoking
• Tracheal intubation (endotracheal intubation, tracheostomy)
• URI
identify the most likely cause (Table 30.2) and the choice of antimicrobial therapy.
Community-Acquired Pneumonia
Community-acquired pneumonia (CAP) is an acute lung
infection that occurs in patients who have not been hospitalized
or lived in a long-term care facility within 14 days of symptom
onset. The decision to treat the patient at home or admit to a
hospital is based on several factors. These include the patient’s
age, vital signs, mental status, presence of co-morbid conditions, and condition. We can use various tools (Table 30.3) to
support clinical judgment.
Hospital-Acquired Pneumonia
Hospital-acquired pneumonia (HAP), or nosocomial pneumonia, is pneumonia in a non-intubated patient that begins 48
hours or longer after admission to hospital and was not present when they were admitted. Ventilator-associated pneumonia
TABLE 30.2
Organisms Causing Pneumonia
Community-Acquired Pneumonia (CAP)
Typical
• Escherichia coli
• Haemophilus influenzaea
• Klebsiella pneumoniaea
• Methicillin resistant staphylococcus aureus (MRSA)
• Moraxella catarrhalis
• Pseudomonas
• Staphylococcus aureusa
• Streptococcus pneumoniaea
Atypical
• Chlamydophila pneumoniae
• Coxiella burnettii
• Influenza A and B
• Legionella pneumophilia
• Mycoplasma pneumoniae
• Mycobacterium tuberculosis
Respiratory Viruses
• Parainfluenza virus
• Respiratory syncytial virus
• Rhinovirus
Other Causes of CAP
• Fungi
• Oral anaerobes
Hospital-Acquired Pneumonia (HAP)
• Escherichia colib
• Haemophilus influenzae
• Klebsiella pneumoniaeb
• Microaspiration of bacteria that colonize the mouth, oropharynx
• Pseudomonas aeruginosab
• Proteus species
• Serratia marcescens
• Staphylococcus aureus
• Streptococcus pneumoniaea
aMost common cause of CAP.
bMost common causes of HAP.
CHAPTER 30
TABLE 30.3
Pneumonia Severity Index (PSI)
The PSI can supplement clinical judgment to determine the severity of
pneumonia and if patients need to be hospitalized.
Factor
Points
Demographics
Age in years
Women
Extended care resident
– 10
+10
Other Conditions
Stroke, kidney disease, heart failure
Active cancer
Liver disease
+10 each
+30
+20
Assessment
Respiratory rate ≥30/min, BP < 90, altered
mental status
Pulse 125/min
Temperature <95°F (35°C) or ≥104°F (4O°C)
Pleural effusion
+20 each
+10
+15
+10
Laboratory Results
pH < 7.35
BUN ≥30 mg/dL, Sodium <130 mEq/L
Glucose 250 mg/dL, Hematocrit < 30%,
pAO2 <60 mm Hg or O2 <90 percent
Scoring:
<70 points
71-90 points
>91 points
+30
+20 each
+10 each
Outpatient
Outpatient vs.
Observation
Inpatient
Source: Community-acquired pneumonia severity index (PSI) for
adults. Retrieved from https://www.clinicalkey.com/#!/tools/calculators/calculator/77-s2.0-99.
(VAP), a type of HAP, refers to pneumonia that occurs more
than 48 hours after endotracheal intubation.6 VAP is discussed
in Chapter 28. Both HAP and VAP are associated with longer
hospital stays, increased associated costs, sicker patients, and
increased mortality.
Once the diagnosis of CAP, HAP, or VAP is made, treatment
is started based on risk factors, speed of onset, clinical presentation, underlying medical conditions, hemodynamic stability,
and the most likely causative pathogen. Empiric antibiotic therapy, the initiation of treatment before a definitive diagnosis or
causative agent is made, should be started as soon as pneumonia
is suspected. Empiric antibiotic therapy is based on the drugs
known to be effective for the most likely cause. Antibiotic therapy is adjusted once the results of sputum cultures identify the
exact pathogen causing the infection.
Types of Pneumonia
There are several types of pneumonia. Viral pneumonia is the
most common type. It occurs in one third of all pneumonia
cases. It may be mild and self-limiting or cause potentially
life-threatening problems, such as acute respiratory failure
(ARF) in influenza. Patients with bacterial pneumonia may be
extremely unwell and need hospital admission. Mycoplasma
Lower Respiratory Problems
599
pneumonia, which has traits of both bacteria and viruses, is
often called “atypical” pneumonia. It is mild and occurs in persons younger than 40 years of age.
Aspiration Pneumonia
Aspiration pneumonia results from the abnormal entry of
material from the mouth or stomach into the trachea and
lungs. Conditions that increase the risk for aspiration include
decreased level of consciousness (e.g., seizure, anesthesia, head
injury, stroke, alcohol use), swallowing problems, and having
a nasogastric (NG) tube with or without enteral feeding. With
loss of consciousness, the gag and cough reflexes are depressed,
making aspiration more likely.
The aspirated material (food, water, vomitus, oropharyngeal
secretions) triggers an inflammatory response. The most common form of aspiration pneumonia is a primary bacterial infection. Typically, the sputum culture shows more than 1 organism,
including aerobes and anaerobes, since they both make up the
flora of the oropharynx.
Until cultures are done and results obtained, initial antibiotic
therapy is based on an assessment of probable cause, severity
of illness, and patient factors (e.g., malnutrition, current use
of antibiotic therapy). For patients who aspirate in hospitals,
antibiotic coverage should include both gram-negative organisms and methicillin-resistant Staphylococcus aureus (MRSA).
Aspiration of acidic gastric contents can cause chemical (noninfectious) pneumonitis, which may not need antibiotic therapy. However, secondary bacterial infection can occur in these
patients 48 to 72 hours later.
Necrotizing Pneumonia
Necrotizing pneumonia is a rare complication of bacterial lung
infection. It causes the lung tissue to turn into a thick, liquid
mass. Cavitation and lung abscesses can occur. This sometimes
happens with CAP. We do not know the exact mechanisms
involved. Common causative organisms include Staphylococcus,
Klebsiella, and Streptococcus. Signs and symptoms include respiratory insufficiency and/or failure, leukocytosis, and abnormalities on chest imaging.7 Treatment includes long-term antibiotic
therapy and possible surgery.
Opportunistic Pneumonia
Opportunistic pneumonia is inflammation and infection of
the lower respiratory tract in immunocompromised patients.
Persons at risk include those with altered immune responses.
This can include people with severe protein-calorie malnutrition or immunodeficiencies (e.g., human immunodeficiency
virus [HIV] infection) and those receiving radiation therapy,
chemotherapy, and any immunosuppressive therapy, including
long-term corticosteroid therapy. In addition to the risk for bacterial and viral pneumonia, the immunocompromised person
may develop an infection from organisms that do not normally
cause disease, such as Pneumocystis jiroveci pneumonia (PJP) or
cytomegalovirus (CMV).8
PJP is occurring with greater frequency in HIV-negative,
immunocompromised persons.8 The onset is slow and subtle. Symptoms include fever, tachypnea, tachycardia, dyspnea,
600
SECTION 6
Problems of Oxygenation: Ventilation
Inflammatory response
• Attraction of neutrophils
• Release of inflammatory mediators
• Accumulation of fibrinous exudates,
red blood cells, and bacteria
Alveoli fill with fluid and debris
(consolidation)
Increased production of mucus
(airway obstruction)
Decreased gas exchange
A
A
A
B
Fig. 30.2 Atelectasis. Scanning electron micrograph of lung parenchyma. (A) Alveoli (A) and alveolar-capillary membrane (arrow). (B)
Effects of atelectasis. Alveoli (A) are partially or totally collapsed. (A,
From Dantzker DR, Bone RC, George RB, editors: Pulmonary and critical care medicine, vol 1, St Louis, 1993, Mosby. B, From Albertine KH,
Williams MC, Hyde DM: Anatomy of the lungs. In RJ Mason, VC Broaddus, JF Murray, et al., editors: Murray and Nadel’s textbook of respiratory medicine, ed 4, Philadelphia, 2005, Saunders.)
Resolution of infection
• Macrophages in alveoli ingest and
remove debris
• Normal lung tissue restored
• Gas exchange returns to normal
Fig. 30.1 Pathophysiologic course of pneumonia.
nonproductive cough, and hypoxemia. The chest x-ray usually
shows diffuse bilateral infiltrates. In widespread disease, the
lungs have massive consolidation.
PJP can be life-threatening, causing ARF and death. Infection
can spread to other organs, including the liver, bone marrow,
lymph nodes, spleen, and thyroid. Bacterial and viral pneumonias first must be ruled out because of the vague presentation
of PJP. Although the causative agent is fungal, PJP does not
respond to antifungal agents. Treatment consists of IV or oral
trimethoprim/sulfamethoxazole, depending on the severity of
disease, overall clinical condition, and the patient’s response.
CMV, a herpes virus, can cause viral pneumonia. Most CMV
infections are asymptomatic or mild. Severe disease can occur
in people with an impaired immune response. CMV is one of
the most important life-threatening infectious complications
after hematopoietic stem cell transplant.9 Antiviral medications
(e.g., ganciclovir, cidofovir) and high-dose immunoglobulin are
part of treatment.
Pathophysiology
Specific pathophysiologic changes related to pneumonia vary
depending on the offending pathogen. Almost all pathogens
trigger an inflammatory response in the lungs (Fig. 30.1).
Inflammation, characterized by an increase in blood flow and
vascular permeability, activates neutrophils to engulf and kill
the offending pathogens. As a result, the inflammatory process attracts more neutrophils, airway edema occurs, and fluid
leaks from the capillaries and tissues into alveoli. Normal O2
transport is affected, leading to manifestations of hypoxia (e.g.,
tachypnea, dyspnea, tachycardia).
Atelectasis, the absence of gas or air in 1 or more areas of
the lung, may occur with pneumonia (Fig. 30.2). Atelectasis
may be asymptomatic. Some patients have extreme shortness
of breath and severe chest pain. Consolidation, a feature typical of bacterial pneumonia, occurs when the normally air-filled
Fig. 30.3 Chest x-ray of a patient with acute bacterial pneumonia. (©
iStock.com/stockdevil.)
alveoli become filled with water, fluid, and/or debris (Fig. 30.3).
This can potentially obstruct airflow, impair gas exchange, and
cause significant respiratory insufficiency. Over time and with
appropriate antibiotic therapy, macrophages lyse and process
the debris. This allows lung tissue to recover and gas exchange
to return to normal.
Clinical Manifestations
The most common presenting symptoms of pneumonia are
cough, fever, chills, dyspnea, tachypnea, and pleuritic chest
pain. The cough may or may not be productive. Sputum may be
green, yellow, or even rust colored (bloody). Viral pneumonia
may initially be seen as influenza, with respiratory symptoms
appearing and/or worsening 12 to 36 hours after onset.
The older or debilitated patient may not have classic symptoms of pneumonia. Confusion or stupor (possibly related to
hypoxia) may be the only finding. The older adult may have
CHAPTER 30
hypothermia, rather than fever. Nonspecific manifestations
include diaphoresis, anorexia, fatigue, myalgias, and headache.
Fine or coarse crackles may be auscultated over the affected
region. If consolidation is present, bronchial breath sounds,
egophony (an increase in the sound of the patient’s voice), and
increased fremitus (chest wall vibrations made by vocalization)
may be present. Patients with pleural effusion may have dullness
to percussion over the affected area.
Complications
A major problem today is pneumonia caused by multidrug-resistant (MDR) pathogens. Common culprits include MRSA
and gram-negative bacilli. Risk factors for MDR pneumonia
include advanced age, immunosuppression, history of antibiotic use, and prolonged mechanical ventilation. Antibiotic susceptibility tests can identify MDR pathogens. The virulence of
these pathogens can severely limit the available and appropriate
antimicrobial therapy. MDR pathogens increase mortality from
pneumonia.
Other complications from pneumonia develop more often in
older adults and those with underlying chronic diseases. These
include:
• Pleurisy, inflammation of the pleura.
• Pleural effusion, or fluid in the pleural space. In most cases,
the effusion is sterile and reabsorbed in 1 to 2 weeks. Sometimes, effusions require aspiration by thoracentesis.
• Bacteremia, bacterial infection in the blood, is more likely to
occur in infections with Streptococcus pneumoniae and Haemophilus influenzae.
• Pneumothorax can occur when air collects in the pleural
space, causing the lungs to collapse.
• ARF is a leading cause of death in patients with severe pneumonia. ARF occurs when pneumonia damages the lungs’
ability to exchange O2 and CO2 across the alveolar-capillary
membrane.
• Sepsis can occur when bacteria within alveoli enter the
bloodstream. Severe sepsis can lead to shock and multisystem organ dysfunction syndrome (MODS) (see Chapter 42).
Lung abscess is not a common complication of pneumonia. It
may occur with pneumonia caused by S. aureus and gram-negative organisms. Empyema, the accumulation of purulent exudate in the pleural cavity, may occur in up to 20% of cases. It
requires antibiotic therapy and drainage of the exudate by a
chest tube or open surgical drainage. Pleurisy, pleural effusion,
and lung abscess are discussed later in this chapter.
Diagnostic Studies
The common diagnostic procedures for pneumonia are outlined
in Table 30.4. History, physical assessment, and chest x-ray often
give enough information to make immediate decisions about
early treatment. Chest x-ray often shows patterns characteristic of
the infecting pathogen and is important in diagnosing pneumonia. X-ray may also show pleural effusions. Bronchoscopy with
bronchial washings or thoracentesis may be done to obtain cell
and fluid samples from patients not responding to initial therapy.
Arterial blood gases (ABGs) may show hypoxemia, hypercapnia, and acidosis. Leukocytosis occurs in most patients with
Lower Respiratory Problems
TABLE 30.4
Pneumonia
601
Interprofessional Care
Diagnostic Assessment
• History and physical assessment
• Chest x-ray
• Sputum: Gram stain, culture and sensitivity test
• Pulse oximetry and/or ABGs
• CBC, white blood cell differential, and routine blood chemistries
• Blood cultures (if indicated)
Management
• O2 therapy
• Critical care management, with mechanical ventilation as needed
• Increased fluid intake (at least 2–3 L/day), IV fluids
• VTE prophylaxis
• Physiotherapy, early mobility
• Balance between activity and rest
Drug Therapy
• Appropriate antibiotic therapy (Table 30.6)
• Antipyretics
• Analgesics
• NSAIDs (if no contraindications)
bacterial pneumonia. The white blood cell (WBC) count is usually greater than 15,000/μL (15 × 109/L) with the presence of
bands (immature neutrophils). Ideally, we should obtain a sputum specimen for culture and Gram stain to identify the organism before starting antibiotic therapy. However, we should not
delay starting antibiotic therapy if we cannot obtain a specimen.
Delays in antibiotic therapy can increase the risk for mortality.
Blood cultures are done for patients who are seriously ill.
C-reactive protein (CRP), procalcitonin, and interleukin 6
(IL-6) are currently being explored as ways to help tell pneumonia from other types of heart and respiratory failure.10
Interprofessional Care
Prompt treatment with the appropriate antibiotic is essential.
Antibiotics are highly effective for both bacterial and mycoplasma
pneumonia. In uncomplicated cases, the patient responds to drug
therapy within 48 to 72 hours. Signs of improvement include
decreased temperature, improved breathing, and less chest discomfort. Abnormal physical findings can last more than 7 days.
Pneumococcal vaccine is used to prevent S. pneumoniae infection (Table 30.5). Although cough suppressants, mucolytics, bronchodilators, and corticosteroids are often prescribed as adjunctive
therapy, the use of these drugs is debatable. However, they may be
prescribed for patients with underlying chronic conditions.
Currently, there is no definitive treatment for most viral
pneumonias. Care is generally supportive. In most circumstances, viral pneumonia is self-limiting and will often resolve
in 3 to 4 days. Antiviral therapy may be used to treat pneumonia
caused by influenza (e.g., oseltamivir, zanamivir) or a few other
viruses (e.g., acyclovir for herpes simplex virus).
Drug Therapy
The HCP selects empiric therapy based on the likely pathogen. Table 30.6 presents the drug therapy for bacterial CAP.
602
SECTION 6
TABLE 30.5
Problems of Oxygenation: Ventilation
Pneumococcal Vaccines
Vaccinea
Recommendations for Use
Pneumococcal conjugate
vaccine (PCV13,
Prevnar 13):
Protect against 13 types
of pneumococcal
bacteria
• Children <2 years
• Adults ≥65 years
• Anyone 2–64 years old with certain medical
conditions (e.g., sickle cell disease, asplenia,
immunodeficiencies, HIV infection, chronic
kidney disease, leukemia, cancer, long-term
immunosuppressive therapy)
• Adults ≥50 years
• Adults 19–64 years old who smoke
• Anyone 2–64 years old who have high risk of
pneumococcal disease (e.g., heart disease, lung
disease, diabetes, alcohol use, cirrhosis, sickle
cell disease, immunocompromised, cancer)
Pneumococcal
polysaccharide vaccine
(PPSV23, Pneumovax
23): Protect against 23
types of pneumococcal
bacteria
aFor more details on scheduling of pneumococcal vaccinations, see
https:www.cdc.gov/pneumococcal/vaccination.html.
TABLE 30.6 Drug Therapy
Bacterial Community-Acquired Pneumonia
Patient Variable
Treatment Options
Outpatient
Healthy
No comorbidities or risk factors for
antibiotic-resistant infection
Beta lactam OR Macrolide OR
­doxycycline
Co-Morbidities
COPD; diabetes; chronic liver,
lung, heart, or renal disease;
cancer; alcohol use; no spleen
Inpatient
Medical Unit
ICU
Special Considerations
•Community-acquired methicillin-resistant Staphylococcus
aureus (CA-MRSA)
•Pseudomonas infection
•Pseudomonas infection in
patient with penicillin allergy
Respiratory fluoroquinolone OR β-Lactam plus macrolide (doxycycline may
be substituted for macrolide)
OR
Beta lactam plus doxycycline plus
macrolide
Respiratory fluoroquinolone OR β-Lactam plus macrolide (doxycycline may
be substituted for macrolide)
β-Lactam plus either azithromycin or
respiratory fluoroquinolone
Vancomycin or linezolid (Zyvox)
Antipneumococcal and antipseudomonal
β-lactam OR
Antipneumococcal, antipseudomonal
β-lactam plus either respiratory fluoroquinolone or ciprofloxacin or levofloxacin
OR Antipneumococcal, antipseudomonal
β-lactam plus aminoglycoside plus either
ciprofloxacin or levofloxacin
Substitute aztreonam for the above
β-lactam
Source: Community acquired pneumonia in adults. Retrieved from https://
www.clinicalkey.com/#!/content/clinical_overview/67-s2.0-77188ebde5b9-49a1-88a0-0211995a4b85#treatment-options-heading-35.
For all types of pneumonia, empiric antibiotic therapy is
based on whether the patient has risk factors for MDR
pathogens. The prevalence and resistance patterns of MDR
pathogens vary among localities and agencies. Therefore,
antibiotic therapy must be adapted to local patterns of antibiotic resistance. Multiple regimens exist. All treatment
should initially include antibiotics that are effective against
both resistant gram-negative and resistant gram-positive
organisms.
Clinical improvement usually occurs in 3 to 5 days. Patients
who do not respond to therapy or deteriorate need aggressive
re-evaluation to assess for noninfectious causes, complications,
coexisting infectious processes, or pneumonia caused by an
MDR pathogen.
We switch the patient from IV to oral antibiotic therapy as
soon as they are improving clinically and able to take oral medication. Stable patients can be discharged on oral antibiotics.
Total treatment time for patients with CAP should be a minimum of 5 days. The patient should be afebrile for 48 to 72 hours
before stopping treatment. Stress the importance of completing
the full course of antibiotic treatment. Longer treatment time
may be needed if initial therapy was not active against the identified pathogen or complications occur.
Nutrition Therapy
Hydration is important to prevent dehydration and thin and
loosen secretions. Carefully monitor fluid intake. If the patient
is an older adult, has heart failure (HF), or has a known preexisting respiratory condition, administer IV fluids carefully to
avoid fluid overload. Pay close attention to intake and output.
Monitor and replace electrolytes as needed.
Weight loss may occur in patients with pneumonia because
of increased metabolic needs, difficulty eating due to dyspnea,
nonspecific abdominal symptoms, and activity intolerance.
Small, frequent meals are easier for dyspneic patients to tolerate. Offer foods high in calories and nutrients. A nutrition
assessment by a dietitian may be done on admission to acute
care.
NURSING MANAGEMENT: PNEUMONIA
Assessment
Table 30.7 presents subjective and objective data to obtain from
a patient with pneumonia.
Clinical Problems
Clinical problems for the patient with pneumonia may include:
• Impaired respiratory function
• Infection
• Fluid imbalance
• Activity intolerance
• Altered body temperature
Additional information on clinical problems and interventions for the patient with pneumonia is shown in eNursing Care
Plan 30.1 on the website for this chapter.
Planning
The overall goals are that the patient with pneumonia will have
(1) no signs of hypoxemia, (2) normal breathing patterns, (3)
clear breath sounds, (4) normal chest x-ray, (5) normal WBC
count, and (6) no complications.
CHAPTER 30
Lower Respiratory Problems
603
TABLE 30.7 NURSING ASSESSMENT
Pneumonia
TABLE 30.8 NURSING MANAGEMENT
Care of the Patient With Pneumonia
Subjective Data
Important Health Information
Health history: Lung cancer, COPD, diabetes, chronic debilitating disease,
malnutrition, immunosuppression, exposure to chemical toxins, dust, or
allergens
Medications: Antibiotics, corticosteroids, chemotherapy, or any immunosuppressants
Surgery or other treatments: Recent abdominal or chest surgery, splenectomy,
endotracheal intubation, enteral feedings, or any surgery with general
anesthesia.
• Monitor respiratory status:
•Breath sounds, noting areas of decreased or absent ventilation, and
presence of adventitious sounds.
•Rate, rhythm, depth, and effort of respirations.
•Characteristics of any secretions.
•Ability to cough effectively and presence of fatigue.
•Assess for signs of hypoxemia.
•Administer antibiotic and IV fluid therapy as ordered.
•Administer medications (e.g., bronchodilators and inhalers) to promote airway patency and gas exchange.
•Keep the head of the bed elevated at least 30 degrees.
•Turn and reposition the patient every 2 hrs to promote lung expansion and
mobilize secretions.
•Encourage the patient to cough, deep breathe, and use the incentive spirometer.
•Implement measures to manage fever (see Table 12.5).
•Administer analgesics as ordered to relieve pain.
•Provide ordered VTE and GI prophylaxis.
•Monitor intake and output.
•Supervise AP:
•Obtain vital signs and report to RN.
•Provide personal hygiene, skin care, and oral care
•Assist with frequent position changes, including early mobility
•Report to RN any change in patient condition.
Functional Health Patterns
Health perception–health management: Smoking, alcohol use, illicit drug use,
recent tract URI, malaise
Nutritional-metabolic: Anorexia, nausea, vomiting
Activity-exercise: Prolonged bed rest or immobility. Fatigue, weakness. Dyspnea, cough.
Cognitive-perceptual: Pain with breathing, nasal congestion, chest pain, sore
throat, headache, abdominal pain, muscle aches
Objective Data
Cardiovascular
•Tachycardia
General
•Fever, restlessness, or lethargy. Splinting of thoracic cavity
Neurologic
•Changes in mental status, ranging from confusion to delirium
Respiratory
•Tachypnea, pharyngitis
•Asymmetric chest movements or retraction, decreased excursion
•Nasal flaring, use of accessory muscles (neck, abdomen)
•Crackles, friction rub on auscultation, dullness on percussion over consolidated areas, ↑ tactile fremitus on palpation
•Pink, rusty, purulent, green, yellow, or white sputum (amount may be scant
to copious)
Possible Diagnostic Findings
•Leukocytosis, positive sputum on Gram stain and culture, Patchy or diffuse
infiltrates, abscesses, pleural effusion, or pneumothorax on chest x-ray
•leftAbnormal ABGs with ↓ or normal PaO2, ↓ or normal PaCO2, and ↑ or
normal pH initially, and later ↓ PaO2, ↑ PaCO2, and ↓ pH
Implementation
Health Promotion
To reduce the risk for pneumonia, teach patients to practice good
health habits, such as frequent hand washing, good nutrition,
adequate rest, regular exercise, and coughing or sneezing into the
elbow rather than hands. Avoiding smoking is one of the most
important health-promoting behaviors. If possible, avoid exposure
to people with URIs. If a URI occurs, it requires prompt attention
with supportive measures (e.g., rest, fluids). If symptoms persist for longer than 7 days, the person should seek medical care.
Identifying patients at risk and taking measures to prevent pneumonia are important. Encourage those at risk for pneumonia (e.g.,
chronically ill, older adult) to obtain needed vaccines.
Collaborate With Respiratory Therapist
•Apply O2 therapy as ordered.
•Perform chest physiotherapy (e.g., percussion, postural drainage).
Collaborate With Dietitian
•Assess and monitor nutrition status.
•Recommend optimal diet.
Collaborate With Physical and Occupational Therapist
•Perform ROM exercises.
•Assist with early and progressive ambulation.
Acute Care
Nursing care for the patient with pneumonia is outlined in Table
30.8. Although many patients with pneumonia are treated on an
outpatient basis, the nursing care plan for a patient with pneumonia (see eNursing Care Plan 30.1) applies to both patients at
home and hospitalized.
Essential nursing care for hospitalized patients with
pneumonia includes monitoring assessment findings and
the response to therapy. We provide supportive measures
according to the patient’s needs. These may include O2
therapy to treat hypoxemia and analgesics to relieve chest
pain. Implement measures to reduce fever (see Table 12.5).
Prompt collection of specimens and timely administration
of antibiotics is critical. Hydration, nutrition support, and
positioning are part of the care plan. Work with the respiratory therapist to monitor the patient’s condition and provide
chest physiotherapy.
Balance rest and activity to each patient’s tolerance. Benefits
of early mobility include improved lung and chest expansion,
mobilization of secretions, and prevention of venous stasis.
604
SECTION 6
Problems of Oxygenation: Ventilation
Practice strict medical asepsis and adherence to infection
control guidelines to reduce the incidence of possible transmission between staff and patients. Staff and visitors should wash
their hands when entering and leaving the patient’s room. Staff
must wash hands or use hand sanitizer before and after providing care and on removing gloves.
Implement measures to reduce the incidence of pneumonia
in patients at higher risk. To prevent aspiration in the patient
who has problems swallowing, elevate the head-of-bed to at
least 30 degrees. Assess for presence of a gag reflex before giving food or fluids. Patients who have an orogastric or NG tube
are at risk for aspiration pneumonia. Although feeding tubes are
small, any interruption in the integrity of the lower esophageal
sphincter can allow reflux of gastric contents. Elevating the head
of the bed can help prevent this complication.
After surgery, treat pain to a comfort level that permits the
patient to deep breathe and cough yet remain awake and alert
and achieve optimum mobility. Twice-daily oral hygiene with
chlorhexidine swabs reduces the risk of pneumonia in postoperative patients.11
In the ICU, strictly adhere to the ventilator bundle (see Table
28.10), a group of interventions aimed at reducing the risk for
VAP. Maintain sterile aseptic technique when suctioning the
patient’s trachea. Use caution when handling ventilator circuits,
tracheostomy tubing, and nebulizer circuits that can become
contaminated from patient secretions.
Ambulatory Care
Teach the patient about the importance of taking every dose of
the prescribed antibiotic (see Table 15.9). Review any drug-drug
and food-drug interactions. Explain the need for adequate rest
to promote recovery. Tell the patient to drink plenty of liquids
(at least 6 to 10 glasses/day, unless contraindicated) and avoid
alcohol and smoking. A cool mist humidifier or warm bath may
help the patient breathe easier. Tell them that it may be several
weeks before their usual sense of well-being returns. Explain
that a follow-up chest x-ray may be done in 6 to 8 weeks to evaluate resolution of pneumonia. The older adult or chronically ill
patient may have a prolonged period of convalescence.
Teaching should include information about available influenza and pneumococcal vaccines. Patients can receive the pneumococcal vaccine and influenza vaccine at the same time but
not in the exact same location. The vaccines cannot be mixed
into 1 injection.
Evaluation
The expected outcomes are that the patient with pneumonia will
have:
• Effective respiratory rate, rhythm, and depth of respirations
• Lungs clear to auscultation
• No complications
TUBERCULOSIS
Tuberculosis (TB) is an infectious disease caused by
Mycobacterium tuberculosis. It usually involves the lungs, but
can infect any organ, including the brain, kidneys, and bones.
BOX 30.2
EQUITY
PROMOTING HEALTH
Tuberculosis
• 88% of TB cases in the United States occur in racial and ethnic minorities.
71.4% of these persons were born outside of the United States.
• Asians have the highest TB rate, followed by Hispanics (30%) and Blacks
(20%).
• American Indian/Alaska Natives, and Native Hawaiian/Pacific Islanders
have the lowest TB rates amongst all ethnic groups (1%).
Source: Centers for Disease Control and Prevention: Health disparities
in TB. Retrieved from https://www.cdc.gov/tb/topic/treatment/default.
htm.
About 25% of the world’s population is infected with TB.12 The
incidence of TB worldwide declined until the mid-1980s. We
are now seeing increasing rates of TB. This is attributed to HIV
disease and the emergence of drug-resistant strains of M. tuberculosis. TB is the leading cause of mortality in patients with HIV
infection.
TB occurs disproportionately in the poor, underserved, and
minorities (Box 30.2). People most at risk include the homeless,
residents of inner-city neighborhoods, foreign-born people,
those living or working in institutions (long-term care facilities,
prisons, shelters, hospitals), IV drug users, overcrowded living
conditions, less than optimal sanitation, and those with poor
access to health care. Immunosuppression from any cause (e.g.,
HIV infection, cancer, long-term corticosteroid use) increases
the risk for active TB infection.
Etiology and Pathophysiology
M. tuberculosis is a gram-positive, aerobic, acid-fast bacillus
(AFB). It is usually spread from person to person by airborne
droplets expectorated when breathing, talking, singing, sneezing, and coughing. A process of evaporation leaves small droplet
nuclei, 1 to 5 μm in size, suspended in the air for minutes to
hours. Another person then inhales the bacteria. Humans are
the only known reservoir for TB. TB is not highly infectious.
Transmission requires close contact and frequent or prolonged
exposure. TB does not spread by touching, sharing food utensils, kissing, or any other physical contact.
Factors that influence transmission include the (1) number
of organisms expelled into the air, (2) concentration of organisms (small spaces with limited ventilation would mean higher
concentration), (3) length of time of exposure, and (4) immune
system of the exposed person. Once inhaled, these small droplets lodge in bronchioles and alveoli. A local inflammatory reaction occurs, and the infection is established. This is called the
Ghon lesion or focus. It represents a calcified TB granuloma, the
hallmark of a primary TB infection. The formation of a granuloma is a defense mechanism aimed at walling off the infection
and preventing further spread. Bacillus replication is inhibited,
stopping the infection.
Most immunocompetent adults infected with TB can completely kill the mycobacteria. Some people have the mycobacteria in a non-replicating dormant state. Of these persons, 5%
to 10% develop active TB infection when the bacteria begin to
CHAPTER 30
TABLE 30.9
Classification of Tuberculosis
Class
Exposure or
Infection
0
No TB exposure
1
TB exposure,
no infection
Latent TB
infection, no
disease
2
3
TB, clinically
active
4
TB, but not
clinically active
5
TB suspect
Lower Respiratory Problems
605
Latent Tuberculosis Infection
(LTBI) Compared to Tuberculosis Disease
TABLE 30.10
Description
LTBI
TB Disease
No TB exposure, not infected (no history of
exposure, negative tuberculin skin test)
TB exposure, no evidence of infection (history
of exposure, negative tuberculin skin test)
TB infection without disease (positive reaction
to tuberculin skin test, negative bacteriologic
studies, no x-ray findings compatible with
TB, no clinical evidence of TB)
TB infection with clinically active disease
(positive bacteriologic studies or both a
significant reaction to tuberculin skin test and
clinical or x-ray evidence of current disease)
No current disease (history of previous
episode of TB or abnormal, stable x-ray
findings in a person with a positive
reaction to tuberculin skin test. Negative
bacteriologic studies if done. No clinical or
x-ray evidence of current disease)
TB suspect (diagnosis pending). Person
should not be in this classification for >3
months
Has no symptoms
Has symptoms that may include:
• Bad cough that lasts ≥3 week
• Pain in the chest
• Coughing up blood or sputum
• Weakness or fatigue
• Weight loss, no appetite
• Chills
• Fever
• Sweating at night
Usually feels sick
May spread TB bacteria to others
Usually has a positive TST or blood
test result showing TB infection
May have an abnormal chest x-ray or
positive sputum smear or culture
Needs treatment for active TB disease
multiply months or years later. While M. tuberculosis is aerophilic (O2 loving) and has an affinity for the lungs, the infection
can spread through the lymphatic system and find good environments for growth in other organs. These include the cerebral
cortex, spine, bone epiphyses, liver, kidneys, lymph nodes, and
adrenal glands.
Once a strain of M. tuberculosis develops resistance to the
first-line drug therapy (isoniazid and rifampin), it is defined
as multidrug-resistant tuberculosis (MDR-TB).13 Extensively
drug-resistant TB (XDR-TB) is a rare type of MDR-TB.
XDR-TB is also resistant to any fluoroquinolone and at least 1
second-line drug.13 Resistance results from several problems,
including incorrect prescribing, lack of case management, and
nonadherence to the prescribed regimen.
Classification
We use several systems to classify TB. The American Thoracic
Society classifies TB based on disease development (Table 30.9).
We also classify TB by (1) its presentation (primary, latent, reactivated) and (2) whether it is pulmonary or extrapulmonary.
Primary TB infection starts when the bacteria are inhaled and
trigger an inflammatory reaction. Most people have effective
immune responses that encapsulate the organisms for the rest
of their lives, preventing the initial infection from progressing
to disease. If the initial immune response is not adequate, the
body cannot contain the organism. As a result, the bacteria replicate and active TB disease results. When active disease develops within the first 2 years of infection, it is called primary TB.
People co-infected with HIV are at greatest risk for developing
active TB.
Post-primary TB, or reactivation TB, is defined as TB disease
occurring 2 or more years after the initial infection. If the site of
Does not feel sick
Cannot spread TB bacteria to others
Usually has a positive TST or blood
test result showing TB infection
Has a normal chest x-ray and a
negative sputum smear
Needs treatment for latent TB
infection to prevent active TB
disease
Source: Centers for Disease Control and Prevention. Tuberculosis (TB)
fact sheets: the difference between latent TB infection and TB disease. Retrieved from https://www.cdc.gov/tb/publications/factsheets/
general/ltbiandactivetb.htm.
TB is pulmonary or laryngeal, the person is infectious and can
transmit the disease to others.
Latent TB infection (LTBI) occurs in a person who does not
have active TB disease (Table 30.10). People with LTBI have a
positive skin test but are asymptomatic. They cannot transmit
the TB bacteria to others but can develop active TB disease later.
Immunosuppression, diabetes, poor nutrition, HIV, glucocorticoid therapy, pregnancy, stress, and chronic disease can reactivate the disease. Treatment of LTBI is as important as primary
TB.
Clinical Manifestations
Symptoms of pulmonary TB usually do not develop until 2 to
3 weeks after infection or reactivation. The primary manifestation is an initial dry cough. It often becomes productive with
mucoid or mucopurulent sputum. Active TB disease may initially present with constitutional symptoms (e.g., fatigue, malaise, anorexia, unexplained weight loss, low-grade fevers, night
sweats). Dyspnea is a late symptom that may signify considerable pulmonary disease or a pleural effusion. Hemoptysis is also
a late symptom.
Sometimes, TB has a more acute, sudden presentation. The
patient may have a high fever, chills, flu-like symptoms, pleuritic pain, a productive cough, and ARF. Lung auscultation
may be normal or reveal adventitious sounds, such as crackles.
Hypotension and hypoxemia may be present.
Immunosuppressed (e.g., HIV-infected) people and older
adults are less likely to have fever and other signs of an infection. In patients with HIV, classic manifestations of TB, such as
fever, cough, and weight loss, may be wrongly attributed to PJP
or other HIV-associated opportunistic diseases. Respiratory
problems in patients with HIV are assessed to determine the
606
SECTION 6
Problems of Oxygenation: Ventilation
cause. A change in cognitive function may be the only initial
presenting sign of TB in an older person.
The manifestations of extrapulmonary TB depend on the
organs infected. For example, renal TB can cause dysuria
and hematuria. Bone and joint TB may cause severe pain.
Headaches, vomiting, and lymphadenopathy may be present
with TB meningitis.
Complications
Properly treated, pulmonary TB typically heals without complications, except for scarring and residual cavitation within
the lung. Significant lung damage, although rare, can occur in
patients who are poorly treated or who do not respond to TB
treatment.
Miliary TB is widespread dissemination of the mycobacterium through the bloodstream to several distant organs. The
infection is characterized by a large amount of TB bacilli and
may be fatal if untreated. It can occur with primary disease
or reactivation of LTBI. Manifestations slowly progress over a
period of days, weeks, or even months. Symptoms vary depending on the organs that are affected. Fever, cough, and lymphadenopathy are present. Hepatomegaly and splenomegaly may
occur.
Pleural TB, a specific type of extrapulmonary TB, can result
from either primary disease or reactivation of a latent infection.
Chest pain, fever, cough, and a unilateral pleural effusion are
common. A pleural effusion is caused by bacteria in the pleural space, which trigger an inflammatory reaction and a pleural
exudate of protein-rich fluid. Empyema is less common than
effusion but may occur from large numbers of TB organisms in
the pleural space. Diagnosis is confirmed by AFB cultures and
a pleural biopsy.
Because TB can infect organs throughout the body, other
acute and long-term complications can result. TB in the spine
(Pott disease) can lead to destruction of the intervertebral disc
and adjacent vertebrae. Central nervous system (CNS) TB can
cause bacterial meningitis. Abdominal TB can lead to peritonitis, especially in HIV-positive patients. The kidneys, adrenal
glands, lymph nodes, and urogenital tract can be affected.
Diagnostic Studies
Tuberculin Skin Test
The tuberculin skin test (TST) (Mantoux test) using purified
protein derivative (PPD) is the standard method to screen people for M. tuberculosis. The test is given by injecting 0.1 mL of
PPD intradermally on the ventral surface of the forearm. We
read the test by inspection and palpation 48 to 72 hours later for
the presence or absence of induration. Induration, a palpable,
raised, hardened area or swelling (not redness) at the injection
site means the person has been exposed to TB and has developed antibodies. Antibody formation occurs 2 to 12 weeks after
initial exposure to the bacteria. Any indurated area present is
measured and recorded in millimeters. Based on the size of the
induration and risk factors, we make an interpretation based on
CDC standards for determining a positive test (see Table 27.15).
Two-step testing with the Mantoux test is recommended for
baseline or initial screening for health care workers and those
who have a decreased response to allergens. If the 1st test is positive, the person does not need the 2nd test. They do, however,
need further evaluation for active disease. If the 1st test is negative, a 2nd test is done 1 to 3 weeks later. Some people with
LTBI or who were previously infected with TB may have a falsenegative result with the 1st test. Repeating the test may stimulate (boost) the body’s ability to react in future tests.14 A positive
reaction to a subsequent test could be a new infection or the
result of the boosted reaction to an old infection. A previously
negative 2 step test ensures that any future positive results can
be accurately interpreted as being caused by a new infection.
Interferon-γ Release Assays
Interferon-γ (INF-γ) release assays (IGRAs) are another screening tool for TB. IGRAs are blood tests that detect INF-γ release
from T cells in response to M. tuberculosis.15 Examples of IGRAs
include QuantiFERON-TB Gold In-Tube test (QFT-GIT) and
the T-SPOT.TB test. Test results are available in a few hours.
IGRAs have several advantages over the TST. IGRAs
require only 1 patient visit, are not subject to reader bias, have
no “booster” phenomenon, and are not affected by bacillus
Calmette-Guérin (BCG) vaccination. The cost of an IGRA is
much higher than the TST. Guidelines suggest that both tests
are viable options. The choice should be based on context and
reasons for testing. Neither IGRAs nor TST can tell between
LTBI and active TB infection. LTBI can only be diagnosed by
excluding active TB.
Chest X-Ray
Although the chest x-ray findings are important, it is not possible to make a diagnosis of TB based solely on chest x-ray
findings. The chest x-ray may appear normal in a patient with
TB. Findings suggestive of TB include upper lobe infiltrates,
cavitary infiltrates, lymph node involvement, and pleural and/
or pericardial effusion. Other diseases, such as sarcoidosis, can
mimic the appearance of TB.
Bacteriologic Studies
Sputum culture is the gold standard for diagnosing TB. We need
3 consecutive sputum specimens, each collected at 8- to 24-hour
intervals, with at least 1 early morning specimen. The initial test
involves microscopic examination of stained sputum smears
for AFB. A definitive diagnosis of TB requires mycobacterial
growth, which can take up to 6 weeks. For patients in whom
suspicion of TB is high, treatment is started while waiting for
culture results. Samples for other suspected TB sites can be collected from gastric washings, cerebrospinal fluid (CSF), or fluid
from an effusion or abscess.
Interprofessional Care
Most patients with TB are treated on an outpatient basis (Table
30.11). Many people can continue to work and maintain their
lifestyles with few changes. Patients with sputum smear–positive TB are considered infectious for the first 2 weeks after
starting treatment. Advise these patients to restrict visitors, and
avoid travel, public transportation, and trips to public places.
Teach them the importance of good hand washing and oral
CHAPTER 30
Lower Respiratory Problems
TABLE 30.11 Interprofessional Care
Pulmonary Tuberculosis
TABLE 30.12
Tuberculosis
Diagnostic Assessment
• History and physical assessment
• Tuberculin skin test (TST)
• QuantiFERON-TB Gold In-Tube test (QFT-GIT) or T-SPOT.TB test
• Chest x-ray
• Bacteriologic studies
• Sputum smear for acid-fast bacilli (AFB)
• Sputum culture
Drug
Management
• Long-term treatment with antimicrobial drugs (Tables 30.12 and 30.13)
• Follow-up AFB smears, cultures, and chest x-rays
• Follow-up care, addressing needs and concerns of patient and close
contacts, and involving community health care workers and social workers
hygiene. Hospitalization may be needed for the severely ill or
debilitated patient.
Drug Therapy
Active disease. The mainstay of TB treatment is drug therapy
(Table 30.12). Because of the growing prevalence of MDR-TB, it is
important to manage the patient with active TB aggressively. Drug
therapy is divided into 2 phases: intensive and continuation (Table
30.13). In most circumstances the treatment regimen for patients
with previously untreated TB consists of a plan with 4 drugs
(isoniazid, rifampin, pyrazinamide, and ethambutol). If drug
susceptibility test results show that the bacteria are susceptible
to all drugs, ethambutol may be stopped. If the patient develops
a toxic reaction to the primary drugs, other drugs can be used,
including rifabutin and rifapentine (Priftin). If pyrazinamide is
not included in the initial phase (e.g., liver disease, pregnancy),
the remaining 3 drugs are used for the initial phase.
DRUG ALERT
Drug Therapy
For Active TB
ethambutol (Myambutol)
isoniazid
pyrazinamide
rifampin
For Drug Resistant TB
Fluoroquinolones
•levofloxacin
•moxifloxacin
Injectable antibiotics
Aminoglycosides
•amikacin
•capreomycin (Capastat)
•kanamycin
bedaquiline (Sirturo)
pretomanid
streptomycin
607
Common Side Effects
Headache, blurred vision, ocular toxicity
(decreased red-green color discrimination)
Liver toxicity, asymptomatic elevation of
aminotransferases (ALT, AST)
Vomiting, confusion, headache
Liver toxicity, joint pain, hyperuricemia
Liver toxicity, thrombocytopenia
Orange discoloration of bodily fluids (sputum,
urine, sweat, tears)
Anorexia, nausea, abdominal discomfort
GI problems, neurologic effects (dizziness,
headache), rash
Hepatitis, GI toxicity
Prolonged QT interval
Ototoxicity, kidney toxicity
Liver toxicity, nausea
Joint and muscle pain
Nausea, vomiting, liver problems
Peripheral neuropathy
Vision problems
Nausea, vomiting, liver problems
Ototoxicity, neurotoxicity, kidney toxicity
Other Drugs Used in TB
rifabutin (Mycobutin) (for
Liver toxicity, thrombocytopenia, neutropenia
TB and co-existing HIV
Orange discoloration of bodily fluids (sputum,
infection)
urine, sweat, tears)
Nausea, vomiting, anorexia
rifapentine (Priftin) (as an
Like those of rifampin
alternate to rifampin)
Isoniazid
ALT, Alanine transaminase; AST, aspartate aminotransferase.
• Alcohol may increase risk for liver toxicity.
• Teach patient to avoid drinking alcohol during treatment.
• Monitor for signs of hepatitis before and while taking drug.
for nonadherence.16 DOT is an expensive but essential public
health measure. In many areas, the public health nurse administers DOT at a clinic site.
Fixed-dose combination drugs may enhance adherence.
Combinations of isoniazid and rifampin and of isoniazid,
rifampin, and pyrazinamide are available to simplify therapy.
The therapy for people with HIV uses the same medications as
outlined in Table 30.13, but in a slightly different schedule. In
the intensive phase, HIV patients take isoniazid, ethambutol,
pyrazinamide, and a rifamycin for the 1st 2 months, then isoniazid and a rifamycin for the last 4 months.17
Teach patients about the adverse effects of drug therapy and
when to seek medical care. The major side effect of isoniazid,
rifampin, and pyrazinamide is nonviral hepatitis. Baseline liver
function tests (LFTs) are done at the start of treatment and
monitored closely (e.g., every 2 to 4 weeks), especially if results
are abnormal.
Latent tuberculosis infection. In people with LTBI, drug
therapy helps prevent a TB infection from developing into active
Sensitivity testing guides the treatment for MDR-TB.
MDR-TB therapy in the initial phase typically includes 5 drugs: 1
or 2 first-line agents, a fluoroquinolone, an injectable antibiotic,
and 1 or more second-line agents, for at least 6 months after sputum culture is negative. This is followed by at least 4 drugs, minus
the injectable antibiotic, for 18 to 24 months. Two newer drugs,
bedaquiline (Sirturo) and Delamanid (Deltyba), are used in combination with other drugs to treat MDR-TB and XDR-TB.
Many people do not adhere to the treatment program and
complete the full course of therapy (Box 30.3). Nonadherence
is a major factor in the emergence of MDR-TB and treatment
failures. Directly observed therapy (DOT) involves providing the antitubercular drugs directly to patients and watching
as they swallow the drugs. It is the preferred way to ensure
adherence for all patients with TB, especially for those at risk
608
SECTION 6
Problems of Oxygenation: Ventilation
TABLE 30.13 Drug Therapy
Tuberculosis Treatment Regimens
BOX 30.3 ETHICAL/LEGAL DILEMMAS
Patient Adherence
Intensive TB Medication
Phase
(2 Months)
Continuation TB
Medication Phase
(4 or 7 Months)
Option #1: Preferred Method
4 drugs:
Daily for 8 weeks
isoniazid
(40–56 doses)
rifampin
pyrazinamide
ethambutola
2 drugs:
isoniazid
rifampin
Daily for 18 weeks
(90–126 doses)
OR
3 times weekly for 18
weeks (54 doses)b
Alternative TB Drug Dosing—Option #1
4 drugs:
Daily for 2 weeks
2 drugs:
3 times weekly for
isoniazid
(14 doses), then
isoni18 weeks (54
rifampin
3 times per
azid
doses)b
pyrazinamide
week for 6
rifamethambutola
weeks (18
pin
doses)b
Alternative TB Drug Dosing—Option #2
4 drugs:
3 times weekly
2 drugs:
3 times weekly for
isoniazid
for 8 weeks (24
isoni18 weeks (54
rifampin
doses)b
azid
doses)b
pyrazinamide
rifamethambutola
pin
aEthambutol may be stopped if drug tests confirm susceptibility to first
line drugs
bAny patient receiving TB medication less than 7 days/week must
receive directly observed therapy (DOT).
Source: Centers for Disease Control and Prevention: Tuberculosis
(TB) fact sheet: general considerations for treatment of TB disease.
Retrieved from https://www. cdc.gov/tb/publications/factsheets/treatment/treatmenthivnegative.htm.
TB disease. Because a person with LTBI has fewer bacteria,
treatment is much easier. Usually only 1 drug is needed. Drug
regimens for LTBI are outlined in Table 30.14.
The standard treatment regimen for LTBI is 9 months of daily
isoniazid. It is an effective and inexpensive drug that the patient
can take orally. This plan is also recommended for patients with
HIV and those with fibrotic lesions on chest x-ray. While the
9-month plan is more effective, adherence issues may make a
6-month plan preferable. An alternative 3-month regimen of
isoniazid and rifapentine may be used for otherwise healthy
patients who we presume are not infected with MDR bacilli.
Patients who are resistant to isoniazid may receive 4-month
therapy with rifampin. Because of severe liver injury and deaths,
the CDC does not recommend the combination of rifampin and
pyrazinamide for treatment of LTBI.
Bacille Calmette-Guérin vaccine. Bacille Calmette-Guérin
(BCG) vaccine is a live, attenuated strain of Mycobacterium
bovis. The vaccine is given to infants in parts of the world with
a high prevalence of TB. In the United States, it is t rarely used
because of the low risk for infection, the vaccine’s variable
effectiveness against adult pulmonary TB, and potential
interference with TST reactivity. The BCG vaccination can result
in a false-positive TST. IGRA results are not affected. The BCG
Situation
While working at a health clinic at a homeless shelter, you discover that F.C.,
a 64-year-old man with tuberculosis (TB), has not been taking his drug therapy.
He tells you that it is hard for him to get to the clinic to obtain his medications,
much less to keep on a schedule. You are concerned about F.C. and the risk
he poses for the other people at the shelter, in the park, and at the meal sites
where he often visits.
Ethical/Legal Points for Consideration
• Adherence is a complex issue involving a person’s culture, values, and
beliefs, perceived risk for disease, access to treatment, availability of
resources, and perceived consequences of failure to adhere to treatment.
• State emergency detention laws provide public health officials with the
legal authority to take action to apprehend and hold a person with TB who
we believe to be a threat to public health.
• The federal government and many states have provisions for quarantine,
detention, and treatment of patients with TB who do not adhere to treatment.
• Advocacy for both the patient and the community obliges you to involve
other health care team members, such as social services, to aid in obtaining
resources or support for the patient to complete a course of treatment.
• With the threats of bioterrorism and the globalization of infectious disease,
it seems unlikely that the government’s power to detain will change anytime soon.
Discussion Questions
1. How would you begin your initial conversation with F.C. about your
concerns?
2. What alternatives of care can we offer to F.C.?
3. Under what circumstances, if any, are HCPs justified in overriding a
patient’s autonomy or decision making?
Source: Kavanagh MM, Gostin LO, Stephens J: Tuberculosis, human
rights, and law reform: addressing the lack of progress in the global
tuberculosis response. Retrieved from https://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1003324.
TABLE 30.14
LTBI Regimens
Drug
isoniazid and
rifapentine
(preferred
method)
rifampin
isoniazid and
rifampin
isoniazid
isoniazid
Drug Therapy
Duration
(Months/
Weeks)
Interval
Number
of Doses
(Minimum)
3 months (12
weeks)
Once weeklya
12
4 months (16
weeks)
3 months (12
weeks)
6 months (24
weeks)
9 months (36
weeks)
Daily
112
Daily
84
Daily
168
Daily
252
aUse directly observed therapy (DOT).
Source: Centers for Disease Control and Prevention. Tuberculosis (TB):
treatment regimens for latent tuberculosis infections (LTBI). Retrieved
from https://www.cdc.gov/tb/topic/treatment/ltbi.htm.
CHAPTER 30
vaccine should be considered only for select persons who meet
specific criteria (e.g., health care workers who are continually
exposed to patients with MDR-TB and when infection control
precautions are not successful).
NURSING MANAGEMENT: TUBERCULOSIS
Assessment
Ask the patient about a previous history of TB, chronic illness,
or any immunosuppressive disease or medications. Obtain a
social and occupational history to determine risk factors for
TB transmission. Assess the patient for productive cough, night
sweats, fever, weight loss, pleuritic chest pain, and abnormal lung
sounds. If the patient has a productive cough, early morning is
the best time to collect sputum specimens for an AFB smear.
Clinical Problems
Clinical problems for the patient with TB may include:
• Impaired respiratory function
• Infection
• Deficient knowledge
• Lack of knowledge
Planning
The overall goals are that the patient with TB will (1) have normal
lung function, (2) adhere to the treatment plan, (3) take measures
to prevent the spread of TB, and (4) have no recurrence.
Implementation
Health Promotion
The goal is to eradicate TB worldwide. Screening programs in
known risk groups are valuable in detecting persons with TB.
For example, the person with a positive TST should have a
chest x-ray to assess for active TB disease. Report people diagnosed with TB to public health authorities for identification and
assessment of contacts and risk to the community. Treatment
of LTBI reduces the number of TB carriers in the community.
Programs to address the social determinants of TB are
needed to decrease TB transmission. Reducing HIV infection,
poverty, overcrowded living conditions, malnutrition, smoking,
and drug and alcohol use can help minimize TB infection rates.
Improving access to health care and education are important.
Acute Care
Patients admitted to the ED or directly to the unit with respiratory symptoms should be assessed for the possibility of TB.
Those strongly suspected of having TB should (1) be placed
on airborne isolation; (2) receive a medical workup, including
chest x-ray, sputum smear and culture; and (3) start appropriate drug therapy. Airborne infection isolation is needed for
the patient with pulmonary or laryngeal TB until the patient is
not infectious. Patients should be placed in a single-occupancy
room with negative pressure and airflow of 6 to 12 exchanges
per hour. Everyone entering the room should wear a high-efficiency particulate air (HEPA) or N95 mask.
Teach patients to cover the nose and mouth with paper tissues every time they cough, sneeze, or produce sputum. The
Lower Respiratory Problems
609
tissues should be thrown into a paper bag and disposed of with
the trash or flushed down the toilet. Emphasize careful hand
washing after handling sputum and soiled tissues. If patients
need to be out of the negative-pressure room, they must wear a
standard surgical mask to prevent exposure to others. Minimize
prolonged visitation to other parts of the hospital.
Identify and screen close contacts of the person with TB.
Anyone testing positive for TB infection needs further evaluation and treatment for either LTBI or active TB disease.
Ambulatory Care
Patients who respond clinically are discharged home if their
household contacts have already been exposed and the patient
is not posing a risk to others. A sputum specimen for AFB
smear and culture should be done monthly until 2 consecutive
specimen cultures are negative. More frequent AFB smears may
be done to assess the early response to treatment and determine infectiousness. Negative cultures are needed to declare the
patient not infectious.
Teach the patient how to minimize exposure to close contacts and household members. Homes should be well ventilated,
especially the areas where the infected person spends a lot of
time. While still infectious, the patient should sleep alone and
spend as much time as possible outdoors. Teach them to minimize time in congregate settings and public transportation.
Teach the patient and caregiver about adherence with the
treatment plan. Most treatment failures occur because the
patient does not take the drug, stops taking it too soon, or takes
it irregularly. Strategies to improve adherence include teaching
and counseling, reminder systems, incentives or rewards, contracts, and DOT.
Notify the public health department. They are responsible
for follow-up on household contacts and assessing the patient
for adherence. If adherence is an issue, the public health department may be responsible for DOT (Box 30.4). Most patients
are considered adequately treated when drug therapy has been
completed, cultures are negative, there is improvement in their
condition, and improvement on chest x-ray.
Because about 5% of patients have relapses, teach the patient
to recognize the symptoms that occur with recurrent TB. If
these symptoms occur, the patient should seek immediate
medical attention. Teach the patient about factors that could
reactivate TB, such as immunosuppressive therapy, cancer, and
prolonged debilitating illness. If the patient has any of these,
we must notify the HCP so that the patient can be monitored
for TB reactivation. In some situations, it is necessary to put
the patient on anti-TB therapy. Because smoking is associated
with poor outcomes, encourage patients who smoke to quit.
Provide patients with teaching and resources to help them stop
smoking.
Evaluation
The expected outcomes are that the patient with TB will have:
• Resolution of the disease
• Normal lung function
• Absence of any complications
• No further transmission of TB
610
SECTION 6
Problems of Oxygenation: Ventilation
Fungal Lung Infections
BOX 30.4 EVIDENCE-BASED PRACTICE
Adherence to TB Treatment Program
TABLE 30.15
You are a nurse working in an outpatient health clinic with C.J., a 42-year-old
woman diagnosed 2 months ago with active TB. She is on directly observed therapy (DOT). You notice C.J. has started to miss and has been late for her appointments. She tells you it is hard to make her appointments as a new job requires
long work hours. She asks if she needs to continue with her visits to get her drugs.
She says she is “feeling better” and does not understand what all the fuss over
the drugs is about. She adds that she is “perfectly capable of taking my own pills.”
Endemic Fungal Infections
Blastomycosis
Blastomyces dermatitidis
Coccidioidomycosis
Coccidioides immitis
Histoplasmosis
Histoplasma capsulatum
Making Clinical Decisions
Best Available Evidence
Guidelines for effective case management of patients with TB include education, home visits, patient reminders, and incentives. TB clinic attendance and
treatment completion rates are higher when patients take part in DOT compared to self-administered therapy. When appointments are missed, phone
calls, Web-based videos, or home visits will engage patients, resulting in
improved attendance and treatment completion.
Clinician Expertise
You are aware that patient-centered care includes being responsive to
patients’ changing needs. You know that patients may stop attending appointments and taking their drugs when feeling well again. This can lead to treatment failure, the need to restart therapy, and multidrug resistance.
Patient Preferences and Values
C.J. tells you she has a busy job and does not always remember her appointments. She stated that she would like to be responsible for taking her drugs.
Implications for Nursing Practice
1. What information you want to obtain from C.J.?
2. What teaching would you provide to C.J. about taking her own medications?
3. How will you determine if C.J. is adhering to the drug treatment plan?
Source: Pradipta IS, Houtsma D, van Boven JFM, et al.: Interventions to
improve medication adherence in tuberculosis patients: A systematic review
of randomized controlled studies, NPJ Prim Care Respir Med 30:21, 2020.
ATYPICAL MYCOBACTERIA
There are more than 30 acid-fast mycobacteria that cause diseases other than TB. These include lung disease, lymphadenitis,
skin or soft tissue disease, and disseminated disease. Atypical
mycobacteria are not airborne or transmitted by droplets. They
can be found in tap water, soil, bird feces, and house dust.
People who are immunosuppressed (e.g., HIV/AIDS) or
have chronic lung disease are most susceptible to infection.
Pulmonary symptoms include cough, shortness of breath,
weight loss, fatigue, and blood-tinged sputum.
Diagnosis is challenging and differs based on the site of the
infection. We cannot tell this type of lung disease from TB either
clinically or radiologically. Diagnostic studies done include a
chest x-ray and 3 sputum specimens tested for AFB. Treatment
may include a prolonged course of antibiotics, depending on the
organism cultured and patient’s condition.
PULMONARY FUNGAL INFECTIONS
Pulmonary fungal pneumonia is an infectious process
in the lungs caused by endemic (native and common) or
Infection
Organism
Opportunistic Fungal Infections
Aspergillosis
Aspergillus niger, Aspergillus fumigatus
Candidiasis
Candida albicans
Cryptococcosis
Cryptococcus neoformans
opportunistic fungi (Table 30.15). Endemic fungal pathogens
cause infection in healthy people and immunocompromised
people in certain areas. For example, Coccidioides, which
causes coccidioidomycosis, is a fungus found in the soil of dry,
low-rainfall areas.18 It is endemic in many areas of the southwestern United States. Opportunistic fungal infections occur
in immunocompromised patients (e.g., those receiving chemotherapy, immunosuppressive drugs) and in patients with
HIV and cystic fibrosis. Pulmonary fungal infections can be
life-threatening.
Pulmonary fungal infections are acquired by inhaling
spores. They are not transmitted from person to person. The
patient does not have to be placed in isolation. The manifestations are like those of bacterial pneumonia. Skin testing, serology, and biopsy methods help identify the infecting
organism.
The choice of antifungal agent is based on the pathogen identified on culture or most likely suspected. Amphotericin B is the
standard therapy for treating serious systemic fungal infections.
It must be given IV to achieve adequate blood and tissue levels
because the GI tract does not absorb it well. Less serious infections can be treated with oral antifungals, such as ketoconazole,
fluconazole (Diflucan), voriconazole (Vfend), and itraconazole
(Sporanox). We monitor therapy effectiveness with fungal serology titers.
LUNG ABSCESS
Etiology and Pathophysiology
A lung abscess is necrosis of lung tissue. It typically results from
bacteria aspirated from the oral cavity in patients with periodontal disease. Lung abscess can also result from IV drug use,
cancer, pulmonary emboli, TB, and various parasitic and fungal
diseases. The abscess usually develops slowly, beginning with an
enlarging area of infection that becomes necrotic and eventually
forms a cavity filled with purulent material. Abscesses usually
contain more than 1 type of microbe, most often anaerobic flora
of the mouth and pharynx.
The lung area most often affected due to aspiration is the
posterior segment of the upper lobes. The abscess may erode
into the bronchial system, causing foul-smelling or sour-tasting
sputum. It may grow toward the pleura and cause pleuritic pain.
Multiple small abscesses, sometimes referred to as necrotizing
pneumonia, can occur within the lung.
CHAPTER 30
Clinical Manifestations and Complications
Manifestations usually occur slowly over a period of weeks
to months, especially if anaerobic organisms are the cause.
Symptoms of abscess caused by aerobic bacteria develop more
acutely and resemble bacterial pneumonia. The most common
is cough-producing purulent sputum (often dark brown) that
is foul smelling and foul tasting. Hemoptysis is common, especially when an abscess ruptures into a bronchus. Other manifestations include fever, chills, weakness, night sweats, pleuritic
pain, dyspnea, anorexia, and weight loss.
Assessment reveals decreased breath sounds on auscultation
over the involved segment of lung. Bronchial breath sounds may
be transmitted to the periphery if the communicating bronchus
becomes patent, and the segment begins to drain. Crackles may
be present in the later stages as the abscess drains.
The infection can spread through the bloodstream and cause
several possible complications. Pulmonary abscess, bronchopleural fistula, bronchiectasis, and empyema from perforation of
the abscess into the pleural cavity can occur.19
Diagnostic Studies
A chest x-ray is often the only test needed to diagnose a lung
abscess. The presence of a single cavitary lesion with an air-fluid
level and local infiltrate confirms the diagnosis. CT scanning
may be helpful if the abscess is not clear on chest x-ray. If there
is drainage via the bronchus, sputum will contain the microorganisms that are present in the abscess. However, expectorated
sputum samples are often contaminated with oral flora, making
it hard to determine the responsible organism(s).
Bronchoscopy may be used to (1) avoid oropharyngeal contamination, (2) collect a specimen if drainage is delayed, or (3)
assess for underlying cancer. Pleural fluid and blood cultures
may be used to identify the offending organisms. Although nonspecific, an elevated neutrophil count may indicate an infection.
Necrotic pulmonary lesions also can be caused by lung infarction, pulmonary embolism, and sarcoidosis.
Interprofessional and Nursing Care
Monitor the patient’s vital signs, LOC, and respiratory rate and
rhythm. Note any signs and symptoms of respiratory distress.
Observe for any signs of hypoxemia. Apply O2 as needed.
Teach the patient how to cough effectively. Chest physiotherapy and postural drainage are not recommended because
they may promote movement of microorganisms into adjacent
bronchi and other lobes of the lungs, extending infection. Rest,
optimal nutrition, and adequate fluid intake promote recovery.
If dentition is poor or dental hygiene is not adequate, encourage the patient to obtain dental care. Collaborate with the social
worker to evaluate options for dental care if the patient has limited resources.
IV antibiotic therapy should be started immediately.
Clindamycin is first-line therapy for its effectiveness against
Staphylococcus and anaerobic organisms. IV antibiotics are
switched to oral antibiotics once the patient shows clinical and
chest x-ray signs of improvement.
Because of the need for prolonged antibiotic therapy,
teach the patient to take antibiotics as directed for the entire
Lower Respiratory Problems
611
prescribed period (see Table 15.9). Sometimes the patient must
return periodically during the course of antibiotic therapy for
repeat cultures and sensitivity tests to ensure that the infecting
organism is not becoming resistant to the antibiotic. When antibiotic therapy is complete, the patient is re-evaluated.
If the patient does not adequately respond to antibiotic treatment, percutaneous drainage of the abscess may be done. A
small catheter, guided by CT or ultrasound, may be placed to
drain the abscess. Surgery is sometimes done when reinfection
of a large cavitary lesion occurs, when an empyema develops, or
to establish a diagnosis when there is evidence of an underlying problem, such as cancer. The usual procedure in such cases
is a lobectomy. A pneumonectomy may be needed for multiple
abscesses.
RESTRICTIVE RESPIRATORY DISORDERS
Disorders that impair the ability of the chest wall and diaphragm
to move with respiration are called restrictive respiratory disorders. There are 2 categories: extrapulmonary conditions, in
which the lung tissue is normal, and intrapulmonary conditions,
in which the primary cause is the lung or pleura. Examples of
extrapulmonary and intrapulmonary conditions are listed in
Table 30.16.
The hallmark characteristic of a restrictive lung disorder is a
reduced total lung capacity (TLC). The hallmark characteristic
of an obstructive disorder is reduced forced expiratory volume
(FEV1). Mixed obstructive and restrictive disorders sometimes
occur together. For example, a patient may have both asthma
Common Causes of
Restrictive Lung Disease
TABLE 30.16
Intrapulmonary Causes
Parenchymal Disorders
• Acute respiratory distress syndrome (ARDS)
• Atelectasis
• Chronic empyema
• Interstitial lung diseases
• Pneumonia
Pleural Disorders
• Pleural effusion
• Pleurisy (pleuritis)
• Pneumothorax
Extrapulmonary Causes
Central Nervous System
• Head injury, central nervous system lesion (e.g., tumor, stroke)
• Opioid and barbiturate overdose
Chest Wall
• Kyphoscoliosis
• Obesity-hypoventilation syndrome
Neuromuscular System
• Amyotrophic lateral sclerosis
• Guillain-Barré syndrome
• Muscular dystrophy
• Myasthenia gravis
612
SECTION 6
Problems of Oxygenation: Ventilation
(an obstructive problem) and pulmonary fibrosis (a restrictive
problem). Pulmonary function tests are the best way to distinguish between restrictive and obstructive respiratory disorders.
ATELECTASIS
Atelectasis is a lung condition characterized by collapsed, airless
alveoli. There may be decreased or absent breath sounds and
dullness to percussion over the affected area. The most common
cause is obstruction of the small airways with secretions. This is
common in patients on bedrest and in almost all postoperative
surgery patients. Normally, the pores of Kohn provide collateral passage of air from one alveolus to another. Deep inspiration opens the pores effectively. For this reason, deep-breathing
exercises, coughing, incentive spirometry, and early mobility
are important to prevent atelectasis and treat the patient at risk
(see Chapter 20).
PLEURISY
Pleurisy (pleuritis) is an inflammation of the pleura. It can be
caused by infectious diseases, cancer, autoimmune disorders, chest
trauma, GI disease, and some drugs. The inflammation usually
subsides once we treat the cause. The pain of pleurisy is typically
abrupt, sharp in onset, and worse with inspiration. The patient’s
breathing is short, shallow, and rapid to avoid unnecessary pleura
and chest wall movement. A pleural friction rub may occur. This
is the sound heard over areas where inflamed visceral pleura and
parietal pleura rub together during inspiration. This sound, like a
squeaking door, is usually loudest at peak inspiration.
Treatment is directed at the underlying cause and providing pain relief. Teach the patient to splint the rib cage when
coughing. If the pain is severe, intercostal nerve blocks may be
considered.
PLEURAL EFFUSION
A pleural effusion is an abnormal collection of fluid in the
pleural space. It is not a disease, but a sign of another condition.
A balance among hydrostatic pressure, oncotic pressure, and
capillary membrane permeability governs movement of fluid
in and out of the pleural space. Fluid accumulation can be due
to increased pulmonary capillary pressure, decreased oncotic
pressure, increased pleural membrane permeability, or obstruction of lymphatic flow.
Types of Pleural Effusions
We classify pleural effusions as transudative or exudative
depending on the protein content. A transudate effusion occurs
mainly in non-inflammatory conditions. It is an accumulation
of protein-poor, cell-poor fluid. The fluid is usually clear, pale
yellow. Causes include (1) increased hydrostatic pressure found
in HF or (2) decreased oncotic pressure from hypoalbuminemia
(e.g., with chronic liver or renal disease). An exudative effusion
results from increased capillary permeability due to an inflammatory reaction. The fluid is rich in protein. They most often
occur with an infection or cancer (called a malignant effusion).
An empyema is a collection of purulent fluid in the pleural
space. Common causes include pneumonia, TB, lung abscess,
and infected surgical chest wounds.
Clinical Manifestations
Common manifestations are dyspnea, cough, and occasional
sharp, non-radiating chest pain that may be worse on inhalation. Breath sounds may be decreased over the affected area. A
chest x-ray may show decreased chest movement on the affected
side. A chest x-ray and CT reveal the volume and location of the
effusion. Additional manifestations seen with empyema include
fever, night sweats, cough, and weight loss.
Interprofessional and Nursing Care
The management of pleural effusions is to treat the underlying
cause. For example, adequate treatment of HF with diuretics
and sodium restriction may result in a decreased incidence of
pleural effusion. The treatment of malignant effusions is more
difficult. These effusions often re-occur and re-accumulate
quickly after thoracentesis.
Treatment options for an empyema include antibiotic therapy (to eradicate the causative organism), percutaneous drainage, chest tube insertion, and intrapleural fibrinolytic therapy
(instilled through the chest tube to dissolve fibrous adhesions).
Some patients may need surgery. Surgical options include
drainage, decortication, or an open window thoracostomy.
Chemical pleurodesis is done to obliterate the pleural space
and prevent re-accumulation of effusion fluid. This procedure
first requires chest tube drainage of the effusion. Once the
fluid is drained, a chemical slurry is instilled into the pleural
space. Talc is the most effective agent used. Other agents we use
include doxycycline and bleomycin. The chest tube is clamped
for 8 hours while the patient is turned in different positions.
This allows the chemical to contact the entire pleural space.
After 8 hours, the chest tube is unclamped and attached to a
drainage unit. Chest tubes are left in place until fluid drainage is
less than 150 mL/day and no air leaks are noted. Fever and chest
pain are common side effects after pleurodesis.
We provide supportive nursing care according to the patient’s
needs. This may include O2 therapy to treat hypoxemia and
analgesics to relieve chest pain. Implement measures to manage fever (see Table 12.5). Hydration, nutrition support, and
positioning are part of the care plan. Work with the respiratory
therapist to monitor the patient’s condition and provide chest
physiotherapy. Care of the patient with a chest tube is described
in Chapter 28.
INTERSTITIAL LUNG DISEASES
Interstitial lung disease (ILD), or diffuse parenchymal lung disease, refers to more than 200 lung disorders in which the tissue
between the air sacs of the lungs (the interstitium) is affected by
inflammation or scarring (fibrosis).20 Most ILDs are rare.
Many times, the cause of an ILD is unknown. Known causes
are inhalation of occupational and environmental toxins, certain drugs, radiation therapy, connective tissue disorders, infection, and cancer. Treatment is aimed at reducing exposure to
CHAPTER 30
the causative agent or treating the underlying disease process.
While scarring is not reversible, treatment with corticosteroids
and immunosuppressant drugs can minimize progression. A
lung transplant may be an option for some patients.
IDIOPATHIC PULMONARY FIBROSIS
Idiopathic pulmonary fibrosis (IPF) is a progressive disorder
characterized by chronic inflammation and formation of scar
tissue in the connective tissue.21 Risk factors include smoking
and exposure to wood and metal dust. IPF affects more men. It
typically first appears between the ages of 50 and 70 years. We
do not know the cause of IPF.
Manifestations include exertional dyspnea, a dry, nonproductive cough, clubbing of the fingers, and inspiratory crackles.
Fatigue, weakness, anorexia, and weight loss may occur as the
disease progresses. Chest x-ray findings are generally nonspecific. Pulmonary function tests may be abnormal, with reduced
vital capacity and impaired gas exchange. Open lung biopsy
using video-assisted thoracic surgery (VATS) often helps to
confirm the pathology. It is the gold standard for diagnosis.
The course is variable, and the prognosis is poor. The median
survival rate is 2.5 to 3.5 years after diagnosis. There is no
known cure for IPF. Many people diagnosed with IPF are first
treated with a corticosteroid, sometimes in combination with
other drugs that suppress the immune system (e.g., methotrexate, cyclosporine). Kinase inhibitor drugs, which block multiple
pathways that are involved with scarring, include nintedanib
(Ofev) and pirfenidone (Esbriet).
O2 therapy and pulmonary rehabilitation should be prescribed for all patients. A lung transplant may be an option for
those who meet criteria.
SARCOIDOSIS
Sarcoidosis is a chronic, multisystem granulomatous disease
of unknown cause that mainly affects the lungs. The disease
may also involve the skin, eyes, liver, kidney, heart, and lymph
nodes. Signs and symptoms vary depending on what organs are
affected. Pulmonary symptoms include dyspnea, cough, and
chest pain. Many patients do not have symptoms.
Staging and treatment decisions are based on chest x-ray,
pulmonary function tests, and severity of symptoms. Some
patients have a spontaneous remission. Treatment is aimed at
suppressing the inflammatory response. Patients are followed
every 3 to 6 months with pulmonary function tests, chest x-ray,
and CT scan to monitor disease progression.
CHEST TRAUMA AND THORACIC INJURIES
Traumatic injuries to the chest contribute to many deaths. Chest
injuries range from simple rib fractures to cardiorespiratory
arrest. We classify the primary mechanisms of injury as either
blunt trauma or penetrating trauma.
Blunt trauma occurs when the chest strikes or is struck by
an object. The impact can cause shearing and compression of
chest structures. The external injury may appear minor, but
Lower Respiratory Problems
613
internally, organs may be severely damaged. Rib and sternal
fractures can easily tear lung tissue. In a high-velocity impact,
shearing forces can result in tearing of the aorta. Compression
of the chest may result in heart or lung contusion, crush injury,
and organ rupture.
In penetrating trauma, a foreign object impales or passes
through the body tissues, creating an open wound. Examples
include knife wounds, gunshot wounds, and injuries with other
sharp objects. Emergency care of the patient with a chest injury
is outlined in Table 30.17. The most common chest emergencies
and their management are described in Table 30.18.
FRACTURED RIBS
Rib fractures are the most common type of chest injury from
blunt trauma. Ribs 5 through 9 are most often fractured because
they are the least protected by chest muscles. A splintered or
displaced fractured rib can damage the pleura, lungs, heart, and
other internal organs.
Manifestations include pain at the site of injury, especially
during inspiration and with coughing. The patient splints the
affected area. They take shallow breaths to try to decrease the
discomfort. Atelectasis and pneumonia may develop because of
pain, decreased chest wall movement, and retained secretions.
The goal of treatment is to decrease pain so that the patient
can breathe adequately and clear secretions. Strapping the chest
with tape or using a thoracic binder is not recommended. These
limit chest expansion and predispose the person to atelectasis
and hypoxemia. NSAIDs, opioids, and thoracic nerve blocks
can be used to reduce pain and assist with deep breathing and
coughing. Surgical plating of fractured ribs may be done for
those patients with extreme chest wall deformity. Teaching
should emphasize deep breathing, coughing, incentive spirometry, appropriate use of pain medications, and when appropriate,
early mobility.
FLAIL CHEST
Flail chest results from the fracture of 3 or more consecutive
ribs, in 2 or more separate places, causing an unstable segment
(Fig. 30.4). It also can be caused by fracture of the sternum and
several consecutive ribs. The resulting chest wall instability
causes paradoxical movement during breathing. During inspiration, the affected part is sucked in, and during expiration, it
bulges out. In other words, the affected (flail) area moves in the
opposite direction with respect to the intact part of the chest.
This paradoxical chest movement may prevent adequate ventilation and increase the work of breathing.
A flail chest is usually apparent on assessment. The patient
has rapid, shallow respirations and tachycardia. Movement of
the thorax is asymmetric and uncoordinated. The patient may
ventilate poorly and try to splint the chest to assist with breathing. Abnormal chest cavity movement, crepitus near the rib
fractures, and chest x-ray all assist in the diagnosis.
Initial therapy consists of ensuring adequate ventilation and
supplemental O2 therapy. The goal is to promote lung expansion and ensure adequate oxygenation. The underlying injured
TABLE 30.17
EMERGENCY MANAGEMENT
Chest Trauma
Etiology
Assessment Findings
Interventions
Blunt
•Assault with blunt object
•Crush injury
•Explosion
•Fall
•Motor vehicle collision
•Pedestrian accident
•Sports injury
Respiratory
•Audible air escaping from chest wound
•↓ Breath sounds on side of injury
•Cough with or without hemoptysis
•Cyanosis of mouth, face, nail beds, mucous membranes
•Dyspnea, respiratory distress
•Frothy secretions
•↓ O2 saturation
•Tracheal deviation
Initial
•If unresponsive, immediately assess circulation, airway, and
breathing.
•If responsive, monitor airway, breathing, and circulation.
•Apply high-flow O2 to keep SpO2 >90%.
•Establish IV access with 2 large-bore catheters. Begin IV fluid
resuscitation as appropriate.
•Remove clothing to assess injury.
•Cover sucking chest wound with nonporous dressing taped on 3
sides (vent dressing).
•Stabilize impaled objects with bulky dressings. Do not remove
object.
•Assess for life-threatening injuries and treat appropriately.
•Place patient in a semi-Fowler’s position if breathing is easier
after cervical spine injury has been ruled out.
•Give small amounts of analgesia as needed for pain and to help
with breathing.
•Prepare for emergency needle decompression if tension pneumothorax or cardiac tamponade present.
Penetrating
•Arrow
•Gunshot
•Knife
•Stick
Cardiovascular
•Asymmetric BP values in arms
•↓ BP
•Chest pain
•Distended neck veins
•Dysrhythmias
•Muffled heart sounds
•Narrowed pulse pressure
•Rapid, thready pulse
Surface Findings
•Abrasions
•Asymmetric chest movement
•Bruising
•Contusions
•Lacerations
•Open chest wound
•Subcutaneous emphysema
TABLE 30.18
Ongoing Monitoring
•Monitor LOC, vital signs, O2 saturation, cardiac rhythm, respiratory rate and rhythm, urine output.
•Anticipate intubation for respiratory distress.
•Release vent dressing if tension pneumothorax develops after
sucking chest wound is covered.
EMERGENCY MANAGEMENT
Chest Injuries
Injury and Description
Manifestations
Intervention
Cardiac Tamponade
Blood rapidly collects in pericardial sac, compresses
myocardium because pericardium does not
stretch, and prevents ventricles from filling.
Muffled, distant heart sounds, hypotension, neck
vein distention, ↑ central venous pressure
Medical emergency. Pericardiocentesis with surgical
repair as appropriate.
Paradoxical movement of chest wall, respiratory
distress. May be associated hemothorax,
pneumothorax, pulmonary contusion
O2 as needed to maintain O2 saturation, analgesia. Positive pressure mechanical ventilation for acute respiratory distress; will also help stabilize flail segment.
Treat associated injuries. Possible surgical fixation for
severe damage to chest wall.
Dyspnea, decreased or absent breath sounds,
dullness to percussion, ↓ Hgb, shock (depending on blood volume lost)
Chest tube insertion with chest drainage system. Autotransfusion of collected blood, treatment of hypovolemia as needed with IV fluid, packed red blood cells.
Dyspnea, ↓ movement of involved chest wall,
decreased or absent breath sounds on the
affected side, hyperresonance to percussion
Chest tube insertion with chest drainage system.
Cyanosis, air hunger, extreme agitation, subcutaneous emphysema, neck vein distention,
hyperresonance to percussion, tracheal deviation away from affected side (late sign)
Medical emergency: needle decompression followed by
chest tube insertion with chest drainage system.
Flail Chest
Fracture of 2 or more adjacent ribs in 2 or more
places with loss of chest wall stability (see Fig.
30.4).
Hemothorax
Blood in the pleural space, may or may not occur in
conjunction with pneumothorax.
Pneumothorax
Air in pleural space (see Fig. 30.5).
Tension Pneumothorax
Air in pleural space that does not escape.
Increased air in the pleural space shifts organs and
increases intrathoracic pressure (see Fig. 30.6).
CHAPTER 30
Lower Respiratory Problems
615
Collapsed
lung
Air
Inspiration
Fig. 30.5 Open pneumothorax. Collapse of lung results from disruption
of chest wall and outside air entering the thoracic cavity.
respiratory distress may be present, including short, shallow,
rapid respirations, dyspnea, and low O2 saturation. On auscultation, breath sounds are absent over the affected area. A chest
x-ray will show air or fluid in the pleural space and reduced lung
volume.
Types of Pneumothoraxes
Expiration
Fig. 30.4 Flail chest causes paradoxical respiration. On inspiration, the
flail section moves inward with mediastinal shift to the uninjured side.
On expiration, the flail section bulges outward with mediastinal shift to
the injured side.
lung may be contused, worsening hypoxemia. Analgesia can
help promote adequate respiration. Some patients may need
mechanical ventilation. In cases of extreme deformity, surgical
fixation of the flail segment may be done. The lung parenchyma
and fractured ribs heal with time. Some patients continue
to have intercostal pain several weeks after the flail chest has
resolved.
PNEUMOTHORAX
A pneumothorax is caused by air entering the pleural cavity.
Normally, negative (subatmospheric) pressure exists between
the visceral pleura (surrounding the lung) and parietal pleura
(lining the chest cavity), known as the pleural space. The pleural space has a few milliliters of lubricating fluid to reduce friction when the tissues move. When the volume of air that enters
this normally subatmospheric space increases, lung volume
decreases. As a result, the change to positive pressure causes a
partial or complete lung collapse.
We can describe a pneumothorax as open (air entering through
an opening in the chest wall) or closed (no external wound).
Penetrating trauma allows air to enter the pleural space through
an opening in the chest wall (Fig. 30.5). A penetrating chest
wound may be called a sucking chest wound, since air enters the
pleural space through the chest wall during inspiration. A pneumothorax should be suspected after any trauma to the chest wall.
If a pneumothorax is small, mild tachycardia and dyspnea
may be the only manifestations. With a larger pneumothorax,
Spontaneous Pneumothorax
A spontaneous pneumothorax typically occurs due to the rupture of small blebs (air-filled sacs) on the surface of the lung.
These blebs can occur in healthy, young people or from lung
disease, such as COPD, asthma, cystic fibrosis, and pneumonia.
Smoking increases the risk for bleb formation. Other risk factors include being tall and thin, male gender, family history, and
previous spontaneous pneumothorax.
Iatrogenic Pneumothorax
Iatrogenic pneumothorax can occur due to laceration or puncture of the lung during medical procedures. For example, transthoracic needle aspiration, subclavian catheter insertion, pleural
biopsy, and transbronchial lung biopsy all have the potential to
injure the lung. Barotrauma from excessive ventilatory pressure
during manual or mechanical ventilation can rupture alveoli,
creating a pneumothorax. Esophageal procedures may result in
a pneumothorax. For example, tearing of the esophageal wall
during insertion of a gastric tube can allow air from the esophagus to enter the mediastinum and pleural space.
Tension Pneumothorax
Tension pneumothorax occurs when air enters the pleural
space but cannot escape. The continued accumulation of air in
the pleural space causes increasingly elevated intrapleural pressures. This results in compression of the lung on the affected
side and pressure on the heart and great vessels, pushing them
away from the affected side (Fig. 30.6). The mediastinum shifts
toward the unaffected side, compressing the “good” lung, which
further compromises oxygenation and ventilation. As the pressure increases, venous return decreases and cardiac output falls.
Tension pneumothorax may result from either an open or
a closed pneumothorax. In an open chest wound, a flap may
act as a one-way valve. Thus, air can enter on inspiration but
cannot escape. Tension pneumothorax can occur with mechanical ventilation and resuscitative efforts. It can also occur if
chest tubes are clamped or become blocked in a patient with a
616
SECTION 6
Problems of Oxygenation: Ventilation
Midline
Superior
vena cava
TABLE 30.19
Tracheal
deviation
Inferior
vena cava
Pneumothorax
Mediastinal shift
Fig. 30.6 Tension pneumothorax. As pleural pressure on the affected
side increases, mediastinal displacement occurs, causing respiratory
and cardiovascular compromise. Tracheal deviation is an external (but
late) sign of mediastinal shift.
pneumothorax. Unclamping the tube or relieving the obstruction may correct this situation.
Tension pneumothorax is a medical emergency. It affects both
the respiratory and cardiovascular systems. Manifestations include
severe dyspnea, marked tachycardia, neck vein distention, and profuse diaphoresis. Decreased or absent breath sounds will be present
on the affected side. Tracheal deviation is a very late sign. If the
problem is not quickly identified and tension in the pleural space is
not relieved (needle compression), the patient is likely to die from
inadequate cardiac output and severe hypoxemia.
Hemothorax
Hemothorax is an accumulation of blood in the pleural space from
injury to the chest wall, diaphragm, lung, blood vessels, or mediastinum. When it occurs with pneumothorax, it is called a hemopneumothorax. The patient with a traumatic hemothorax needs
immediate insertion of a chest tube for evacuation of the blood.
Sometimes, blood drained from a chest tube can be reinfused back
into the patient (autotransfusion) after the injury. However, this
requires special equipment and set-up prior to chest tube insertion.
Chylothorax
Chylothorax is the presence of lymphatic fluid in the pleural
space. The thoracic duct is disrupted either traumatically or
from cancer, allowing lymphatic fluid to fill the pleural space.
This milky white fluid is high in lipids. Normal lymphatic flow
through the thoracic duct is 1500 to 2500 mL/day. This amount
can increase up to 10-fold after ingesting fats. Some cases heal
with conservative treatment (chest drainage, bowel rest, diet).
Octreotide may reduce the flow of lymphatic fluid. Surgery
(thoracic duct ligation) and pleurodesis (the artificial production of adhesions between the parietal and visceral pleura) are
options for some persons.
Interprofessional Care
Treatment of a pneumothorax depends on its severity, underlying cause, and hemodynamic stability of the patient. If the
Causes of Pulmonary Edema
• Acute respiratory distress syndrome (ARDS)
• Altered capillary permeability of lungs: aspiration, inhaled toxins, inflammation (e.g., pneumonia), severe hypoxia, near-drowning
• Anaphylactic (allergic) reaction
• Hypoalbuminemia: nephrotic syndrome, liver disease, nutritional disorders
• Left ventricular (heart) failure
• Lymph system cancer (e.g., non-Hodgkin lymphoma)
• Overhydration with IV fluids
• O2 toxicity
• Unknown causes: neurogenic condition, opioid overdose, reexpansion
pulmonary edema, high altitude
patient is stable and has minimal air and/or fluid accumulated
in the intrapleural space, no treatment may be needed since the
condition may resolve spontaneously.
Pre-hospital emergency care consists of covering the wound
with an occlusive dressing that is secured on 3 sides (vent dressing). During inspiration, as negative pressure is created in the
chest, the dressing pulls against the wound, preventing air from
entering the pleural space. During expiration, as the pressure
rises in the pleural space, the dressing is pushed out and air
escapes through the wound and from under the dressing. If
the object that caused the open chest wound is still in place,
pre-hospital care providers will not remove it. They will stabilize
the impaled object with a bulky dressing and arrange transport
to the nearest medical facility.
In acute care, the most definitive and common treatment
of pneumothorax and hemothorax is to insert a chest tube
and connect it to water-seal drainage. Repeated spontaneous
pneumothorax may need surgical treatment with a partial pleurectomy, stapling, or pleurodesis to promote adherence of the
pleurae to one another. Tension pneumothorax is a medical
emergency, requiring urgent needle decompression followed by
chest tube insertion to water-seal drainage. Care of the patient
with chest tubes is described in Chapter 28.
VASCULAR LUNG DISORDERS
PULMONARY EDEMA
Pulmonary edema is an abnormal accumulation of fluid in the
alveoli and interstitial spaces of the lungs. It is a complication of
various heart and lung problems (Table 30.19). In severe cases,
pulmonary edema can be a life-threatening medical emergency.
The most common cause of pulmonary edema is left-sided HF.
The patient often presents with varying degrees of dyspnea,
diaphoresis, and wheezing, depending upon the severity of pulmonary edema and underlying medical condition. A 3rd heart
sound may be present. Sputum may be blood-tinged and frothy
sputum. A chest x-ray is the best option for confirming the
diagnosis.
Treatment is often directed towards finding the underlying
cause of the edema and reducing the amount of fluid in the
lungs. Goals include simultaneously improving oxygenation,
ventilation, and cardiac output.
CHAPTER 30
Place the patient in a semi or high Fowler’s position.
Administer O2 to keep SpO2 greater than 90%. This may require
low or high flow O2 delivery devices, non-invasive ventilation
(e.g., Bi-PAP), or mechanical ventilation. Preload reduction
may be accomplished by giving IV diuretics (e.g., furosemide) or
nitroglycerine. Small amounts of IV morphine can reduce afterload. Cardiac output can be supported with IV Dobutamine.
Monitor the patient’s vital signs, work of breathing, breath
sounds, urinary output, electrolyte balance, and response to
treatment.
PULMONARY EMBOLISM
Etiology and Pathophysiology
Pulmonary embolism (PE) is the blockage of 1 or more pulmonary arteries by a thrombus, fat or air embolus, or tumor tissue.
A PE consists of material that gains access to the venous system and then to the pulmonary circulation. The PE travels with
blood flow through ever-smaller blood vessels until it lodges
and obstructs perfusion of the alveoli. The lower lobes are most
often affected.
Most PEs arise from deep vein thrombosis (DVT) in the
deep veins of the legs. Venous thromboembolism (VTE) is the
preferred term to describe the spectrum from DVT to PE.
Other sites of origin of PE include femoral or iliac veins, right
side of the heart (atrial fibrillation), and pelvic veins (especially
after surgery or childbirth). Upper extremity DVT sometimes
occurs in the presence of central venous catheters or arterial
lines. These cases may resolve with removal of the catheter. A
saddle embolus refers to a large thrombus lodged at an arterial
bifurcation (Fig. 30.7).
Less common causes include fat emboli (from fractured long
bones), air emboli (from improperly administered IV therapy), bacterial vegetation on heart valves, amniotic fluid, and
cancer.22 Risk factors for PE include immobility or reduced
mobility, surgery within the last 3 months (especially pelvic
and lower extremity surgery), history of VTE, cancer, obesity,
Lower Respiratory Problems
617
oral contraceptives, hormone therapy, smoking, prolonged air
travel, HF, pregnancy, and clotting disorders.
Clinical Manifestations
The signs and symptoms of PE are varied and nonspecific,
making diagnosis difficult. Manifestations depend on the type,
size, and extent of emboli. Small emboli may go undetected or
cause vague, transient symptoms. Symptoms may begin slowly
or appear suddenly. Dyspnea is the most common presenting
symptom in patients with PE. Mild to moderate hypoxemia may
occur. Other manifestations include tachypnea, cough, chest
pain, hemoptysis, crackles, wheezing, fever, accentuation of pulmonic heart sound, tachycardia, and syncope. Massive PE may
cause a sudden change in mental status, hypotension, feelings of
impending doom, and cardiorespiratory arrest.
Complications
About 10% of patients with massive PE die within the 1st hour.
Identifying the patient “at-risk” for VTE is essential. Treatment
with anticoagulants significantly reduces mortality.
Complications include pulmonary infarction and pulmonary hypertension. Pulmonary infarction (death of lung tissue)
is most likely when there is (1) occlusion of a large or medium-sized pulmonary vessel (more than 2 mm in diameter), (2)
insufficient collateral blood flow from the bronchial circulation, or (3) pre-existing lung disease. Infarction results in alveolar necrosis and hemorrhage. Sometimes the necrotic tissue
becomes infected, and an abscess may develop. Pleural effusions
are common.
Pulmonary hypertension results from hypoxemia or from
involvement of a large surface area of the pulmonary bed. As
a single event, a PE rarely causes pulmonary hypertension.
Recurrent PEs or PEs that do not completely resolve gradually reduce capillary bed blood flow over time. This may
eventually cause chronic thromboembolic pulmonary hypertension.23 Dilation and hypertrophy of the right ventricle occurs.
Depending on the severity of pulmonary hypertension and how
Large coiled central
clot extending into
and obstructing both
pulmonary arteries
Peripheral emboli
(multiple small formed
clot fragments in
peripheral arteries)
Pulmonary
trunk
Fig. 30.7 Saddle pulmonary embolus. This embolus straddles the bifurcation of a major artery, with the clot
extending down into both right and left branches of the major vessel.
618
SECTION 6
Problems of Oxygenation: Ventilation
quickly it develops, outcomes can vary. Some patients dying
within months while and others live for decades.
TABLE 30.20 Interprofessional Care
Acute Pulmonary Embolism
Diagnostic Studies
Diagnostic Assessment
• History and physical assessment
• Chest x-ray
• Continuous ECG monitoring
• Pulse oximetry, ABGs
• Spiral (helical) CT scan (gold standard for ventilated or non-ventilated
patient); if unavailable, computed tomography angiography (CTA) or
pulmonary angiography
• Ventilation-perfusion (V/Q) lung scan (best for non-ventilated patient)
• Potentially useful lab tests (but not diagnostic); D-dimer level, troponin
level, b-natriuretic peptide level
• Ultrasound of upper or lower extremities (based on likely source)
ABG analysis is important but does not diagnose a PE. The PaO2
may be low because of inadequate oxygenation from occluded
pulmonary vessels preventing matching of perfusion to ventilation. The pH is often normal unless respiratory alkalosis develops because of prolonged hyperventilation or to compensate for
lactic acidosis caused by shock.
Abnormal findings may be seen on a chest x-ray (atelectasis,
pleural effusion) and ECG (nonspecific ST segment and T wave
changes), but they are not diagnostic for PE. Serum troponin
levels and b-type natriuretic peptide (BNP) levels are often high.
D-dimer is a laboratory test that measures the amount of
cross-linked fibrin fragments. These fragments are the result of
clot degradation. The disadvantage of D-dimer testing is that it
is neither specific (many other conditions cause increases) nor
sensitive, because up to 50% of patients with a small PE have
normal results. Patients with suspected PE and an elevated
D-dimer level but normal venous ultrasound may need a spiral
CT or lung scan.
A spiral (helical) CT scan (CT angiography or CTA) is the
most common test to diagnose PE. An IV injection of contrast
media is needed to view the pulmonary blood vessels. The scanner continuously rotates around the patient while obtaining
views (slices) of the pulmonary vasculature. This allows us to
see all anatomic regions of the lungs. Computer reconstruction
gives a 3-D picture and assists in seeing PEs.
If a patient cannot have contrast media, a ventilation-perfusion (V/Q) scan is done. The V/Q scan has 2 parts. It is most
accurate when both are done:
1.Perfusion scanning involves IV injection of a radioisotope. A
scanning device images the pulmonary circulation.
2.Ventilation scanning involves inhalation of a radioactive
gas, such as xenon. Scanning reflects the distribution of
gas through the lung. The ventilation portion requires the
patient’s cooperation. It may not be possible to perform in
the critically ill patient, especially if the patient is intubated.
Interprofessional Care
To reduce mortality, we start treatment as soon as we suspect a
PE (Table 30.20). The goals are to (1) facilitate optimal cardiorespiratory function, (2) ensure adequate blood flow, (3) prevent
further growth or extension of thrombi, and (4) prevent and
avoid further recurrence and any complications.
Immediate assessment should focus on cardiorespiratory status, which varies by the size and location of the PE. O2 should be
given by mask or cannula when hypoxemia is present. The FIO2
is titrated based on ABG analysis. In some situations, mechanical ventilation is needed to maintain adequate oxygenation.
Respiratory measures—including turning, coughing, deep
breathing, and incentive spirometry—are important to help
prevent atelectasis. Pain from pleural irritation or reduced coronary blood flow is treated with opioids. If HF is present, diuretics are used. If manifestations of shock are present, IV fluids and
vasopressor agents are given as needed to support circulation.
Management
• Supplemental O2, intubation if needed
• Monitor hemoglobin, assess patient for bleeding
• Monitor activated partial thromboplastin time and international normalized ratio levels
• Balance activity and rest
• Inferior vena cava filter
• Pulmonary embolectomy in life-threatening situation
Drug Therapy
• Unfractionated heparin IV
• Low-molecular-weight heparin (e.g., enoxaparin [Lovenox])
• Factor Xa Inhibitors (e.g., apixaban [Eliquis], edoxaban)
• Thrombin Inhibitors (e.g., dabigatran [Pradaxa])
• Warfarin (Coumadin) for long-term therapy
• Fibrinolytics (e.g., activase) for life-threatening situation
• Analgesia
Drug Therapy
Immediate anticoagulation is required for patients with PE. Drug
therapy for patients with acute PE occurs in 3 phases: initial (for
the first 7 days), longer (up to 6 weeks), and extended (6 months
and beyond). Subcutaneous low-molecular-weight heparin
(LMWH) (e.g., enoxaparin, fragmin, fondaparinux) is the recommended treatment for patients with acute PE. LMWH is safer
and more effective than unfractionated heparin. Monitoring the
aPTT is not necessary or useful with LMWH. Unfractionated IV
heparin is effective but hard to titrate to therapeutic levels.
Warfarin (Coumadin), an oral anticoagulant, should be
started at the time of diagnosis. Warfarin should be given for
at least 3 to 6 months and then reevaluated. Alternatives to
warfarin include apixaban (Eliquis), dabigatran (Pradaxa), and
edoxaban (Savaysa). Anticoagulant therapy may be contraindicated if the patient has complicating factors, such as liver problems (causing changes in the clotting), overt bleeding, a history
of hemorrhagic stroke, heparin-induced thrombocytopenia
(HIT), or other blood dyscrasias.
Some HCPs use direct thrombin inhibitors (see Table 41.10)
in the treatment of PE. Similarly, fibrinolytic agents, such as
tissue plasminogen activator (tPA) or alteplase (Activase), may
help dissolve the PE and the source of the thrombus in the pelvis
or deep leg veins, thus, decreasing the risk for recurrent emboli.
Fibrinolytic therapy is discussed in Chapter 37.
CHAPTER 30
Pulmonary
embolism
IVC filter
with hook
Blood clot caught
in IVC filter
Deep vein
thrombosis
(DVT)
Fig. 30.8 Inferior vena cava (IVC) filter. This small device is placed in
the inferior vena cava. It helps trap blood clots that may travel from the
lower extremities up towards the brain and heart.
Lower Respiratory Problems
619
Initially, keep the patient on bed rest in a semi-Fowler’s position to facilitate breathing. Assess cardiopulmonary status with
careful monitoring of vital signs, cardiac rhythm, pulse oximetry,
ABGs, and lung sounds. Apply O2 therapy as directed. Maintain
a patent IV line for medications and fluid therapy. Monitor laboratory results to ensure therapeutic ranges of INR (for warfarin) and aPTT (for IV heparin). Monitor platelet counts for
thrombocytopenia and the development of HIT. Observe the
patient for complications of anticoagulant and fibrinolytic therapy (e.g., bleeding, bruising). Implement fall precautions once
the patient can be out of bed.
The patient may be anxious because of pain, inability to
breathe, and fear of death. Provide emotional support and reassurance to help relieve the patient’s anxiety.
Teaching about long-term anticoagulant therapy is essential.
Anticoagulant therapy continues for at least 3 months. Patients
with large or recurrent emboli may be treated indefinitely with
anticoagulants. INR levels are drawn at intervals and warfarin
dosage is adjusted. Some patients are monitored by nurses in an
anticoagulation clinic.
Long-term management of PE is similar to that for the patient
with VTE (see more about VTE in Chapter 41). Discharge planning is aimed at preventing worsening of the current condition
and avoiding complications and recurrence. Reinforce the need
for the patient to return to the HCP for regular follow-up care.
PULMONARY HYPERTENSION
Surgical Therapy
Hemodynamically unstable patients with massive PE in whom
thrombolytic therapy is contraindicated may be candidates for
pulmonary embolectomy. Embolectomy, the removal of emboli,
can be achieved through a diagnostic imaging (vascular catheter) or surgical approach. It can help decrease right ventricular
afterload. Surgical outcomes have improved in recent years, in
part due to rapid diagnosis and enhanced surgical procedures.
Percutaneous interventional techniques, surgical embolectomy, ultrasound-guided catheter thrombolysis, and aspiration
thrombectomy are newer, moderately invasive procedures for
PE. In patients who are at high risk and for whom anticoagulation is contraindicated, an inferior vena cava (IVC) filter may be
the treatment of choice (Fig. 30.8). This device, inserted through
the femoral vein, is placed at the level of the renal veins in the
inferior vena cava. Once inserted, the filter expands and prevents the movement of large clots upwards and into the pulmonary system. Complications are rare but include misplacement,
migration, and perforation.
In pulmonary hypertension there is an elevated pulmonary
artery pressure (greater than 20 mm Hg) from an increase in
resistance to blood flow through the pulmonary circulation.
Normally, the pulmonary circulation is characterized by low
resistance and low-pressure vessels. In pulmonary hypertension, the pulmonary pressures are high.
There are 5 classes of pulmonary hypertension.24 Each class
(group) is based on cause:
Group 1: Attributed to medication, specific diseases, genetic
(inherited) link, or idiopathic
Group 2: Related to left-sided HF
Group 3: Related to the lungs and hypoxia
Group 4: Related to the cardiovascular system and thromboembolism
Group 5: Multifactorial (and often unclear) origins (e.g., hematologic, metabolic, renal involvement)
Pulmonary hypertension can occur as a primary disease (idiopathic pulmonary arterial hypertension) or as a secondary complication of a respiratory, heart, autoimmune, liver, or connective
tissue problem (secondary pulmonary arterial hypertension).
NURSING MANAGEMENT: PULMONARY
EMBOLISM
IDIOPATHIC PULMONARY ARTERIAL
HYPERTENSION
Prevention of PE begins with prevention of DVT. Identifying
the “at risk” patient is essential. Nursing measures aimed at prevention of PE are similar to those for prophylaxis of VTE. These
include the use of intermittent pneumatic compression devices,
early ambulation, and anticoagulant medications.
Etiology and Pathophysiology
Idiopathic pulmonary arterial hypertension (IPAH) was previously known as primary pulmonary hypertension (PPH). The
cause of IPAH is unknown. It is related to connective tissue diseases, cirrhosis, and HIV. The exact relationship between these
620
SECTION 6
Problems of Oxygenation: Ventilation
PATHOPHYSIOLOGY MAP
Insult occurs (hormonal, mechanical, other)
Pulmonary endothelial injury
• Smooth muscle proliferation
• Vascular scarring
Sustained pulmonary hypertension
Right ventricular hypertrophy
Cor pulmonale
Right-sided heart failure
Although IPAH has no cure, treatment can relieve symptoms,
improve quality of life, and prolong life. If untreated, IPAH can
rapidly progress, causing right-sided HF and death within a few
years. New drug therapy has greatly improved survival. Drug
therapy consists of agents that dilate the pulmonary blood vessels, reduce right ventricular overload, and reverse remodeling
(Table 30.21). Diuretics are used to manage peripheral edema.
Anticoagulants reduce the risk of thrombus formation. Because
hypoxia is a potent pulmonary vasoconstrictor, low-flow O2
gives symptomatic relief. The goal is to keep O2 saturation 90%
or greater.
Surgical therapy includes pulmonary thromboendarterectomy (PTE), in which clots are removed from the pulmonary
arteries. It is a technically demanding, high risk procedure,
done only at certain centers. Atrial septostomy (AS) is a palliative procedure that involves the creation of an intra-atrial
right-to-left shunt to decompress the right ventricle. It is used
for some patients awaiting a lung transplant. A lung transplant
is an option for patients who do not respond to drug therapy
and progress to severe right-sided HF. Disease recurrence has
not been reported in persons who had a lung transplant.
Fig. 30.9 Pathogenesis of pulmonary hypertension and cor pulmonale.
disorders and IPAH is unclear. Similarly, the pathophysiology of
IPAH is poorly understood. We believe that some type of insult
(e.g., hormonal, mechanical) to the pulmonary endothelium
may occur, causing a cascade of events leading to vascular scarring, endothelial dysfunction, and smooth muscle proliferation
(Fig. 30.9). IPAH affects more females.
Clinical Manifestations and Diagnostic Studies
The classic symptoms are dyspnea on exertion and fatigue.
Exertional chest pain, dizziness, and syncope may occur. These
are related to the inability of cardiac output to increase in response
to increased O2 demand. Abnormal heart sounds may be heard,
including an S3. Eventually, as the disease progresses, dyspnea
occurs at rest. Pulmonary hypertension increases the workload
of the right ventricle and causes right ventricular hypertrophy (a
condition called cor pulmonale) and, eventually, HF.
Right-sided cardiac catheterization is the definitive test
to diagnose any type of pulmonary hypertension. It gives an
accurate measurement of pulmonary artery pressures, cardiac
output, and pulmonary vascular resistance. Diagnostic evaluation often includes ECG, chest x-ray, pulmonary function tests,
echocardiogram, and CT scan. Confirmation of IPAH requires
a workup to exclude conditions that may cause secondary pulmonary hypertension.
The mean time between onset of symptoms and the diagnosis is about 2 years. By the time patients become symptomatic,
the disease is already in the advanced stages and the pulmonary
artery pressure is 2 to 3 times normal values.
Interprofessional and Nursing Care
Early recognition is essential to interrupt the vicious cycle
responsible for disease progression. Encourage patients to
report unexplained shortness of breath, syncope, chest discomfort, and feet and ankle edema to their HCP.
SECONDARY PULMONARY ARTERIAL
HYPERTENSION
Secondary pulmonary arterial hypertension (SPAH) occurs when
another disease causes a chronic increase in pulmonary artery
pressures. The primary disease can cause anatomic or vascular
changes that result in the pulmonary hypertension. SPAH can
develop due to parenchymal lung disease, left ventricular dysfunction, intracardiac shunts, chronic PE, or systemic connective tissue disease.25
The symptoms can reflect the underlying disease, but some
are directly related to SPAH. These include dyspnea, fatigue,
lethargy, and chest pain. Initial physical findings can include
right ventricular hypertrophy and signs of right-sided HF
(increased pulmonic heart sound, S4 heart sound, peripheral
edema, hepatomegaly).
Diagnosis of SPAH is like that of IPAH. With SPAH, we treat
the underlying primary disorder. When irreversible pulmonary
vascular damage has occurred, therapies for IPAH are started.
A PTE may offer a cure for patients with chronic pulmonary
hypertension caused by PE.
COR PULMONALE
Cor pulmonale is enlargement of the right ventricle caused by
a primary respiratory disorder. Almost any disorder that affects
the respiratory system can cause cor pulmonale. The most
common cause is COPD. Pulmonary hypertension is usually a
pre-existing condition in the person with cor pulmonale. Overt
HF may be present. Fig. 30.9 outlines the cause and pathogenesis of pulmonary hypertension and cor pulmonale.
Clinical Manifestations and Diagnostic Studies
Manifestations are subtle and often masked by symptoms of the
lung problem. Common symptoms include exertional dyspnea,
CHAPTER 30
Lower Respiratory Problems
621
TABLE 30.21 Drug Therapy
Pulmonary Hypertension
Drug
Mechanism of Action
Calcium Channel Blockers
diltiazem (Cardizem, cardizem
•↓ BP
LA)
•Act on vascular smooth muscle, causing dilation
nifedipine (Procardia)
•Lower pulmonary artery pressure
Endothelin Receptor Antagonists
ambrisentan (Letairis)
•Binds to endothelin-1 receptors and blocks
bosentan (Tracleer)
the constriction of pulmonary arteries
macitentan (Opsumit)
•Promotes relaxation of pulmonary arteries
•↓ Pulmonary artery pressure
Phosphodiesterase (Type 5) Enzyme Inhibitors
sildenafil (Revatio)
•Promote smooth muscle relaxation in lung
tadalafil (Adcirca)
vasculature
Vasodilators
iloprost (Ventavis)
treprostinil (Tyvaso)
Vasodilators
epoprostenol (Flolan, Veletri)
treprostinil (Remodulin)
Considerations
•Successful in a very small number of patients
•Only used in patients who do not have right-sided HF
•Used at high doses in comparison to other uses of calcium channel blockers
•Given orally
•For patients with New York Heart Association (NYHA) class II to IV
symptoms
•Hepatotoxic
•Monitor liver function tests monthly
•Given orally
•Contraindicated in patients taking nitroglycerin, since may cause refractory hypotension
•Synthetic analogs of prostacyclin (PGI2)
•Dilate systemic and pulmonary arterial
vasculature
•Help relieve dyspnea
•Given by inhalation
•For patients with NYHA class III or IV HF
•Given 6–9 times a day using a disk inserted into a nebulizer
•Can cause orthostatic hypotension. Do not give to patients with systolic
BP <85 mm Hg.
•Promote pulmonary vasodilation and reduce
pulmonary vascular resistance
•Relieves dyspnea and chest congestion
•For patients who do not respond to calcium channel blockers or have
NYHA class III or IV right-sided HF
•Given by continuous IV (central line) or continuous subcutaneous route
•Half-life of epoprostenol is short. Potential clinical deterioration from
abrupt withdrawal if infusion disrupted
tachypnea, cough, and fatigue. Physical signs include evidence
of right ventricular hypertrophy on ECG and an increase in
intensity of S2. Chronic hypoxemia leads to polycythemia and
increased total blood volume and viscosity. Polycythemia is
often present in cor pulmonale from COPD.
If HF accompanies cor pulmonale, peripheral edema, weight
gain, distended neck veins, full, bounding pulse, and enlarged
liver may occur. Various laboratory tests and imaging studies are
used to confirm the diagnosis of cor pulmonale (Table 30.22).
Interprofessional and Nursing Care
Early identification is essential before changes to the heart occur
that may be irreversible. Management is directed at determining the cause and treating the underlying problem.
Long-term O2 therapy, the mainstay of treatment to correct
the hypoxemia, reduces vasoconstriction and pulmonary hypertension. All other interventions are tailored for each patient. If
fluid, electrolyte, and/or acid-base imbalances are present, they
must be corrected. Diuretics may help decrease plasma volume
and reduce the workload on the heart but must be used with
caution. In some cases, decreases in fluid volume from diuresis
can worsen heart function. Bronchodilator therapy is needed
if the underlying respiratory problem is due to an obstructive
disorder.
Other treatments may include vasodilator therapy, calcium
channel blockers, anticoagulants, digitalis, and phlebotomy. All
have varying degrees of success. Chronic management of cor
pulmonale from COPD is like that described for COPD (see
Chapter 31).
ENVIRONMENTAL LUNG DISEASES
Environmental or occupational lung diseases result from
inhaled dust or chemicals. The extent of lung damage is influenced by the toxicity of the inhaled substance, amount and duration of exposure, and individual susceptibility. Environmentally
induced lung disease includes pneumoconiosis, chemical pneumonitis, and hypersensitivity pneumonitis.
Pneumoconiosis is a general term for a group of lung diseases caused by inhalation and retention of mineral or metal
dust particles. The literal meaning of pneumoconiosis is “dust in
the lungs.” We classify these diseases by the origin of the dust
(e.g., silicosis, asbestosis, berylliosis). For example, silicosis
occurs from inhaling silica from sand and rock. Coal worker’s pneumoconiosis (CWP), or black lung, is caused by inhaling large amounts of coal dust. It is a hazard for underground
coal miners. The inhaled substance is ingested by macrophages,
which releases substances that cause cell injury and death.
622
SECTION 6
TABLE 30.22
Cor Pulmonale
Problems of Oxygenation: Ventilation
Interprofessional Care
Diagnostic Assessment
• History and physical assessment
• ABGs, SpO2
• Serum and urine electrolytes
• b-Type natriuretic peptide (BNP)
• ECG
• Chest x-ray
• Echocardiography
• CT scan, MRI
• Cardiac catheterization
Management
• Treat the cause (which may be difficult, often involves improving O2
delivery to the patient and right ventricular function)
• O2 therapy
• Low-sodium diet
Drug Therapy (Depending on the Primary Cause)
• Bronchodilators
• Diuretics (use with caution)
• Pulmonary vasodilators
• Calcium channel blockers
• Inotropic agents
• Digitalis
• Anticoagulation therapy
Fibrosis occurs from tissue repair after inflammation. Breathing
problems become evident after many years of repeated exposure, resulting in diffuse pulmonary fibrosis (excess connective
tissue).
Asbestos is a group of minerals composed of microscopic
fibers. For many years, asbestos was used for insulation and
to help fireproof buildings. When disturbed, asbestos releases
tiny filament particles into the air. Once inhaled, the tiny
fibers become deposited within the lung. Asbestosis causes
chronic lung inflammation. People with repeated exposure
are at a greater risk for disease. Lung cancer, either squamous
cell carcinoma or adenocarcinoma, is the most frequent cancer from asbestos exposure. There is a lapse of at least 15 to 19
years between first exposure and development of lung cancer.
Mesothelioma, both pleural and peritoneal, is associated with
asbestos exposure.26
Chemical pneumonitis results from exposures to toxic chemical fumes. There are 2 types of chemical pneumonitis: acute and
chronic. In the acute form, there is diffuse lung injury characterized by pulmonary edema. Chronically, the clinical picture
is that of bronchiolitis obliterans (obstruction of the bronchioles
due to inflammation and fibrosis). The chest x-ray is normal or
shows hyperinflation.
Hypersensitivity pneumonitis, or extrinsic allergic alveolitis, is a form of parenchymal lung disease seen when a person
inhales an antigen to which they are allergic. There are acute,
subacute, and chronic forms. Examples include bird fancier’s
lung (exposure to particles in feathers and droppings of birds)
and farmer’s lung (inhalation of hay dust particles).
Clinical Manifestations
Symptoms of many environmental lung diseases may not occur
until at least 10 to 15 years after the initial exposure to the
inhaled irritant. Manifestations common to all pneumoconiosis
include dyspnea, cough, wheezing, and weight loss. Pulmonary
function studies often show reduced vital capacity. A chest x-ray
often shows lung involvement specific to the primary problem.
CT scans have been useful in detecting early lung involvement.
COPD is the most common complication of environmental
lung disease. Other associated problems include acute pulmonary edema, lung cancer, mesothelioma, and TB. Appearance
of these symptoms and complications are often the reason the
patient seeks medical care. Cor pulmonale is a late complication. It is more common in conditions where there is diffuse
pulmonary fibrosis.
Interprofessional and Nursing Care
The best approach to managing environmental lung diseases is
to prevent or decrease environmental and occupational exposure. Teach those at risk about the use of appropriate PPE.
Wearing masks and ensuring well-designed, effective ventilation systems are in place are appropriate for some occupations.
Smoke inhalation by nonsmokers has led to laws requiring a
smoke-free workplace. Periodic inspections and monitoring
of workplaces by agencies such as the Occupational Safety and
Health Administration (OSHA) and the National Institute for
Occupational Safety and Health (NIOSH) reinforce employers’ obligations to provide a safe work environment. NIOSH is
responsible for workplace safety and health regulations in the
United States.
Encourage regular medical check-ups for those in high-risk
occupations. Early diagnosis is essential to halting the disease
process. Care is directed toward preventing disease progression
and monitoring, improving, or controlling respiratory symptoms.
Treatment depends on the cause and severity of the condition.
Acute care may include O2 therapy, IV fluid, percussion therapy,
inhaled bronchodilators, corticosteroids, and NSAIDs. Some
patients need mechanical ventilation. Longer term care includes
pulmonary rehabilitation. Patients should be immunized against
pneumococcal pneumonia and influenza. Discontinuing exposure to the offending inhalant and smoking cessation may or
may not be effective in stopping disease progression.
LUNG TRANSPLANTATION
Lung transplantation has become an important alternative
option for patients with end-stage lung disease. Unfortunately,
the limiting factor is the lack of donors. A variety of pulmonary
problems are potentially treatable with a lung transplant (Table
30.23). Better patient selection criteria, improvements in surgical techniques, enhanced immunosuppression, and excellent
postoperative care have resulted in improved survival rates.
Preoperative Care
Patients being considered for a lung transplant have an extensive evaluation. Absolute contraindications include cancer
CHAPTER 30
TABLE 30.23
Lung Transplant
Common Indications for a
• Progressive lung disease and greater than 50% chance of death in the
next 2 years without a lung transplant
• Chronic obstructive pulmonary disease (COPD)
• Cystic fibrosis
• Emphysema with α1-antitrypsin deficiency
• Idiopathic pulmonary fibrosis
• Interstitial lung disease
• Pulmonary arterial hypertension
within the past 2 years (excluding some types of skin cancer),
untreatable advanced dysfunction of another major organ system (e.g., heart, liver, renal failure), uncorrectable bleeding condition, mycobacterium tuberculosis, severe obesity (BMI >35kg/
m2), and significant psychosocial problems.27 The patient and
family must be able to cope with complex postoperative care
(e.g., adherence to immunosuppressive therapy, monitoring
for infection). Many transplant centers require outpatient pulmonary rehabilitation before surgery to maximize physical
conditioning.
In the United States, the United Network for Organ Sharing
(UNOS) designates recipients of donor lungs based on a
lung allocation score (LAS). The LAS helps prioritize waiting list recipients based on the urgency of need and expected
post-transplant survival expectations.
Patients who are accepted as transplant candidates must
always carry a pager in case a donor organ becomes available.
They must be prepared to be at their transplant center at a
moment’s notice. Patients may have to limit their travel in case
they need to quickly return to the transplant center.
Surgical Procedure
Four types of lung transplant procedures are available: single-lung, bilateral lung, heart-lung, and transplantation of lobes
from a living-related donor.
A single-lung transplant involves a thoracotomy incision on
the affected side of the chest. The opposite lung is ventilated
while the diseased lung is excised, and the donor lung implanted.
There are 3 anastomoses: bronchus, pulmonary artery, and
pulmonary veins. In a bilateral lung transplant, the incision is
made across the sternum and the donor lungs are implanted
separately. A median sternotomy incision is used for a heartlung transplant procedure. Lobar transplantation from living
donors is reserved for those who urgently need a transplant and
are unlikely to survive until a donor becomes available. Most
of these recipients are patients with cystic fibrosis. The donors
are their parents or relatives. Once anastomosis is complete, the
lung is gently reinflated, perfusion is re-established, chest tubes
are inserted, and the surgical incision is closed.
Postoperative Care
Immediate postoperative care often includes mechanical ventilation and hemodynamic monitoring in the ICU. IV therapy, immunosuppression, nutrition support, detection of early
rejection, and preventing or treating complications, including
Lower Respiratory Problems
623
infection, are priorities. Once hemodynamic stability has been
achieved and mechanical ventilation discontinued, the patient
is transferred to a high-acuity observation or surgical unit.
Lung transplant recipients are at high risk for multiple
complications. Infections are the leading cause of death, especially within the 1st year after transplant.28 Bacterial bronchitis and pneumonia are the most common infections. CMV,
fungi, viruses, and mycobacteria are also causative agents.
Noninfectious issues may include VTE, diaphragmatic dysfunction, and cancer.
Immunosuppressive therapy usually includes a 3 drug regimen of tacrolimus, mycophenolate mofetil (CellCept), and
prednisone. (The mechanisms of action of these drugs are discussed in Table 14.17.) Drug levels are monitored on a regular
basis. Lung transplant recipients usually receive higher levels of
immunosuppressive therapy than other organ recipients.
Acute rejection is fairly common. Between 28% and 64% of
patients will have 1 episode of acute rejection in the 1st year
after their transplant.29 When acute rejection occurs, it typically
occurs in the first 5 to 10 days after the transplant. Signs include
low-grade fever, fatigue, dyspnea, dry cough, and O2 desaturation. Accurate diagnosis of rejection is by transbronchial biopsy
completed via bronchoscopy. Treatment consists of high doses
of IV corticosteroids for 3 days, followed by high doses of oral
prednisone. In patients with persistent or recurrent acute rejection, antilymphocyte therapy may be useful.
Bronchiolitis obliterans (BOS) is a manifestation of chronic
rejection in lung transplant patients. BOS is characterized by
airflow obstruction that progresses over time. The onset is
often subacute, with gradual development of exertional dyspnea, nonproductive cough, wheezing, and/or low-grade fever.
Airway obstruction is not responsive to bronchodilators and
corticosteroid therapy. Additional immunosuppressive agents
may be used to treat chronic rejection. Because acute rejection
is a major risk factor for BOS, preventing acute rejection is key
to decreasing chronic rejection.
Before discharge, the patient needs to be able to perform
self-care activities, including managing their medication plan,
and know when to call the transplant team. Patients are taught
pulmonary clearance measures, including chest physiotherapy
and deep-breathing and coughing techniques to help minimize
complications. Home spirometry is used to monitor trends in
lung function. Teach patients to keep medication logs, laboratory results, and spirometry records. An outpatient rehabilitation program can improve physical endurance.
After discharge, the transplant team follows the patient for
transplant-related issues. Patients return to their HCP for health
maintenance and routine illnesses. Care coordination among
the transplant team, inpatient team, and primary care team
is essential for ongoing successful management. Information
about organ transplants, histocompatibility, rejection, and
immunosuppressive therapy is found in Chapter 14.
LUNG CANCER
Lung cancer is the leading cause of cancer-related deaths in
the United States.30 Lung cancer accounts for 25% of all cancer
624
SECTION 6
Problems of Oxygenation: Ventilation
deaths, more than those caused by breast, prostate, and colon
cancer combined. In 2021, around 235,000 new cases of lung
cancer will be diagnosed, and 131,000 Americans will die.30
Although lung cancer has a high mortality and low cure rate,
advances in medical treatment are improving the response
to treatment.
Etiology
Smoking causes 80% to 90% of all lung cancers.31 There is no safe
form of tobacco or tobacco product. Using smokeless tobacco,
pipes and cigars, hookah and waterpipe, bidis, and kreteks all
pose significant risk for lung cancer.
Tobacco smoke contains over 7000 chemicals, of which 250
are harmful. Of the harmful substances in tobacco smoke, 69
interfere with normal cell development and are linked to lung
cancer. Exposure to tobacco smoke causes changes in the bronchial epithelium. These changes usually return to normal with
smoking cessation. The risk for lung cancer gradually decreases
with smoking cessation, reaching that of nonsmokers within 10
to 15 years of quitting.
The risk for developing lung cancer is directly related to total
exposure to tobacco smoke. Measures of exposure include the
total number of cigarettes smoked in a lifetime, age of smoking onset, depth of inhalation, tar and nicotine content, and
the use of unfiltered cigarettes. Nonsmokers can also develop
lung cancer. Sidestream smoke (smoke from burning cigarettes,
cigars) has the same carcinogens found in mainstream smoke
(smoke inhaled and exhaled by the smoker). This exposure to
secondhand smoke creates a health risk for nonsmoking adults
and children.
Other risk factors include exposure to high levels of pollution, radiation (especially radon exposure), and asbestos. Heavy
or prolonged exposure to industrial agents, such as radon, coal
dust, asbestos, chromium, silica, arsenic, and diesel exhaust,
increases risk, especially in smokers.31
Marked variations exist in a person’s tendency to develop
lung cancer. Differences in incidence, risk factors, and survival
exist between men and women (Box 30.5). Genetic, hormonal,
and molecular influences may contribute to these differences.
At the same time, the incidence and survivability vary between
racial and ethnic populations (Box 30.6).
Pathophysiology
We think most primary lung tumors arise from mutated epithelial cells. The growth of mutations, which are caused by carcinogens, is influenced by various genetic factors. Once underway,
epidermal growth factor promotes tumor development. Tumor
cells grow slowly, taking 8 to 10 years for a tumor to reach 1
cm in size, the smallest lesion detectable on x-ray. Lung cancers
occur mainly in the segmental bronchi or beyond and usually
occur in the upper lobes.
There are 2 broad subtypes of primary lung cancer: non–
small cell lung cancer (NSCLC) (84%) and small cell lung cancer (SCLC) (13%) (Table 30.24).32 Lung cancers metastasize
mainly by direct extension and through the blood and lymph
system. The common sites for metastasis are the lymph nodes,
liver, brain, bones, and adrenal glands.
BOX 30.5 BIOLOGIC SEX CONSIDERATIONS
Lung Cancer
Men
• Have a 1 in 15 chance of developing lung cancer (smokers and nonsmokers)
• Diagnosed with lung cancer more than women
• Die from lung cancer more than women
• Male smokers are 10 times more likely to develop lung cancer than nonsmokers
• Lung cancer incidence and deaths are decreasing in men
Women
• Have a 1 in 17 chance of developing lung cancer (smokers and nonsmokers)
• Lung cancer incidence and deaths are increasing in women.
• Develop lung cancer after fewer years of smoking than men
• Develop lung cancer at a younger age than men
• Nonsmoking women are at greater risk for developing lung cancer than
nonsmoking men
• Women with lung cancer live, on the average, 12 months longer than men
BOX 30.6
EQUITY
PROMOTING HEALTH
Lung Cancer
Blacks
• Have the highest incidence of lung cancer
• Are more likely to die from lung cancer than any other ethnic group
• Have a higher rate of lung cancer among men than in other ethnic groups
Whites
• Have the 2nd highest death rate from lung cancer
• Have a higher rate of lung cancer among women than in other ethnic groups
Asians/Pacific Islanders and Hispanics
• Have the lowest rates of lung cancer in both men and women
Source: American Lung Association: Lung cancer fact sheet. Retrieved
from https://www. lung.org/lung-health-diseases/lung-disease-lookup/
lung-cancer/resource-library/lung-cancer-fact-sheet.
Other Types of Lung Tumors
SCLC and NSCLC account for 97% of lung tumors. The other
3% include:
• Hamartomas, the most common benign tumor, is a
slow-growing congenital tumor composed of fibrous tissue,
fat, and blood vessels.
• Mucous gland adenoma is a benign tumor arising in the
bronchi. It consists of columnar cystic spaces.
• Mesotheliomas are either malignant or benign. They start in
the visceral pleura. Malignant mesotheliomas are related to
asbestos exposure. Benign lesions are localized.
Secondary metastases from other cancers can occur. Cancer cells
from another part of the body reach the lungs through the pulmonary capillaries or lymphatic network. The main cancers that spread
to the lungs often start in the breast, GI, or genitourinary tract.
Paraneoplastic Syndrome
Lung cancer can cause paraneoplastic syndrome. Paraneoplastic
syndrome may be initiated by hormones, cytokines, enzymes
(secreted by tumor cells), or antibodies (made by the body in
CHAPTER 30
TABLE 30.24
Type
Lower Respiratory Problems
625
Types of Primary Lung Cancer
Growth Rate
Characteristics
Response to Therapy
Non–Small Cell Lung Cancer (NSCLC)
Adenocarcinoma
Moderate
• Accounts for 40% of lung cancers
• Most common lung cancer in United States
• Most common cancer in people who have not smoked
• Found in peripheral areas of lung
• Often has no manifestations until widespread metastasis is present
Large cell
Rapid
• Accounts for 10% of lung cancers
(undifferentiated)
• Composed of large cells that are anaplastic
cancer
• Often arise in bronchi
• Is highly metastatic via lymphatics and blood
Squamous cell
Slow
• Accounts for 25%–30% of lung cancers
cancer
• Centrally located
• Causes early symptoms of nonproductive cough and hemoptysis
• Does not have a strong tendency to metastasize
Small Cell Lung Cancer (SCLC)
Small cell cancer
Very rapid
• Accounts for about 10%–15% of lung cancers
• Very aggressive form of lung cancer
• Spreads early via lymphatics and bloodstream
• Frequent metastasis to brain
• Associated with endocrine problems
• Surgical resection may be tried depending
on staging
• Does not respond well to chemotherapy
• Surgery is not usually done because of high
rate of metastases
• Tumor may be radiosensitive but often recur
• Surgical resection may be tried
• Adjuvant chemotherapy and radiation
• Depending on the staging, life expectancy
is better than for SCLC
• Chemotherapy mainstay of treatment; more
responsive to chemotherapy than NSCLC
• Radiation used as adjuvant therapy and
palliative measure
• Overall poor prognosis
response to the tumor) that destroy healthy cells. Sometimes, paraneoplastic syndrome manifests before the cancer is diagnosed.
Examples of paraneoplastic syndrome include hypercalcemia, syndrome of inappropriate antidiuretic hormone secretion
(SIADH), adrenal hypersecretion, polycythemia, and Cushing
syndrome. SCLCs are most often associated with paraneoplastic syndrome. The conditions may stabilize with treatment of
the underlying cancer. SIADH, adrenal hypersecretion, and
Cushing syndrome are discussed in Chapter 54.
Clinical Manifestations
The manifestations of lung cancer are usually nonspecific. They
may appear late in the disease process. Symptoms may be masked
by a chronic cough attributed to smoking or smoking-related lung
disease. Manifestations depend on the type of primary lung cancer, its location, and extent of metastatic spread. Lung cancer often
presents as a lobar pneumonia that does not respond to treatment.
The most common symptom and often the one that is
reported first is a persistent cough. The patient may have dyspnea or wheezing. Blood-tinged sputum may be present because
of bleeding caused by the cancer. Chest pain, if present, may be
localized or unilateral, ranging from mild to severe.
Later manifestations include nonspecific systemic symptoms, such as anorexia, nausea and vomiting, fatigue, and
weight loss. Hoarseness may be present due to laryngeal nerve
involvement. Dysphagia, unilateral paralysis of the diaphragm,
and superior vena cava obstruction may occur because of intrathoracic spread of the cancer. Lymph nodes are often palpable in
the neck or axillae. Mediastinal involvement may lead to pericardial effusion, cardiac tamponade, and dysrhythmias.
Diagnostic Studies
A chest x-ray is the first diagnostic test done for patients with
suspected lung cancer. The x-ray may be normal or identify a
Fig. 30.10 Lung cancer lesion. (© iStock.com/Sutthaburawonk.)
lung mass or infiltrate (Fig. 30.10). Evidence of metastasis to
the ribs or vertebrae and a pleural effusion may be seen on chest
x-ray. CT scanning is used to further evaluate the lung mass. CT
scans can identify the location and extent of masses in the chest,
any mediastinal involvement, and lymph node enlargement.
Sputum cytology can identify cancer cells, but sputum samples are rarely used in diagnosing lung cancer because cancer
cells are not always present in the sputum. A definitive diagnosis
requires a biopsy. Cells for biopsy can be obtained by CT-guided
needle aspiration, bronchoscopy, mediastinoscopy, or VATS. If
a thoracentesis is done to relieve a pleural effusion, the fluid is
analyzed for cancer cells.
626
SECTION 6
TABLE 30.25
Lung Cancer
Problems of Oxygenation: Ventilation
Interprofessional Care
Diagnostic Assessment
• History and physical assessment
• Chest x-ray
• Bronchoscopy
• Cytologic study of bronchial washings or pleural space fluid
• Transbronchial or percutaneous fine-needle aspiration
• CT scan, MRI, PET
• Mediastinoscopy
• Video-assisted thoracoscopic surgery (VATS)
• Laboratory tests: CBC, electrolytes, BUN, creatinine, WBC and differential,
liver function tests, calcium chemistries
Management
• Surgery (segmental or wedge resection, lobectomy, pneumonectomy)
• Radiation therapy
• Chemotherapy
• Targeted therapy and immunotherapy
• Prophylactic cranial radiation
• Bronchoscopic laser therapy
• Photodynamic therapy
• Airway stenting
• Radiofrequency ablation
Accurate assessment of lung cancer is critical for staging
and determining appropriate treatment. Bone scans and CT
scans of the brain, pelvis, and abdomen assess for metastases. A CBC with differential, electrolyte panel, and liver and
renal function tests are done. Sometimes pulmonary function
tests may be done. MRI and/or positron emission tomography
(PET) may be used to evaluate and stage lung cancer. Table
30.25 outlines the diagnostic assessment and management of
lung cancer.
Staging
Staging of NSCLC is done using the TNM staging system.33
Under the TNM system, cancer is grouped into 4 stages with
A or B subtypes. A simplified version of staging of NSCLC is
shown in Table 30.26. Patients with stages I, II, and IIIA disease
may be surgical candidates. Stage IIIB or IV disease is usually
inoperable and has a poor prognosis. Many NSCLCs are not
resectable at the time of diagnosis.
Staging of SCLC by TNM has not been useful because this
cancer is aggressive and always considered systemic. The stages
of SCLC are limited and extensive. Limited means that the tumor
is only on 1 side of the chest and regional lymph nodes. Extensive
SCLC means that the cancer extends beyond the limited stage.
Unfortunately, most patients with SCLC have extensive disease
at time of diagnosis.
Screening for Lung Cancer
Many medical groups recommend cancer screening for highrisk patients. Adults ages 50 to 80 with a history of smoking
(20 pack-year smoking history or currently smoke) or who quit
smoking but less than 15 years ago should have annual screening for lung cancer.34 Screening is done using low-dose CT.
TABLE 30.26
Lung Cancer
Staging of Non–Small Cell
Stages Characteristics
0
I
A
B
II
A
B
III
A
B
C
IV
A
B
Cancer cells found in first layer of cells in the respiratory airway
or alveoli
Tumor is small and localized to lung. No lymph node involvement
Tumor <3 cm, minimally invasive
Tumor 3–4 cm and invading main airway (but not into right or left
bronchi), visceral pleura.
Increased tumor size, some lymph node involvement
Tumor 4–5 cm with invasion of main airway (but not right or left
bronchi), visceral pleura
Tumor 5–7 cm involving the bronchus and lymph nodes near
bronchi on same side of chest; tumor 5–7 cm with visceral and
parietal pleura, diaphragm, phrenic nerve involvement; 2 or
more tumors in same lobe of lung
Increased spread of tumor
1 or more tumors ≤5 cm or smaller spread to the nearby (same side)
structures (chest wall, pleura, pericardium), or metastases into
diaphragm, hear, bone, and regional lymph nodes below carina
1 or more tumors >5 cm in the same lung, involving heart,
trachea, esophagus, mediastinum; lymph node involvement
(same side or opposite side, or below carina),
Tumor >5 cm and more than 1 tumor in a different lobe of the
lung; lymph nodes on opposite side involved
Distant metastasis (to the other lung)
Metastases to the other lung, pleura, pericardium; 1 new tumor
outside of chest
Metastases widespread and 2 or more tumors outside of the chest
Interprofessional Care
Surgical Therapy
Surgical resection is the treatment of choice in NSCLC stages
I to IIIA without mediastinal involvement. Resection gives the
best chance for a cure. Factors that affect survival include the
size of the primary tumor and preexisting co-morbidities. For
other NSCLC stages, patients may have surgery in conjunction
with radiation therapy, chemotherapy, and targeted therapy.
Surgical procedures include segmental or wedge resection
procedures, lobectomy (removal of 1 or more lobes of the lung),
or pneumonectomy (removal of 1 entire lung). VATS may be
used to treat lung cancers near the outside of the lung. Surgery
is generally not done for SCLC because of its rapid growth and
dissemination at the time of diagnosis.
When the tumor is operable, the patient’s cardiopulmonary
status must be evaluated to determine the ability to have surgery. Pulmonary function studies, ABGs, and anesthesia and
critical care consults are often done to assess the patient’s cardiopulmonary status and overall surgical risk.
Radiation Therapy
Radiation therapy may be used as treatment for both NSCLC
and SCLC. Radiation therapy may be given as curative, palliative, or adjuvant therapy in combination with surgery, chemotherapy, or targeted therapy.
Radiation therapy may be the primary therapy in the person
who cannot undergo surgical resection because of co-morbidities. Radiation therapy relieves dyspnea and hemoptysis from
CHAPTER 30
bronchial obstructive tumors and treats superior vena cava syndrome. It can treat pain from metastatic bone lesions or brain
metastasis. Radiation before surgery can reduce the tumor
mass before surgical resection. Complications of radiation therapy include esophagitis, skin irritation, nausea and vomiting,
anorexia, and radiation pneumonitis (see Chapter 16).
Stereotactic body radiotherapy (SBRT), or stereotactic radiosurgery (SRS), is a type of radiation therapy that uses high doses
of radiation delivered to tumors outside the CNS. SBRT uses special positioning procedures and radiology techniques to deliver a
higher dose of radiation to the tumor and expose only a small part
of healthy lung. It does not destroy the tumor, but damages tumor
DNA. Therapy is given over 1 to 3 days. SBRT is an option for
patients with early-stage lung cancers who cannot have surgery.
Chemotherapy
Chemotherapy is the main treatment for SCLC. In NSCLC,
chemotherapy may be used to treat nonresectable tumors or as
adjuvant therapy to surgery. A variety of chemotherapy drugs
and multidrug protocols are used. Chemotherapy for lung cancer typically consists of combinations of 2 of these drugs: etoposide, carboplatin, cisplatin, paclitaxel, vinorelbine, docetaxel,
gemcitabine, and pemetrexed (Alimta).
Targeted Therapy
Targeted therapy uses drugs that block the growth of molecules
involved in specific aspects of tumor growth (see Chapter 16).
Because this therapy inhibits growth rather than directly killing
cancer cells, targeted therapy may be less toxic than chemotherapy.
One targeted therapy for NSCLC is tyrosine kinase inhibitors. They
block signals for growth in the cancer cells. Agents include cetuximab (Erbitux), erlotinib (Tarceva), afatinib (Gilotrif), gefitinib
(Iressa), osimertinib (Tagrisso), and necitumumab (Portrazza).
Another type of kinase inhibitor is used to treat patients with
NSCLC who have an abnormal anaplastic lymphoma kinase
(ALK) gene. Drugs in this class include crizotinib (Xalkori), brigatinib (Alunbrig), and ceritinib (Zykadia). These drugs directly
inhibit the kinase protein made by the ALK gene that is responsible for cancer development and growth.
Another targeted therapy used to treat lung cancer inhibits
the growth of new blood vessels (angiogenesis) by targeting
vascular endothelial growth factor. Bevacizumab (Avastin) is an
angiogenesis inhibitor.
Immunotherapy
Nivolumab (Opdivo), atezolizumab (Tecentriq), and pembrolizumab (Keytruda) are drugs that target PD-1, a protein on T cells
that normally helps keep these cells from attacking other cells
in the body. By blocking PD-1, these drugs boost the immune
response against cancer cells. This can shrink some tumors or
slow their growth. Nivolumab and pembrolizumab can be used
in people with metastatic NSCLC whose cancer has progressed
after other treatments and with tumors that express PD-1.
Other Therapies
Prophylactic cranial irradiation. Patients with SCLC have
early metastases, especially to the CNS. Most chemotherapy
Lower Respiratory Problems
627
does not penetrate the blood-brain barrier. As a result, after
successful systemic treatment, the patient is at risk for brain
metastases. Pro­phy­lactic radiation can decrease the incidence
of brain metastases and may improve survival rates in patients
with limited SCLC.
Bronchoscopic laser therapy. Bronchoscopic laser therapy
makes it possible to remove obstructing bronchial lesions. The
laser’s thermal energy is transmitted to the target tissue. It is a
safe and effective treatment of endobronchial obstructions from
tumors. Symptoms of airway obstruction are relieved due to
thermal necrosis and tumor shrinkage. The procedure may be
repeated as needed.
Photodynamic therapy. Photodynamic therapy (PDT) is
a form of treatment for early-stage lung cancers that uses a
combination of a drug and a specific type of light. Cancer
cells are killed when the drug, known as a photosynthesizer, is
exposed to a specific wavelength of light. Porfimer (Photofrin)
is the most used photosynthesizer. After an IV injection, it
selectively concentrates in tumor cells in the esophagus and
outer layers of the airways. After a set time (usually 48 hours),
the tumor is exposed to laser light via bronchoscopy, activating
the drug and causing cell death. Necrotic tissue is removed with
bronchoscopy a few days later. This process can be repeated as
needed. PDT can affect nutrient delivery to cancer cells and
stimulate the immune system to attack the cancer cells.
Airway stenting. Stents are used alone or in combination
with other techniques for relief of dyspnea, cough, or respiratory
insufficiency. The stent is inserted during a bronchoscopy. The
advantage of a stent is that it supports the airway wall against
collapse or external compression and can delay extension of
tumor into the airway lumen. At this time, we do not know
which patients will benefit most from airway stents.
Radiofrequency ablation. Radiofrequency ablation therapy
is used to treat small NSCLC lung tumors that are near the
outer edge of the lungs. This therapy is an alternative to surgery
in patients who cannot or choose not to have surgery. A thin,
needle-like probe is inserted through the skin into the tumor.
CT scans are used to guide placement. An electric current is
then passed through the probe, which heats and destroys cancer
cells. Local anesthesia is used for this outpatient procedure.
NURSING MANAGEMENT: LUNG CANCER
Assessment
It is important to determine the patient and caregiver’s understanding of the condition, diagnostic tests (those completed as
well as those planned), treatment options, and prognosis. Assess
the patient’s anxiety level and support available from family and
significant others. Subjective and objective data that you should
obtain are described in Table 30.27.
Clinical Problems
Clinical problems for the patient with lung cancer may include:
• Impaired respiratory function
• Difficulty coping
• Pain
• Deficient knowledge
628
SECTION 6
Problems of Oxygenation: Ventilation
TABLE 30.27 NURSING ASSESSMENT
Lung Cancer
Subjective Data
Important Health Information
Health history: Exposure to secondhand smoke, airborne carcinogens
(e.g., asbestos, radon, hydrocarbons), other pollutants. Urban living
environment. Chronic lung disease (e.g., TB, COPD, bronchiectasis).
History of cancer.
Medications: Cough medicines, bronchodilators, expectorants, other respiratory medications
Functional Health Patterns
Health perception–health management: Smoking history, including what was
smoked, amount per day, and number of years. Family history of lung cancer. Frequent respiratory tract infections
Activity-exercise: Fatigue. Persistent cough (productive or nonproductive). Dyspnea at rest or with exertion, hemoptysis (late symptom)
Cognitive-perceptual: Chest pain or tightness, shoulder and arm pain, headache, bone pain (late symptom)
Objective Data
Cardiovascular
•Pericardial effusion, cardiac tamponade, dysrhythmias (late signs)
General
Fever, nose and/or throat infection, neck and axillary lymphadenopathy, paraneoplastic syndrome (e.g., syndrome of inappropriate ADH secretion)
GI
•Anorexia, nausea, vomiting, weight loss, dysphagia (late)
Musculoskeletal
•Pathologic fractures, muscle wasting (late)
Neurologic
•Confusion, disorientation, unsteady gait (brain metastasis)
Respiratory
•Wheezing, hoarseness, stridor, dyspnea on exertion (unilateral diaphragm
paralysis), pleural effusions (late signs)
Skin
•Edema of neck and face (superior vena cava syndrome), digital clubbing.
Jaundice (liver metastasis)
Other Possible Diagnostic Findings
•Lesions and any metastases found on chest x-ray, CT scan, MRI, PET scan
•Positive sputum or bronchial washings for cytologic studies.
•Positive fiberoptic bronchoscopy and biopsy findings
Planning
The overall goals are that the patient with lung cancer will have a
(1) patent airway, (2) adequate tissue oxygenation, (3) minimal
discomfort, and (4) understanding about the type of lung cancer, and (5) a realistic outlook about treatment and prognosis.
Implementation
Health Promotion
The best way to halt the epidemic of lung cancer is to prevent
people from smoking, help smokers stop smoking, and decrease
exposure to environmental pollutants. Because most smokers
start in the teenage years, prevention of teen smoking has the
most significant role in reducing the incidence of lung cancer.
A wealth of material is available to the smoker who is interested
in smoking cessation.
Modeling healthy behavior by not smoking, promoting smoking cessation programs, and actively supporting education and
policy changes related to smoking are important nursing activities. Many changes have occurred because we know that secondhand smoke is a health hazard. Laws prohibit smoking in most
public places and limit public smoking to designated areas.
Acute Care
Care of the patient with lung cancer initially involves support
and reassurance during diagnostic evaluation. It is important
to recognize the multiple stressors that occur when someone
receives a lung cancer diagnosis. The stress response is a normal and adaptive response but can become detrimental when
stress is overwhelming and intense. Patients have the stress
of their symptoms, including dyspnea and cough. Diagnostic
and therapeutic interventions provide more stress by placing
patients in unfamiliar environments with unusual and perhaps
painful procedures. Emotional stressors include waiting for
test results and awareness of the high mortality rate from lung
cancer. Worries about role performance and ability to care for
their family while undergoing cancer treatment provide further
stress. Assess every patient since each will have unique stressors.
The insight gained will help the patient and caregiver cope with
the stress of both illness and treatment.
Patient-centered care depends on the diagnosis and plan for
treatment. Teach signs and symptoms to report (e.g., hemoptysis, dysphagia, chest pain, hoarseness). Provide comfort, teach
ways to reduce pain, and monitor for drug side effects. Teach
the patient to recognize signs and symptoms that may indicate
progression or recurrence of disease. Be available to listen to
the patient and their families. Encourage them to share their
thoughts, fears, and concerns. Foster appropriate coping strategies for both the patient and caregiver and help them access
resources to deal with the illness.
Care of the patient undergoing radiation therapy and chemotherapy is discussed in Chapter 16.
CHECK YOUR PRACTICE
You are completing discharge teaching with E.S., a 72- year-old patient who
had a lobectomy for NSCLC. She tells you, “I’m not going to give up smoking
my cigarettes because I am just going to die anyhow. I might as well enjoy
smoking while I can.”
• How would you respond?
Ambulatory Care
Counseling patients on smoking cessation and prevention is
essential in decreasing mortality from lung cancer. Assess smoking cessation readiness. Some patients may not perceive value in
quitting smoking once they have a diagnosis of lung cancer. As
CHAPTER 30
nurses, however, we can encourage the patient to perhaps quit
or decrease the number of cigarettes smoked per day. We might
be able to gain support from family members who may wish to
quit smoking with the patient. Explain the importance of maintaining a smoke-free environment in the home, particularly if
O2 will be in use. If the treatment plan includes home O2, the
teaching plan must include the safe use of O2.
For many patients with lung cancer, little can be done to
significantly prolong their lives. Radiation therapy and chemotherapy can provide palliative relief from distressing symptoms.
Constant pain may become a major problem. Measures used
to relieve pain are discussed in Chapter 9. Care of the patient
with cancer is discussed in Chapter 16. The palliative care team
should be involved as the patient and family move toward the
Lower Respiratory Problems
629
end of life (see Chapter 10). Social workers and spiritual care
advisors are invaluable in end-of-life situations. The team can
provide information about disability, financial planning, and
community resources for end-of-life care, such as hospice and
home care.
Evaluation
The expected outcomes are that the patient with lung cancer will:
• Have adequate breathing patterns
• Maintain adequate oxygenation
• Have minimal to no pain
• Convey feelings openly and honestly, with a realistic attitude
about prognosis
Case Study
Pneumonia and Lung Cancer
Patient Profile
J.H. is a 52-year-old male who comes to the ED with shortness
of breath. He says it has really increased over the past several
months. J.H. has not been to a doctor for many years, as he is
often “too busy with work.” His wife told him to get his “cough
checked out.”
(© iStockphoto/
Subjective Data
Thinkstock.)
• 38 pack-year history of cigarette smoking
• Has had 25-lb weight loss despite a normal appetite in the past few months
• Admits to a “smoker’s cough” for the past 2 to 3 years
• Recently started coughing up a small amount of blood-tinged sputum
• Married and the father of 3 adult children
Objective Data
Physical Assessment
• Thin, pale man who looks older than stated age
• Height 6 ft (182.9 cm); weight 135 lb (61.2 kg)
• Intermittently confused and anxious
• Vital signs: temperature 102.6°F (39.2°C), heart rate 120, respiratory rate 36
(shallow, slightly labored), BP 98/54
• Lung auscultation: Coarse crackles (left upper and left lower lobes) that clear
with cough; decreased breath sounds (right middle lobe and right lower lobe)
• Chest wall has limited excursion on right side
Diagnostic Studies
• ABGs: pH 7.51, PaO2 62 mm Hg, PaCO2 30 mm Hg, HCO3− 22 mEq/L
• SpO2 saturation 88% (room air)
• Chest x-ray: Right lung (RML, RLL) consolidation, with visible mass around
right bronchus; small pleural effusion (<150mL) on the right side
• Bronchoscopy: Biopsy of mass reveals small cell lung cancer (SCLC)
Interprofessional Care
• Diagnosis: Pneumonia with SCLC
• Follow-up and discuss with patient and family appropriate treatment options
Discussion Questions
1. Recognize: How would you classify J.H.’s pneumonia? Why is this
­important?
2. Analyze: Which findings concern you?
3. Analyze: What is your analysis of J.H.’s ABG results?
4. Plan: How would you expect other health care team members to be
involved in J.H.’s care?
5. Prioritize: Based on the assessment data presented, what are the priority
clinical problems?
6. Prioritize: What are the priority nursing interventions for J.H.?
7. Act: Identify activities that you can delegate to assistive personnel (AP).
8. Act: You are planning a meeting with J.H. and his family at 1400 hours to
discuss their needs. The morning of the meeting, the HCP informs you that
J.H. is terminally ill. Who will you include in this meeting?
9. Act: J.H.’s children tell you that they are worried they will get lung cancer,
since their father has it and they grew up around his secondhand smoke.
They want to know what kind of screening is available for them. How will
you respond?
10. Evaluate: How would radiation therapy help J.H.?
Answers available at http://evolve.elsevier.com/Lewis/medsurg.
B R I D G E T O N C L E X E X A M I N A T I O N
The number of the question corresponds to the same-numbered
outcome at the beginning of the chapter.
1.When caring for a patient with acute bronchitis, the nurse
will prioritize interventions by
a. auscultating lung sounds.
b. encouraging fluid restriction.
c. administering antibiotic therapy.
d. teaching the patient to avoid cough suppressants.
2.Which patient(s) have the greatest risk for aspiration pneumonia? (select all that apply)
a. Patient who had thoracic surgery
b. Patient with acute opioid overdose
c. Patient who had a myocardial infarction
d. Patient who is receiving nasogastric enteral feeding
e. Patient who has a traumatic brain injury from blunt
trauma
SECTION 6
Problems of Oxygenation: Ventilation
3.An appropriate nursing intervention to help a patient with
pneumonia manage thick, purulent secretions would be to
a. perform postural drainage every hour.
b. provide analgesics every 3 hours to promote comfort.
c. administer O2 as prescribed to maintain optimal O2 levels.
d. teach them how to cough effectively and expectorate
secretions.
4.A patient with TB is admitted to the hospital and placed
in a single patient room on airborne precautions. What
should the nurse teach the patient? (select all that apply)
a. No visitors will be allowed while in airborne isolation.
b. Expect regular TB skin testing to evaluate for infection.
c. Adherence to precautions includes coughing into a
paper tissue.
d. Take all medications for full length of time to prevent
multidrug-resistant TB.
e. Wear a standard isolation mask if leaving the airborne
infection isolation room.
5.When caring for a patient with a lung abscess, what is the
nurse’s priority intervention?
a. Postural drainage
b. Antibiotic administration
c. Obtaining a sputum specimen
d. Asking the patient about a family history of lung cancer
6.The patient with a right-side pleural effusion has stable vital
signs and O2 at 6 L/min via nasal cannula. A right-side chest
tube is attached to straight drainage. Which actions would
the nurse include in the plan of care? (select all that apply)
a. Placing the patient on NPO status
b. Administering analgesia as ordered
c. Maintaining high-Fowler’s position
d. Encouraging deep breathing and coughing
e. Monitoring color and amount of chest tube drainage
7.You are caring for a patient with several traumatic injuries
after a multiple-vehicle accident. Which assessment finding
would lead you to suspect a flail chest?
a. Chest-tube is draining bright red blood
b. Tracheal deviation to the unaffected side
c. Paradoxical chest movement during respiration
d. Little to no movement of the involved chest wall
8.When planning care for a patient at high risk for pulmonary embolism, the nurse prioritizes
a. maintaining the patient on strict bed rest.
b. using intermittent pneumatic compression devices.
c. encouraging the patient to cough and deep breathe.
d. encouraging a fluid intake of 2000 mL per 8-hour shift.
REFERENCES
1.Centers for Disease Control and Prevention (CDC), National
Center for Health Statistics: Deaths and mortality. Retrieved from
https://www.cdc.gov/nchs/fastats/deaths.htm.
2.CDC: Fast facts: pertussis. Retrieved from http://www.cdc.gov/
pertussis/fast-facts.html.
3.CDC: Vaccine information statement (VIS)-Tdap: tetanus,
diphtheria, and pertussis. Retrieved from http://www.cdc.gov/
vaccines/hcp/vis/vis-statements/tdap.html.
9.The nurse would closely monitor patients exposed to a
chlorine leak from a local factory for
a. pulmonary edema.
b. anaphylactic shock.
c. respiratory acidosis.
d. acute tubular necrosis.
10.Management of a patient after a lung transplant includes
which measures? (select all that apply)
a. Mechanical ventilation in the early postoperative period
b. Assisting with a lung biopsy if acute rejection is suspected
c. IV fluid therapy accompanied by accurate intake and
output
d. Immunosuppressant therapy, which usually involves a 3
drug regimen
e. Pulmonary clearance measures, including deep-breathing and coughing
11.Nursing care of a patient with Stage 4 lung cancer would
include
a. Coordinating a referral to palliative care
b. Limiting visitors to decrease infection risk
c. NPO status and starting parenteral nutrition
d. Avoiding talking about the cancer diagnosis
1. a; 2. b, d, e; 3. d; 4. c, d, e; 5. b; 6. b, c, d, e; 7. c; 8. b; 9. a; 10. a,
b, c, d, e; 11. a.
630
For rationales to these answers and even more NCLEX review
questions, visit http://evolve.elsevier.com/Lewis/medsurg.
EVOLVE WEBSITE/RESOURCES LIST
http://evolve.elsevier.com/Lewis/medsurg
Review Questions (Online Only)
Key Points
Answer Keys for Questions
• Rationales for Bridge to NCLEX Examination Questions
• Answer Guidelines for Case Study
Student Case Studies
• Patient With Lung Cancer
• Patient With Pulmonary Embolism and Respiratory Failure
Nursing Care Plans
• eNursing Care Plan 30.1: Patient With Pneumonia
Conceptual Care Map Creator
Audio Glossary
Content Updates
4.CDC: Pertussis (whooping cough): diagnosis confirmation.
Retrieved from https://www.cdc.gov/pertussis/clinical/diagnostic-testing/diagnosis-confirmation.html.
*5.World Health Organization (WHO): WHO reveals leading causes
of death and disability worldwide: 2000-2019. Retrieved from
https://www. www.who.int/news/item/09-12-2020-who-revealsleading-causes-of-death-and-disability-worldwide-2000-2019.
*6.Modi AR, Kovacs CS: Hospital-acquired and ventilator-associated
pneumonia: diagnosis, management, and prevention, Clev Clin J
of Med 87:633, 2020.
CHAPTER 30
7.Saha BK: Rapidly progressive necrotizing pneumonia: remember
the streptococcus anginous group! Retrieved from https://www.
ncbi.nlm.nih.gov/pmc/articles/PMC7406454/.
*8.Salzer HJF, Schafer G, Hoenigl M, et al: Clinical, diagnostic, and
treatment disparities between HIV-infected and non-HIV-infected immunocompromised patients with pneumocystis
jirovecii pneumonia. Retrieved from https://www.karger.com/
Article/Pdf/487713.
9.Einsele H, Ljungman P, Boeckh M: How I treat CMV reactivation after allogeneic hematopoietic stem cell transplantation,
Blood 135:1619, 2020.
*10.Karakioulaki M, Stolz D: Biomarkers in pneumonia-beyond
procalcitonin, Int J Mol Sci 20:2019, 2004.
*11.Warren C, Medei MK, Wood B, et al.: A nurse-driven oral care
protocol to reduce hospital-acquired pneumonia, AJN 119:44,
2019.
12.WHO: Tuberculosis. Retrieved from https:// www.who.int/newsroom/fact-sheets/detail/tuberculosis.
13.CDC: Fact sheet: Multi-drug resistant tuberculosis (MDR-TB).
Retrieved from: https://www.cdc.gov/tb/publications/factsheets/
drtb/mdrtb.htm.
14.Massachusetts Department of Public Health: Booster or recall
effect and two-stage tuberculin skin testing. Retrieved from
https://www.mass.gov/service-details/booster-or-recall-effectand-two-stage-tuberculin-skin-testing.
*15.Zhou G, Luo Q, Luo S, et al.: Interferon-γ release assays or
tuberculin skin test for detection and management of latent
tuberculosis infection: a systematic review and meta-analysis,
Lancet Infect Dis 20:1457, 2020.
*16.Pradipta IS, Houtsma D, van Boven JFM, et al: Interventions to
improve medication adherence in tuberculosis patients: a systematic review of randomized controlled studies. Retrieved from
https://www.nature.com/articles/s41533-020-0179-x.
17.CDC: Tuberculosis fact sheet: special considerations for treatment of TB disease in persons infected with HIV. Retrieved from
https://www.cdc.gov/tb/publications/factsheets/treatment/treatmenthivpositive.htm.
18.CDC: Fungal diseases: where valley fever comes from. Retrieved
from https://www.cdc.gov/fungal/diseases/coccidioidomycosis/
causes.html.
19.Kamangar N: Lung abscess clinical presentation. Retrieved from
https://emedicine.medscape.com/article/299425-clinical.
20.Wong AW, Ryerson CJ, Guler SA: Progression of fibrosing interstitial lung disease. Retrieved from https://respiratory-research.
biomedcentral.com/articles/10.1186/s12931-020-1296-3.
Lower Respiratory Problems
631
21.Lee J: Idiopathic pulmonary fibrosis. Retrieved from https://www.
merckmanuals.com/en-ca/professional/pulmonary-disorders/
interstitial-lung-diseases/idiopathic-pulmonary-fibrosis.
22.Duffett L, Castellucci LA, Forgie MA: Pulmonary embolism: update on management and controversies. Retrieved from https://
www.bmj.com/content/bmj/370/bmj.m2177.full.pdf
23.Kim NH, Delcroix M, Jais X, et al: Chronic thromboembolic
pulmonary hypertension. Retrieved from https:// erj.ersjournals.
com/content/53/1/1801915.
24.Yaghi S, Novikov A, Trandafirescu T: Clinical update on pulmonary hypertension, J Invest Med 68:821, 2020.
25.University of Wisconsin School of Medicine and Public Health
Primary and secondary pulmonary hypertension. Retrieved
from https://www.uwhealth.org/thoracic-surgery/primary-and-secondary-pulmonary-hypertension/11358#.
26.American Cancer Society: Risk factors for malignant mesothelioma. Retrieved from https://www.cancer.org/cancer/malignant-mesothelioma/causes-risks-prevention/risk-factors.html.
27.Cheronis N, Rabold E, Singh A, et al.: Lung transplantation in
COPD, Crit Care Nurs Q 44:61, 2021.
28.Bos S, Vos R, Van Raemdonck DE, et al.: Survival in adult lung
transplantation: where are we in 2020? Curr Opin Organ Transplant 25:268, 2020.
*29.Parulekar AD, Kao CC: Detection, classification, and management of rejection after lung transplantation, J Thorac Dis
11:S1732, 2019.
30.American Cancer Society: Key statistics for lung cancer. Retrieved from https://www.cancer.org/cancer/lung-cancer/about/
key-­statistics.html
31.CDC: Lung cancer: what are the risk factors for lung cancer? Retrieved from https://www.cdc.gov/cancer/lung/basic_info/risk_factors.htm.
32.Bohnenkamp S, Lacovara J: Non-small cell lung cancer: Part 1,
Med-Surg Nursing 29:411, 2020.
33.Lababede O, Meziane MA: The eighth edition of TNM staging
of lung cancer: Reference chart and diagrams, Oncologist 23:844,
2018.
*34.US Preventive Services Task Force: Screening for lung cancer:
US Preventive Services Task Force recommendation statement,
JAMA 325:962, 2021.
*Evidence-based information for clinical practice.