combinations. Antimicrob Agents Chemother (Bethesda). 1970;10:195.
Philadelphia, PA: Lippincott Williams & Wilkins; 2005:365.
the uptake of 14 C-labeled streptomycin by enterococci. J Clin Invest. 1971;50:2580.
from patients with infective endocarditis. Antimicrob Agents Chemother. 1980;18:944.
correction appears in Antimicrob Agents Chemother. 1995;39:2835]. Antimicrob Agents Chemother.
combinations of cell wall-active agents. J Infect Dis. 1996;173:909.
endocarditis. Antimicrob Agents Chemother. 1981;20:405.
experimental Enterococcus faecalis endocarditis. J Antimicrob Chemother. 1997;39:519.
used? Clin Infect Dis. 2002;34:159.
Murray BE. Vancomycin-resistant enterococcal infections. N EnglJ Med. 2000;342:710.
Rice LB. Emergence of vancomycin-resistant enterococci. Emerg Infect Dis. 2001;7:183.
States, 1989–1993. MMWR Morb Mortal Wkly Rep. 1993;42:597.
System Report, data summary from January 1992 through June 2004, issued October 2004. Am J Infect
Treatment of Infective Endocarditis. New York, NY: Grune and Stratton; 1981:123.
feedings. Antimicrob Agents Chemother. 2005;49:3676.
Scand J Infect Dis. 2007;39:75.
Munoz-Price LS et al. Emergence of resistance to daptomycin during treatment of vancomycin-resistant
Enterococ-cusfaecalis infection. Clin Infect Dis. 2005;41:565.
endocarditis: impact of protein binding? Ann Pharmacother. 2008;42:289.
hospital. Medicine (Baltimore). 1997;76:94.
Pierrotti LC, Baddour LM. Fungal endocarditis, 1995–2000. Chest. 2002;122:302.
Diseases Society of America. Clin Infect Dis. 2009;48:503.
Melamed R et al. Successful non-surgical treatment of Candida tropicalis endocarditis with liposomal
amphotericin B (AmBisome). Scand J Infect Dis. 2000;32:86.
Terrell CL. Antifungal agents. Part II. The azoles. Mayo Clin Proc. 1999;74:78.
human immunodeficiency virus infection [Letter]. Clin Infect Dis. 1992;15:1062.
and associated with endophthalmitis and folliculitis. Clin Infect Dis. 1992;14:422.
Antimicrob Agents Chemother. 2015;59:2365.
Tunkel AR et al. Enterobacter endocarditis. Scand J Infect Dis. 1992;24:233.
Cooper R, Mills J. Serratia endocarditis. A follow-up report. Arch Intern Med. 1980;140:199.
prognostic indicator in infective endocarditis. Am J Med. 1985;78:262.
Reyes MP, Lerner AM. Current problems in the treatment of infective endocarditis due to Pseudomonas
aeruginosa. Rev Infect Dis. 1983;5:314.
and gentamicin. J Infect Dis. 1977;136:327.
aminoglycosides against Pseudomonas aeruginosa. Rev Infect Dis. 1984;6(Suppl 3):S678.
organisms, including Pseudomonas aeruginosa. Am J Med. 1985;78:251.
Dickinson G et al. Efficacy of imipenem/cilastatin in endocarditis. Am J Med. 1985;78(6A):117.
surgery. Arch Dis Child. 1997;76:68.
Pseudomonas aeruginosa endocarditis. Antimicrob Agents Chemother. 1985;28:428.
Child JS. Risks for and prevention of infective endocarditis. Cardiol Clin. 1996;14:327.
guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease
Acute bronchitis is a commonly encountered clinical diagnosis exhibited
by cough for more than 5 days and generally does not require treatment
ACUTE EXACERBATION OF CHRONIC OBSTRUCTIVE
Antibiotics should be provided to patients with acute exacerbations of
chronic obstructive pulmonary disease (AECOPD) if three primary
symptoms (increased dyspnea, increased sputum volume, and increased
sputum purulence) are present, if two primary symptoms are present
and increased sputum purulence is one of the symptoms, or with
required mechanical ventilation.
Hospitalized patients with AECOPD should both be optimally treated,
and their COPD management be assessed to decrease the likelihood of
readmission. Baseline COPD medications should be examined and
adjusted based on disease severity. Additionally, an assessment of
patients’ understanding of the role of medications (maintenance therapy
vs. rescue medications), ability to use inhalers correctly, access to
prescribed medications, and discussions regarding pulmonary
rehabilitation should take place. Consideration for pharmacologic venous
thromboembolism prophylaxis should also be made in this high-risk
Vaccinations to prevent influenza and Streptococcus pneumoniae in
patients with COPD or previous pneumonia reduce disease-associated
The first decision after a diagnosis of community-acquired pneumonia
(CAP) is to determine the need for hospitalization. Several predictive
rules including the pneumonia severity index (PSI) and CURB-65
(confusion, uremia, increased respiratory rate, low blood pressure, and
age ≥65 years) have been developed to facilitate site-of-care decision
The most frequently isolated bacterial pathogen causing CAP, regardless
of epidemiologic factors and severity of illness, is S. pneumoniae.
The most important consideration when selecting empiric therapy is to
identify patients at risk for infection with drug-resistant S. pneumoniae
Patients who continue to have a positive laboratory test result for
influenza more than 48 hours after the onset of illness are at high risk of
requiring hospitalization, or who are not improving should also be
HOSPITAL-ACQUIRED, VENTILATOR-ASSOCIATED, AND
HEALTH CARE–ASSOCIATED PNEUMONIA
Hospital-acquired pneumonia (HAP) is defined as pneumonia that
occurs at least 48 hours after hospital admission. Ventilator-associated
pneumonia (VAP) refers to pneumonia that arises 48 to 72 hours after
endotracheal intubation. Health care–associated pneumonia (HCAP) is
diagnosed in any patient who has been hospitalized in an acute-care
hospital for 2 or more days within 90 days of infection; resided in a
nursing home or long-term care facility; received intravenous antibiotic
therapy, chemotherapy, or wound care within the past 30 days of the
The major difference in the bacteriology between CAP and
HAP/HCAP/VAP is a shift to gram-negative pathogens, MDR
pathogens, and methicillin-resistant Staphylococcus aureus (MRSA) in
Risk factors for pneumonia caused by MDR pathogens include
antimicrobial therapy in the previous 90 days, current hospitalization of 5
days or more, immunosuppressive disease or therapy, or any risk factor
Patients with early-onset pneumonia (<5 days) and no MDR risk factors
can be treated with a single agent, including a non-antipseudomonal
third-generation cephalosporin or ertapenem, ampicillin/sulbactam, or an
combination of antibiotics active against Pseudomonas aeruginosa. This
regimen usually includes an antipseudomonal β-lactam, plus either an
aminoglycoside or ciprofloxacin/levofloxacin. Vancomycin or linezolid
should be added if MRSA risk factors are present or if there is a high
incidence at the health care facility.
Acute bronchitis (AB) is defined as an acute, self-limiting respiratory illness of the
upper bronchi accompanied by cough for more than 5 days that can last up to 3
1–3 AB may be associated with or without purulent sputum production, and
2 Patients can be diagnosed with AB when there is no evidence of
pneumonia and when acute asthma, an acute exacerbation of chronic obstructive
pulmonary disease (AECOPD), or the common cold have been ruled out as the cause
3 While the true incidence of AB is unknown, it is considered to be one of
the most common conditions encountered in clinical practice, accounting for more
than 6.7 million outpatient visits per year.
Pathophysiology and Epidemiology
AB is characterized by the inflammatory response to infection in the epithelium of the
bronchi. Further progression of this inflammation leads to thickening of the tracheal
2 Sloughing of cells from the tracheobronchial epithelium and inflammatory
mediators causes bronchospasm and reduced forced expiratory volume in 1 second
) that usually improves after 5 weeks. Spread of pathogen and inflammatory
response correlate with patient symptoms. Although bacteria can be isolated from
sputum, bacterial invasion of the bronchial tree rarely occurs, and the role of
bacterial pathogens in AB is limited.
5 The vast majority of cases of AB are presumed
Cough lasting for more than 5 days is the hallmark sign of AB. Although the illness is
self-limited, cough can last for up to 3 weeks (typical duration 10–20 days). Sputum
production occurs in up to 50% of cases, but it does not indicate bacterial infection.
Fever is unusual in most cases; when present, it should prompt investigation for
influenza (during appropriate seasons) or for pneumonia (if other clinical signs are
Antimicrobials do not significantly reduce symptoms of AB, and their use increases
the risk of adverse drug events and antimicrobial resistence.
United States and abroad recommend against the use of antimicrobial agents for the
9 Despite the evidence refuting their use, greater than 70% of AB
cases are treated with antibiotics in the United States. Furthermore, the agents used
for AB are increasingly broad-spectrum drugs, further exacerbating bacterial
10 Non-antimicrobial treatment considerations include
bronchodilators or antitussives depending on symptoms, even though evidence to
support the use of many of these modalities is limited.
QUESTION 1: A.R. is a 50-year-old man presenting with a chief complaint of cough. His symptoms have
blood pressure of 130/70 mm Hg, and respiratory rate of 18 breaths/minute with accompanying oxygen
coughing, but it is otherwise normal. What signs and symptoms in A.R. are consistent with AB?
Persistent cough in the absence of other symptoms including fever or myalgia is
3 Cough can last up to 3 weeks and is usually self-limited. The
typical duration of symptoms in AB is 5 to 14 days.
2 Pneumonia must be ruled out;
however, normal oxygen saturation and lack of focal signs on pulmonary physical
examination makes this diagnosis less likely. Sputum production is common, although
not present in all cases of AB. Symptoms can be present at night, contributing to
CASE 67-1, QUESTION 2: What are the most likely causes of A.R.’s case of AB?
The causative agent for AB is identified in a minority of cases; however, when
pathogens are isolated, they are usually of viral etiology.
bacterial pathogens are associated with AB and should primarily be considered in
patients with underlying COPD, mechanical ventilation (tracheobronchitis), or in
cases of outbreaks and exposures (e.g., Bordetella pertussis). A list of common
pathogens with their specific symptoms is included in Table 67-1.
Sick contacts, duration of incubation (2–7 days for viruses vs. weeks for atypical
bacteria), and previous exposures should be considered when determining the
etiologic agent responsible for AB. Specific symptoms reveal infection caused by
specific pathogens, such as an inspiratory whoop and post-tussive emesis (B.
pertussis), pharyngitis and cough lasting longer than 4 weeks (Mycoplasma
pneumoniae), hoarseness with low-grade fever (Chlamydophila pneumoniae), or
cough with fever and myalgias (influenza).
2 Given A.R.’s lack of sick contacts with
bacterial infections (his son’s recent colds are most likely of viral etiology), time
course of present illness, and absence of symptoms suggestive of influenza, a viral
etiology (other than influenza) is most likely to be the cause of his symptoms.
Clinical Diagnosis and Treatment
CASE 67-1, QUESTION 3: Should A.R. be provided an antimicrobial agent for his AB?
Antibiotics have not been shown to substantially reduce the duration of illness in
8 Thus, guidelines recommend against the routine use of antimicrobial therapy for
9 Despite these recommendations, antimicrobials are frequently prescribed
Inappropriate use of antimicrobial therapy is a public health
concern because it may lead to adverse events and antimicrobial resistance. One
exception to avoidance of antimicrobial therapy in AB is if B. pertussis infection
(whooping cough) is suspected. In these cases, antibiotic therapy with a macrolide
antibiotic is recommended, and patients should remain in isolation for the first 5 days
of treatment to prevent disease transmission.
In A.R.’s case, no antimicrobial agent
CASE 67-1, QUESTION 4: Should a sputum culture be obtained from A.R.? What other diagnostics should
Obtaining a sputum sample for culture to determine the presence of the causative
agent or diagnostic screening for atypical pathogens is not routinely indicated for AB.
The rationale is that most of the identified pathogens have no specific treatment (viral
illnesses), and the isolated organisms often are not true pathogens. Diagnostic
screening, however, should be performed during influenza season or during outbreaks
of B. pertussis or other atypical pathogens for infection control purposes. The use of
their widespread use cannot be recommended at this time.
CASE 67-1, QUESTION 5: What symptom-guided therapies should be offered to A.R.?
Influenza Quick onset with fever, chills, headache, and cough. Myalgias are common and may be
Parainfluenza Epidemics in autumn. Outbreaks may occur in nursing homes. Croup in child at home
suggests presence of the organism.
About 45% of family members exposed to infant with bronchiolitis become infected.
Outbreaks prominent in winter or spring. Twenty percent of adults have ear pain.
Adenovirus Similar presentation as influenza; abrupt onset of fever.
Rhinovirus Fever is uncommon and infection generally mild.
uncommon. Marked leukocytosis with lymphocytic predominance can occur.
Incubation period is 2–3 weeks. Outbreaks in military personnel and students have been
Incubation period is 3 weeks. Onset of symptoms, which include hoarseness before
cough, is gradual. Outbreaks reported in nursing homes, college students, and military
Source: Wenzel RP, Fowler AA 3rd. Clinical practice. Acute bronchitis. N EnglJ Med. 2006;355:2125.
Symptom-guided therapies include the use of inhaled β-agonists (albuterol) for
shortness of breath, particularly in patients with underlying reactive airway disease;
inhaled or systemic steroids for persistent cough; nonsteroidal anti-inflammatory
drugs (NSAIDs), aspirin, or acetaminophen to alleviate myalgias or fever; or
antihistamines (brompheniramine), antitussives (codeine, dextromethorphan, or
benzonatate), or mucolytics (guaifenesin) for cough. These symptom-guided
treatments, however, are not backed by strong evidence demonstrating a clear benefit
1–3,11,12 As such, each of these treatments should be approached
with an appropriate consideration of the balance between perceived benefit and risk
of adverse events. Given A.R.’s troublesome cough that has kept him up at night, a
trial of an antitussive such as dextromethorphan is a reasonable first option. NSAIDs
should be avoided given his concurrent aspirin use and lack of clear indication. An
inhaled β-agonist or steroid is also not necessary at this time.
CASE 67-1, QUESTION 6: Should a chest radiograph be ordered for A.R.? What other illnesses may be
considered as the cause of his symptoms?
It is important to distinguish AB from pneumonia with chest radiograph or other
imaging tests when fever, tachycardia, tachypnea; physical examination findings such
as egophony or rales; or hypoxemia or mental status changes (especially in the
3 Clinical differentiation of AB fromAECOPD, postnasal drip,
gastroesophageal reflux disorder (GERD), and asthma must also be made (discussed
separately in this chapter and in Chapter 23 Upper Gastrointestinal Disorders, and in
Chapter 18 Asthma, respectively). In A.R.’s case, no signs of pneumonia are seen on
physical examination or on reviewing symptomatology; therefore, no chest
radiograph is warranted. Frequent symptoms over time or risk factors for COPD
would warrant an investigation for chronic bronchitis. Wheezing or frequent AB
outbreaks and GERD symptoms would guide evaluations for asthma or
gastrointestinal disorders, respectively.
An evaluation of A.R.’s expectations for therapy is important to alleviate concerns
about the decision to not to prescribe antimicrobials. Overuse of antibiotics in AB is
often driven by either prescriber knowledge or patient request. Communication is key
with each patient to provide insight into the potential causative agents of AB, the
natural course of the disease, the role of symptomatic relief, and reasons for avoiding
prescriptions for antibiotics.
Definition, Incidence, and Epidemiology
According to the Global Initiative for Chronic Obstructive Lung Disease (GOLD),
Chronic Obstructive Pulmonary Disease (COPD) is a persistent and progressive
reduction in airflow that results from repeated exposure to noxious particles. The
chronic inflammation in the lungs results in a narrowing of the small airways,
destruction of alveoli, and loss of elastic recoil. Of note, COPD may or may not be
accompanied by increased sputum production and chronic cough. This disease is also
characterized by acute exacerbations (AECOPD), which is defined as a worsening of
symptoms that is more severe than the typical day-to-day variations that patients
experience during the stable phase of their disease. Acute exacerbations of COPD
typically require a change in medication to relieve symptoms and improve
16 Maintenance therapy for COPD (discussed separately in Chapter 19
Chronic Obstructive Pulmonary Disease) is often targeted to reduce the severity and
COPD is associated with high health care expenditures, decreased quality of life,
significant morbidity, and high mortality around the world. AECOPD is responsible
for most of this burden. In the United States and Canada, COPD is the third and fourth
leading cause of death, respectively. In 2009 in the United States, 1.5 million
emergency department visits and 715,000 hospitalizations were attributable to
17 Direct health care costs associated with COPD in 2010 were estimated to
be $29.5 billion in the United States.
17 AECOPD is associated with a decrease in
quality-of-life measurements and an increase in the rate of decline in lung function,
particularly if not treated early.
The primary precipitating factors for AECOPD are infection of the bronchial tree
18–20 As many as one-third of the cases of AECOPD do not have a
Bacteria, viruses, and pollutants lead to inflammatory responses.
inflammation, associated with increases in interleukin-8, tumor necrosis factor-α, and
neutrophils, contributes to pulmonary remodeling, decreased ciliary clearance of
mucus, worsening airflow obstruction, and the respiratory symptoms associated with
Viruses have been identified as the etiologic cause of AECOPD in up to one-third
of the cases, while bacteria have been identified in up to one-half of cases.
micro-organisms most commonly associated with AECOPD include Haemophilus
influenza, Streptococcus pneumoniae, and Moraxella catarrhalis. In patients with
GOLD 3 (severe) or GOLD 4 (very severe) COPD, Pseudomonas aeruginosa is more
16 Many patients with COPD are also colonized with bacteria during the
stable phase of their illness.
21 Evidence suggests that either an increased burden of
the same colonizing microorganism(s) or acquisition of a new bacterial species may
be associated with exacerbating COPD symptoms.
21 Decreases in adaptive immune
responses occur as COPD disease progresses, making patients susceptible to more
frequent exacerbations caused by bacterial pathogens. Additionally, pathogens
associated with exacerbations tend to increase in virulence and antimicrobial
resistance as the underlying disease progresses.
prolonged infection and colonization in patients with COPD is suggested by
interactions between both viruses and bacteria altering immune respone.
Clinical Presentation and Diagnosis
Common features of AECOPD include the following: breathlessness, increased
cough, increased sputum volume, and increased sputum purulence. In contrast to AB,
purulent sputum in AECOPD is associated with an acute bacterial infection.
less specific symptoms include insomnia, fatigue, tachycardia, tachypnea, and a
decrease in exercise tolerance. Patients often report a decrease in ability to conduct
Diagnostic considerations in the evaluation of patients with AECOPD include
pulse oximetry and arterial blood gases, electrocardiogram, and complete blood
count including white blood cell (WBC) differential. Chest radiographs are helpful to
pneumonia, pneumothorax, or pleural effusion. An assessment of comorbidities,
such as the presence of heart failure or lung diseases (e.g., asthma or lung cancer),
should be performed to aid in both prognosis and diagnosis.
samples for Gram stain and culture are not generally recommended, but it may be
helpful if patients are failing initial therapies.
Pharmacotherapy directed at AECOPD includes bronchodilators and supplemental
oxygen, antimicrobial therapy to decrease the burden of microorganisms, and
corticosteroids targeting the inflammatory response.
(aminophylline or theophylline) are rarely used owing to conflicting and limited
evidence of efficacy and concerns about toxicity.
treatment considerations include decisions regarding the site-of-care and the level of
respiratory support. These nondrug considerations are not discussed in detail in this
chapter but are available in the GOLD Guidelines.
QUESTION 1: T.H. is an 81-year-old white woman presenting to the emergency department (ED) because
Arterial blood gases: pH, 7.34, PCO2
Blood urea nitrogen (BUN), 15 mg/dL
Serum creatinine (SCr), 1.21 mg/dL
Brain natriuretic peptide, 66 pg/mL
Thyrotropin, 1.63 micro-international units/mL
Chest radiograph indicated small pleural effusions, but it was otherwise negative for infiltrates or
(obtained 1 year ago) indicated an FEV1
to forced vital capacity ratio of 0.39 and an FEV1
How would you stage the severity of this exacerbation for T.H.?
T.H. has several risk factors for a poor outcome, including the presence of atrial
fibrillation and severe COPD defined by her home oxygen requirement and low
Clinical signs and symptoms consistent with a severe exacerbation include the use
of accessory respiratory muscles, paradoxical chest wall movements, worsening or
new cyanosis, peripheral edema, hemodynamic compromise, signs of right heart
failure, and alterations in mental status. T.H. has two of these factors: reduced
alertness and use of accessory muscles.
Supplemental oxygen to alleviate hypoxemia is a foundation of treatment for
AECOPD. Controlled provision of oxygen should be implemented to provide an
oxygen saturation of greater than 90% or a Pao2 of greater than 60 mm Hg. Hypoxia
that is not easily reversible warrants further examination for venous
thromboembolism, pneumonia, or other causes. A repeat arterial blood gas should be
obtained within 1 hour of initiation of supplemental oxygen to assess for carbon
dioxide retention or acidosis.
The use of short-acting bronchodilators should be initiated promptly in all patients
with AECOPD. β-Agonists, such as albuterol, with or without an anticholinergic
agent (ipratropium), are the preferred agents.
If the patient does not respond, a
methylxanthine (theophylline or aminophylline) may be considered as second-line
therapy. There is no role for long-acting bronchodilators in AECOPD at this time.
CASE 67-2, QUESTION 3: Does T.H. need to be treated with antimicrobial therapy?
The “cardinal” symptoms of AECOPD include increases in sputum purulence,
23 The use of cardinal symptoms as a method of staging
AECOPD severity has been used in several prospective studies and is recommended
Experts advocate for the use of antibiotics for AECOPD, particularly when two or
three cardinal symptoms are present.
18 Specifically, the GOLD Guidelines
recommend antibiotics for patients with three cardinal symptoms (increased dyspnea,
increased sputum volume, and increased sputum purulence); when two cardinal
symptoms are present if increased sputum purulence is one of the symptoms; or in all
patients requiring mechanical ventilation for their AECOPD.
T.H. is exhibiting all three of the cardinal symptoms and therefore should receive
antibiotics. Likely benefits would be enhanced treatment success, prevention of
relapse, decreased risk for rehospitalization, improvement in pulmonary function,
and reduction of the severity of her exacerbation.
CASE 67-2, QUESTION 4: Which antimicrobial agent should be selected for treating T.H.? What duration
of treatment would be recommended?
Given T.H.’s history, diminished mental status, and risk factors for poor outcomes,
intravenous (IV) administration seems appropriate for the initial antibiotic
administration. Potential risk factors for P. aeruginosa should be evaluated. If T.H.
demonstrates risk factors for P. aeruginosa, an anti-pseudomonal β-lactam, such as
cefepime, would be an appropriate initial agent. If no risk factors for P. aeruginosa
as moxifloxacin or levofloxacin should be selected. All these therapies are active
against drug-resistant S. pneumoniae (DRSP). If T.H. improves on one of these
parenteral agents and is ready for discharge, T.H. could transition to an oral
respiratory fluoroquinolone or high doses of amoxicillin/clavulanate.
Another important consideration for initial selection of antimicrobials is an
evaluation of antibiotic history. Alternative antimicrobials from another class should
be considered if patients have been previously treated in the last 3 months.
Additionally, if no improvements in symptoms occur within 72 hours, consider
obtaining a sputum sample for directed therapy.
The duration of treatment of antibiotics for AECOPD suffers from lack of solid
evidence-based recommendation. Given findings from CB investigations, a duration
of 5 to 10 days has been suggested, but this is an area in need of further research.
CASE 67-2, QUESTION 5: Should T.H. be treated with corticosteroids? If so, which dose and duration
In the setting of AECOPD, systemic corticosteroids help to improve lung function,
shorten recovery time, and prevent relapses. Based on available evidence, the GOLD
Guidelines recommend a corticosteroid regimen of 40 mg/day of prednisone for 5
16 This regimen would be appropriate for T.H.,
although an equivalent intravenous regimen could be considered if she was not able
to take an oral regimen. Higher doses and longer durations of therapy have not been
found to confer a clinical advantage, and intravenous and oral regimens are
In those patients receiving more than 3 weeks of
steroids or multiple course of steroids in the previous months, tapering the dose
should be considered. Although it is more expensive, nebulized budesonide may be
considered as an alternative to oral corticosteroids for treatment of AECOPD.
CASE 67-2, QUESTION 6: What factors should be assessed for T.H. during her hospitalization, and what
follow-up should be planned to help assure she recovers fully and is not readmitted for COPD?
Hospitalized patients with AECOPD should both be optimally treated, and their
COPD management be assessed to decrease the likelihood of readmission. T.H.’s
baseline COPD medications should be examined and adjusted based on disease
severity (see Chapter 19 Chronic Obstructive Pulmonary Disease for details).
Additionally, an assessment of her understanding of the role of medications
(maintenance therapy vs. rescue medications), ability to use inhalers correctly,
access to her prescribed medications, and discussions regarding pulmonary
rehabilitation should take place.
17 Consideration for pharmacologic venous
thromboembolism prophylaxis (see Chapter 11 Thrombosis) should also be made in
PREVENTION OF COMMON RESPIRATORY
CASE 67-2, QUESTION 7: Which vaccines should be considered for T.H. as part of her COPD
Vaccination records for influenza and S. pneumoniae should be evaluated in T.H.
Annual influenza vaccination is recommended for all patients ≥6 months with COPD,
and it has been shown to reduce the risk of AECOPD.
pneumoniae with the 23-valent polysaccharide vaccine is recommended for patients
≥19 years old with COPD. Unlike the influenza vaccine, however, vaccination
against S. pneumoniae has not been clearly linked with a reduced risk of AECOPD.
The pneumococcal vaccine is recommended by guidelines, however, as part of the
overall health plan of the patient.
Definition, Incidence, and Epidemiology
Pneumonia is an infection of the lung parenchyma. Community- acquired pneumonia
(CAP) refers to pneumonia acquired in the absence of health care system exposure
(i.e., hospital, long-term care, chronic antibiotic exposure). Diagnosis is dependent
upon clinical features and radiologic evidence of an infiltrate, but it may be further
supported by physical examination and/or hypoxemia.
Current estimates show that CAP accounts for 24.8 cases per 10,000 discharges in
the US adult population with the elderly being primarily affected (65–79 years:
63/10,000; ≥80 years: 164.3/10,000).
In the pediatric population, CAP accounts for
15.7 cases per 10,000 discharges, with infants and young children showing increased
29 The overall mortality rate for patients ≥65 years is
5.6% and is more pronounced in hospitalized patients (8.5%) compared to
30 Seventeen percent of older patients who develop CAP will
Development of CAP occurs through the inhalation of infectious particles via
droplets or aerosols, or the aspiration of oral flora. Rarely, hematogenous spread of
bacteria from distant sources into the lungs may occur, as well as direct extension of
infection to the lung from contiguous areas, such as the pleural or subdiaphragmatic
Once bacteria reach the tracheobronchial tree, defects in local pulmonary defenses
facilitate infection. Contributing factors include inflammation-mediated injury to
bronchial epithelium leading to depressed mucociliary clearance and a blunted
cellular and humoral response. Patients with underlying or acquired
immunodeficiencies are at an increased risk.
Clinical Presentation and Diagnosis
In the majority of CAP cases, patients present acutely with high fever, chills,
tachypnea, tachycardia, and productive cough. Physical examination findings are
usually localized to a specific lung zone and can include crackles, rhonchi, bronchial
dullness, or egophony. On rare occasions, CAP exhibits a subacute presentation with
fever, nonproductive cough, constitutional symptoms, and absent or diffuse findings
on lung examination. Children with CAP may present with vomiting.
A chest radiograph or other imaging technique revealing an infiltrate is required
32 Radiographic manifestations of diseases such as
congestive heart failure and malignancy can obscure the infiltrate, reinforcing the
need to utilize both clinical and chest radiographic findings.
Pretreatment blood cultures and a respiratory sample (expectorated or induced
sputum or endotracheal aspirate in intubated patients) should be obtained for culture
and Gram stain. Although these cultures are often negative, when they are positive,
they allow fine-tuning of the empirical antibiotic selection.
Antibiotic therapy for CAP is empirical in the majority of cases and should always
be based on the most likely pathogen(s), underlying patient characteristics, and the
severity of disease. Based on these variables, clinicians can triage patients for risk of
infection caused by antibiotic-resistant pathogens and appropriately tailor therapy.
results include the following:
Arterial blood gases: pH 7.42, PO2
What signs, symptoms, and tests are consistent with CAP in J.T.?
In the majority of cases, patients with CAP present with cough with sputum
production, dyspnea, and pleuritic chest pain.
33 Patients may show signs of the
systemic inflammatory response syndrome, including tachycardia, tachypnea, fever,
34 Auscultatory examination often reveals decreased
breath sounds, crackles or rhonchi, or egophony in patients with consolidation. Signs
and symptoms associated with severe pneumonia are grouped into minor and major
criteria defined by the Infectious Disease Society of America (IDSA)/American
Thoracic Society (ATS) Guidelines for CAP.
32 Minor criteria include respiratory
rate greater than 30 breaths/minute at admission; ratios of the Pao2
) less than 250 mm Hg; systolic blood pressure
(SBP) less than 90 mm Hg, or diastolic blood pressure (DBP) less than 60 mm Hg;
confusion; multilobar infiltrates; SBP less than 90 mm Hg despite aggressive fluid
resuscitation; BUN of at least 20 mg/dL; leukopenia; thrombocytopenia; and
hypothermia. Major criteria include requirement of mechanical ventilation and
requirement of vasopressors for more than 4 hours.
Clinical findings and a positive infiltrate by chest radiograph or other imaging
technique is required for the diagnosis of pneumonia.
32 Patients who are hospitalized
based on clinical symptoms absent of positive imaging should have repeat imaging
performed 24 to 48 hours post-admission.
CASE 67-3, QUESTION 2: Given the clinical condition of J.T. in the ED, where should her care be
The first decision after a diagnosis of CAP is to determine whether the patient
requires hospitalization. Several predictive rules have been developed to facilitate
site-of-care decision making. The two best-studied tools that are endorsed by the
IDSA/ATS guidelines are the pneumonia severity index (PSI) and the CURB-65 rule.
The PSI uses individually scored demographic characteristics (age, gender,
nursing home residence), comorbidities (liver disease, CHF, renal disease,
neoplasm), physical examination findings (mental status, RR, SBP, temp, HR), and
, glucose, Hct, BUN); the total PSI score categorizes patients
into one of five classes that are associated with an escalating risk of death (Table 67-
35 The CURB-65, developed by the British Thoracic Society, is a simple tool that
focuses on five assessments: confusion (owing to pneumonia), uremia (BUN >19
mg/dL), respiratory rate of at least 30 breaths/minute, SBP less than 90 mm Hg
systolic or DBP less than 60 mm Hg, and age of at least 65 years.
receives one point, and the cumulative score is associated with a specific (rising
with higher score) 30-day mortality risk. Based on the score, subsequent care should
be as follows: 0–1 = outpatient; 2 = admission to ward; ≥3 = ICU care. Both scales
identify patients at low risk of death, but the CURB-65 has been found to be more
discerning of patients who need ICU care and with the highest risk of death.
need for ICU admission can be subjective; however, the IDSA/ATS guidelines
recommend that patients with three or more minor criteria, or at least one major
criteria for severe CAP, be admitted to the ICU.
CASE 67-3, QUESTION 3: What testing should be performed to obtain a microbiologic diagnosis in J.T.?
Patient J.T. can be assessed as follows using the PSI: 45-year-old woman (35
points [45 for age – 10 for gender female]), respiratory rate greater than 30
breaths/minute (20 points), heart rate greater than 125 beats/minute (20 points),
temperature greater than 40°C (15 points), hematocrit less than 30% (10 points), and
altered mental status (20 points). A total score of 120 points places J.T. in risk strata
IV (30-day mortality risk: 9.3%–27%), and she should be admitted to the hospital,
potentially to the ICU. Using the CURB-65, J.T. has a score of 3 (30-day mortality of
9.2%) based on uremia, confusion, and increased respiratory rate, and she should be
Microbiologic testing is optional for outpatients with CAP. However, the
IDSA/ATS guidelines recommend attempting to make a microbiologic diagnosis in
patients with CAP who are hospitalized.
32 Microbiologic diagnosis (via sputum or
endotracheal aspirate) can help guide empiric therapy as well as identify rare and
usual etiologies and cluster cases.
Predicted Pneumonia Mortality and Recommended Site of Care
System and Score Predicted 30-Day Mortality (%) Recommended Site of Care
PSI strata I–II (≤70) 0.1–0.7 Outpatient
PSI strata III (71–90) 0.9–2.8 Admit to hospital ward
PSI strata IV–V (≥91) 9.3–27 Admit to hospital; consider ICU
CURB-65 score 0–1 0.7–2.1 Outpatient
CURB-65 score 2 9.2 Admit to hospital ward
CURB-65 score ≥3 14.5–57 Admit to ICU
care unit; PSI, pneumonia severity index.
Urine antigen tests for pneumococcus and Legionella pneumophila serogroup 1 are
available for patients with severe CAP. Both tests are sensitive (>80%) and specific
(>90%), and have the advantage of detecting pathogens after antibiotics have been
The IDSA/ATS guidelines recommend consideration of influenza testing during
traditional “flu season” and during times of an outbreak.
should be via reverse transcriptase polymerase chain reaction (RT-PCR), which is
the most sensitive and specific method, with a quick turnaround time for results (4–6
38 Rapid influenza antigen detection tests may be used, but because of lower
sensitivity and specificity RT-PCR is recommended to confirm negative test results
reported by the rapid antigen test. Viral isolation in standard cell culture should be
routinely performed with respiratory specimens during the influenza season.
CASE 67-3, QUESTION 4: What pathogens are most likely in J.T.?
The major pathogens for CAP are summarized in Table 67-3. The most frequently
isolated bacterial pathogen, regardless of epidemiologic factors and severity of
illness, accounting for approximately 27% of CAP worldwide, is S. pneumoniae.
No comments:
Post a Comment
اكتب تعليق حول الموضوع