Woolfrey2012 PDF
Woolfrey2012 PDF
Woolfrey2012 PDF
t h e Pr a c t i c a l E m e r g e n c y
Department Perspective
a,b,c,
Karen G.H. Woolfrey, MD, FRCP(C) *
KEYWORDS
Pneumonia Community-acquired Classification Treatment
Adult Pneumococcus
PATHOGENESIS
The challenge in the ED is not in making the diagnosis of pneumonia but rather in iden-
tifying the cause of the infection such that the appropriate antibiotic treatment can be
instituted in a timely manner. This strategy is of particular importance in those patients
with higher risk of mortality (ie, hospitalized inpatients). Because microbiological
testing results are not available at the time of the ED assessment, the initial therapy
with antibiotics is empiric.
To facilitate the decision-making process with regard to the institution of empiric
antibiotics, it is helpful to classify pneumonia. The traditional classification was based
on the terminology of typical or atypical pneumonia. The traditional clinical
Fig. 2. Host conditions that predispose to pneumonia. URTI, upper respiratory tract
infection.
Fig. 3. (A) CXR, posteroanterior, lobar consolidation. (B) CXR, lateral, lobar consolidation.
252 Woolfrey
likely offending agent. This practical classification is important for the ED in guiding
treatment. Hence, the history in the ED should focus not only on the pattern of symp-
toms but also on the setting in which the pneumonia is acquired, any geographic travel
or animal exposures in conjunction with any host risk factors that could predispose to
certain types of infection and also predict patient outcome. The classification can be
broadly divided into 4 categories: CAP; hospital-acquired pneumonia (HAP); health
care-associated pneumonia (HCAP); and ventilator-associated pneumonia (VAP).
Community-acquired pneumonia (CAP) is defined as an acute infection of the
pulmonary parenchyma, occurring outside the hospital, with clinical symptoms
accompanied by the presence of an infiltrate on CXR6 The diagnosis of CAP requires
that a patient has not been hospitalized or in a nursing home in the previous 14 days.
The most common pathogens implicated in the development of CAP are Strepto-
coccus pneumoniae, Mycoplasma pneumoniae, Hemophilus influenzae, Clamydo-
philia sp, and viruses.
Two classifications of pneumonia are associated with exposure to the health care
environment. HAP is a new respiratory infection that presents more than 48 hours after
hospital admission. HCAP is infection in patients hospitalized for 2 or more days in the
previous 90 days. This group includes patients undergoing dialysis or chemotherapy,
chronic wound care, or home intravenous antibiotics care, the immunocompromised
patient population, and patients from nursing home facilities.
VAP is pneumonia that is diagnosed more than 48 hours after a patient has been
intubated and placed on a ventilator in the intensive care unit (ICU).
Fig. 5 provides a schematic view of this classification of pneumonia and the path-
ogenic organisms most commonly associated with infection. The latter 3 classes
(HAP, VAP, and HCAP) are predominately associated with gram-negative bacteria.
Acinetobacter is a pathogen associated with VAP specifically, and the 3 encapsulated
bacteria (Streptococcus pneumoniae, Klebsiella, and H influenzae) are all associated
with particularly higher morbidity and mortality.7
Pneumonia in Adults 253
Mortality from pneumonia varies depending on the causative organism, but Strep-
tococcus pneumoniae has the highest mortality. The incidence of Streptococcus
pneumoniae in 2008 was 100/100,000 adults/y. The mortality statistics for pneumo-
coccal pneumonia in 2005 published by the World Health Organization were 1.6
million deaths worldwide. Even in developed countries the statistics indicate 10% to
20% mortality. The greatest risk of pneumococcal pneumonia is usually among people
who have chronic illness such as lung, heart, or kidney disease, sickle cell anemia, or
diabetes. But high rates are also noted in patients recovering from severe illness,
those residing in nursing homes or chronic care facilities, and those patients older
than 65 years.8 Other high mortality causes include Klebsiella, Legionella, and
methicillin-resistant Staphylococcus aureus (MRSA).
The clinical symptoms that characterize pneumonia caused by various agents often
overlap, and the interobserver variability of physical findings has been shown to be
high. This finding has led to an approach of antibiotic treatment of pneumonia in the
ED, which is mostly empiric. However, to facilitate diagnostic decision making, various
epidemiologic conditions have been shown to be related to specific pathogens in
patients with pneumonia.9 These classic associations are shown in Table 1.
The typical cardiovascular reaction to fever is tachycardia. However, certain pneu-
monias may be associated with fever and relative bradycardia (Faget sign). These
pneumonias include Legionella, Mycoplasma, and tularemia. Other infections associ-
ated with this clinical sign include yellow fever, typhoid fever, brucellosis, and Colo-
rado tick fever.
It is also often useful to consider the pathogenic organisms in pneumonia with
respect to age of the host. Table 2 shows the most typical organisms based on age
classification.
DIAGNOSTIC TESTS
Laboratory Tests
Complete blood count
The white blood cell count (WBC) is neither sensitive nor specific to identify the likely
causative agent of pneumonia (ie, bacterial or viral), but may be correlated with the
severity of illness.10,11 However, the WBC count may be useful in 2 scenarios: first,
neutropenia, which may indicate immunosuppression; and second, lymphopenia,
which may indicate immunosuppression from AIDS.
254
Woolfrey
Table 1
Epidemiologic conditions, risk factors, and classic presentations of pneumonia associated with specific pathogens
Pneumonia in Adults
contagious and lethal
Mycobacterium tuberculosis Alcoholics; lung abscess; HIV
(early); IVDU
255
256
Woolfrey
Table 1
(continued )
Pathogen Symptoms Associated Condition Radiographic/Laboratory Findings
Acinetobacter Alcoholics; VAP
HIV (early)
Streptococcus pneumoniae; H
influenzae; M tuberculosis
HIV (late) Opportunistic infection; CD4 <200; increased LDH; low
Pneumocystis jiroveci; progressive SOB oxygen saturation
Cryptococcus; Histoplasma;
Aspergillus; Mycobacterium
kansasii; Pseudomonas
aeruginosa; H influenzae
Abbreviations: CA-MRSA, community-acquired MRSA; COPD, chronic obstructive pulmonary disease; GI, gastrointestinal; HIV, human immunodeficiency virus;
IVDU, intravenous drug use; LDH, lactate dehydrogenase; LFT, liver function test; SARS, severe acute respiratory syndrome; SOB, shortness of breath.
a
Structural lung disease: bronchiectasis.
b
Hotel or cruise ship stay within the previous 2 weeks.
Pneumonia in Adults 257
Table 2
Age related pneumonia pathogens
will result in a change in antibiotic management or that the test is likely to have high
yield. The specific guidelines recommend therefore the use of sputum cultures in
the following 8 circumstances: ICU admission; failure of outpatient antibiotic manage-
ment; cavitary infiltrates; active alcohol abuse; severe obstructive or structural lung
disease; positive Legionella urinary antigen test (UAT); positive pneumococcal UAT;
or pleural effusion.
Serologic testing
Serologic testing is available for Chlamydia sp, Legionella, and some fungi. In the ED
these investigations are useful only from a retrospective perspective because they
usually require both acute and convalescent serum titers. Rapid antigen tests are
also available for influenza and respiratory syncytial virus (RSV). These tests may be
useful as an adjunctive ED test for infection control purposes for hospital inpatients
and as an aid in decision making regarding family and contact prophylaxis.
UATs are commercially available for Streptococcus pneumoniae and Legionella
pneumophilia. These tests have the highest diagnostic yield in patients with more
severe illness. These antigen tests are rapid, simple to use, have high specificity in
adults (<90%), and, most importantly, have the ability to detect the organism after
antibiotics have been started.20,21
Serologic testing can be useful as an aid to tailoring antibiotic management. This
finding is of particular importance for the identification of Mycobacterium or the iden-
tification of antibiotic-resistant strains. The latter have been implicated in increased
mortality22 and in increased risk of clinical failure.23 The identification of certain path-
ogens may have important epidemiologic implications. These implications include
severe acute respiratory syndrome (SARS), influenza, legionnaire disease, and agents
of bioterrorism. Cost is the greatest impedance to testing in all patients. The cost/
benefit ratio must be considered.24
Microbiological testing in severe CAP in patients admitted to the ICU has been
shown to both identify the causative agent and lead to changes in antibiotic therapy,
both of which, in this setting, have had a positive impact on patient outcome.25
Imaging Modalities
CXR
The diagnosis of CAP is based on the presence of select clinical features (cough,
fever, sputum production, or pleuritic chest pain) and is supported by imaging of
the lung. The CXR remains the reference standard for the diagnosis of pneumonia.
It has been shown to have greater sensitivity and specificity than the physical exam-
ination of the chest for diagnosis of pneumonia.26 The CXR is not only useful in making
the diagnosis of pneumonia but also in aiding in differentiating pneumonia from other
common causes of cough and fever, or in identifying an alternative diagnosis.
There is considerable overlap in the classic CXR appearances associated with
specific pathogens. However, CXR has low sensitivity for the diagnosis of pneumonia
in the very elderly population and in the neutropenic population.
Computed tomography scan/magnetic resonance imaging
Computed tomography (CT) of the chest has been shown to have greater sensitivity
than CXR for the diagnosis of pneumonia. However, the clinical significance of these
findings when the CXR is negative is unclear.27 For patients who are hospitalized with
suspected pneumonia but have a negative CXR, it is recommended to treat the condi-
tion empirically and repeat the CXR in 24 to 48 hours.
CT scanning has been shown to be beneficial for the diagnosis of pneumonia in the
neutropenic patient.27,28 CT scanning can be useful in those patients who do not
Pneumonia in Adults 259
respond to initial therapy. In addition to ruling out other diagnoses such as pulmonary
emboli, a CT scan can disclose other reasons for antibiotic failure, including pleural
effusions, lung abscess, or central airway obstruction. Magnetic resonance imaging
has been shown to have similar sensitivity compared with CT and has been recom-
mended for follow-up examinations in this patient population to minimize repeated
radiograph exposure.29
Ultrasonography
Recently the use of bedside ultrasonography has been studied in the ED diagnosis of
pulmonary conditions including pneumonia. Bedside lung ultrasonography has been
shown to be 96% sensitive and 96% specific in the diagnosis of radio-occult (negative
CXR) pleural-pulmonary lesions.30 A recent systematic review31 has also shown
bedside lung ultrasonography to be an ideal tool for the diagnosis of emergency
pulmonary conditions, with the benefit of the absence of radiation.
Diagnostic and treatment decisions for pneumonia are based on assessing the
severity of illness. These assessments also affect the decision between inpatient
and outpatient treatment and ICU admission versus admission to a general ward.
Scoring Systems
Two scoring systems have been developed that can assist in the identification of
patients who may be candidates for outpatient treatment: CURB-65 is a severity of
illness score,32 and the PSI33 is a prognostic model (Table 3).
The use of these objective criteria must be supplemented by physician judgment.
Factors such as patient compliance to oral medication and outpatient social support
Table 3
Comparison of CURB-65 and PSI scores
CURB - 65 PSI
Confusion 11 Age
Blood urea nitrogen >7 mmol/L 11 Female 10
Respiratory rate >30 11 Nursing home resident 110
Systolic blood pressure <90 mm Hg or diastolic Neoplastic disease history 130
blood pressure <60 mm Hg 11
Age >65 y 11 Liver disease 120
Congestive heart failure 110
Cerebrovascular disease 110
Renal disease 110
Altered mental status 120
Respiratory rate >29 120
Systolic blood pressure <90 120
Temperature <35 C or >39.9 C 115
Pulse >124 110
pH <7.35 130
Blood urea nitrogen <29 120
Sodium <130 120
Glucose >13.8 110
Hematocrit <30% 110
Partial pressure oxygen <60 110
Pleural effusion on radiograph 110
260 Woolfrey
systems should be taken into account. The ATS has also developed criteria to assist in
the decision making regarding which patients require higher-level monitoring or an
ICU admission directly from the ED.7
The PSI uses a 2-step approach to risk assessment. Patients are first identified as
low-risk and recommended for outpatient management. The low-risk patients are
those less than 50 years, who do not have significant comorbid conditions, and
who have no concerning features on physical examination. Patients who do not
meet these low-risk criteria are then classified into categories based on age, comorbid
illness, abnormal physical examination findings, and laboratory abnormalities. Scoring
is divided into 5 classes and each class is associated with a predicted mortality: class
1, points 0, mortality 0.1%; class 2, points less than 70, mortality 0.6%; class 3, points
71–90, mortality 2.8%; class 4, points 91–130, mortality 8.2%; class 5, points greater
than 130, mortality 29.2%. Classes 1, 2, and 3 are considered low-risk patients, class
4, moderate-risk, and class 5, high-risk. Hospital admission is recommended for those
patients who score more than 91 (class 4). This score has been shown to decrease
overall admission rates and decrease health care costs.34 However, the scoring
system does not consider dynamic observation of patients over time, the ability to
take oral medications, home supports, and access to follow-up.
CURB-65 is a more simplified tool that uses 5 criteria to determine patients at lower
risk for adverse events. These criteria are confusion; uremia (blood urea nitrogen
[BUN] >7 mmol/L); respiratory rate (>30); blood pressure (<90 systolic, or >60 dia-
stolic); age 65 years or greater. Each criterion is rated equally for a total score of 5.
The risk of 30-day mortality increases with increasing score. A score of 1 point is
the lowest-risk group, with an estimated 2.7% 30-day mortality; outpatient treatment
is recommended. Two points is the moderate-risk group, with a 6.8% 30-day
mortality; either outpatient treatment with close follow-up or inpatient treatment is rec-
ommended in this group. Three points is the severe group, with an estimated 14%
mortality; inpatient treatment is recommended in this group with consideration for
an ICU admission. Four and 5 points are the highest-risk groups. There is an estimated
27.8% mortality in these groups and an ICU admission is recommended.
Comparison of the PSI and CURB-65 scores reveals that they are equivalent in pre-
dicting mortality.35 Both the 28-day mortality and the inhospital mortality for PSI level V
and CURB >/- 3 were equivalent.36 Both scoring indices have also been shown to
accurately predict outcomes in patients with HCAP.37 However, there are no random-
ized trials of hospital admission strategies that directly compare the 2 scoring
systems. In addition, no prospective criteria have been validated for the decision-
making process for an ICU admission.38 PSI also underperforms in the elderly popu-
lation.39 This finding is suspected secondary to the inappropriate weight given to the
age variable in the scoring system. This situation is of concern because elderly
patients often have atypical presentations and worse outcomes.
The ATS has developed criteria to assist with inhospital disposition decision making.
These criteria are divided into major and minor criteria. Direct admission to an ICU or
high-level monitoring unit is recommended for patients with either of the major criteria
or with 3 of the minor criteria. Major criteria are invasive mechanical ventilation or
septic shock with the need for vasopressors. Table 4 shows the minor criteria for
severe CAP.
MANAGEMENT
The goal of therapy is eradication of the infecting microorganism, with resultant reso-
lution of clinical disease. Antimicrobials are the mainstay of treatment. The ATS
Pneumonia in Adults 261
Table 4
Minor criteria for severe CAP
Table 5
Recommended antibiotic treatment
ambulatory patients with pneumonia without comorbid conditions, risk factors for
DRSP, or recent antibiotic use is not recommended because of the concern for the
development of fluoroquinolone resistance.40 Comorbidity or recent antimicrobial
therapy increased the likelihood of infection with DRSP, and enteric gram-negative
bacteria. In these patients, therapeutic options include either a respiratory fluoroqui-
nolone or a combination therapy with a b-lactam antibiotic effective against Strepto-
coccus pneumoniae plus a macrolide. Recommended b-lactams include: high-dose
amoxicillin or amoxicillin clavulanate. Oral cephalosporins can also be used as alter-
natives. Agents in the same class as the patient has been receiving previously should
not be used to treat patients with recent antibiotic exposure.
For patients who are admitted to a hospital ward, the combination treatment of
a b-lactam plus a macrolide or monotherapy with a fluoroquinolone has been shown
to be associated with a significant reduction in mortality compared with that of the
administration of a cephalosporin alone.41 The choice between dual or monotherapy
should be based on the patient’s previous 3-month antibiotic exposure. Initial therapy
for admitted patients is usually intravenous, but oral therapy can be considered for
patients without risk factors for severe pneumonia, especially with highly bioavailable
agents such as fluoroquinolones.42
Patients admitted to the ICU with pneumonia are those who are usually diagnosed
with severe pneumonia initially from the ED. The antimicrobial treatment in this patient
population must be broader. The minimum recommended treatment of these patients
is a b-lactam plus either azithromycin or a fluoroquinolone. For all patients admitted to
the ICU, antimicrobial coverage should include that for Streptococcus pneumoniae
and Legionella. This combination therapy is recommended for at least 48 hours or until
results of diagnostic tests are known. In the mechanically ventilated ICU patient, treat-
ment with a fluoroquinolone alone has been associated with inferior outcome.43
In the critically ill ICU patient with severe pneumonia, many microorganisms other
than Streptococcus pneumoniae and Legionella sp must be considered. Of particular
importance is Pseudomonas sp and gram-negative bacteria.44 Therefore, standard
empiric treatment regimes in this population should include coverage for Strepto-
coccus pneumoniae, Legionella sp, and H influenzae, all of the atypical organisms,
Enterobacteriaceae sp, and Pseudomonadaceae sp (see Table 5). Penicillin-allergic
patients should have the b-lactam substituted with azetreonam, a synthetic monocy-
clic b-lactam antibiotic. The excess mortality associated with MRSA indicates empiric
coverage for this organism in this patient population. For suspected MRSA (end-stage
renal disease, injection drug abuse, previous influenza, and previous recent antibiotic
use) vancomycin or linezolid should be added.
shown clinical improvement. Criteria for clinical stability include temperature less than
37.8 C, heart rate less than 100/min, respiratory rate less than 24/min, systolic blood
pressure greater than 90 mm Hg; room air oxygen saturation of greater than 90%; and
normal mental status.47 This transition should be balanced with an assessment of the
ability to ingest oral medications in patients with normal functioning gastrointestinal
tracts.
Duration of Treatment
It is recommended that the duration of treatment be a minimum of 5 days and that the
patient be afebrile for 48 to 72 hours before discontinuation of treatment. The patient
should not possess any signs of clinical instability at the time of discontinuation of
treatment.47 Few controlled trials have evaluated the optimum duration of antibiotic
therapy in either inpatients or outpatients. However, most patients with CAP are
treated for 7 to 10 days or longer.
Noninvasive Positive Pressure Ventilation
In patients with pneumonia, noninvasive positive pressure ventilation (NPPV) has been
shown to be well tolerated, safe, and associated with a significant reduction in respi-
ratory rate, need for endotracheal intubation, and duration of ICU stay. NPPV does not
decrease overall duration of overall hospitalization or inhospital mortality, except in the
subgroup of patients with pneumonia and underlying chronic obstructive pulmonary
disease (COPD).48 However, other studies of patients with hypoxic respiratory failure
have failed to show a benefit of NPPV, with many patients eventually requiring intuba-
tion.49 Hence, these conflicting data do not support the routine use of NPPV in patients
with severe pneumonia, with the exception of patients with underlying COPD. The ATS
and the IDSA currently recommend a cautious trial of NPPV for refractory hypoxemia
in patients with severe pneumonia.7
Hypotensive, Fluid-resuscitated Patients with Severe Pneumonia
Corticosteroids have been studied in patients with septic shock and have yielded no ben-
efit. A recent 2010 Cochrane review of 20 randomized trials revealed that corticosteroids
did not change 28-day mortality. Furthermore, corticosteroids did show a statistically
significant increase in adverse events such as hyperglycemia and hypernatremia.50,51
Recombinant human activated protein C (APC) has also been studied in patients
with severe sepsis. A Cochrane Review of 4434 adult patients yielded no benefit.
There was no difference in mortality between the control group and those who
received APC, regardless of the severity of the sepsis. However, use of APC was asso-
ciated with a higher risk of serious bleeding.52
Diffuse Bilateral Pneumonia and Acute Respiratory Distress Syndrome
Mortality for patients with severe diffuse bilateral pneumonia or acute respiratory
distress syndrome (ARDS) is extremely high. The ARDSnet trial revealed a significant
reduction in mortality with the use of low tidal volume ventilation (6 mL/kg ideal body
weight) or what has become known as a lung protective ventilation strategy. With this
intervention, the number needed to treat (NNT) to avoid 1 death is 9 (NNT 5 9).53,54 The
ATS therefore has made a level 1 recommendation that patients with diffuse bilateral
pneumonia or ARDS should be mechanically ventilated with low tidal volumes.
DRSP
Antibiotic resistance patterns vary considerable among countries/regions and evolve
over time. Globally, 1.6 million people die of invasive pneumococcal disease annually.
264 Woolfrey
This incidence is highest in extremes of age, in patients with comorbidity, and in those
with defects in immunity. The development of drug-resistant strains of microorgan-
isms has placed a challenge on effective treatment options.55,56
Emergency physicians should be aware that the patients at the highest risk of infec-
tion with DRSP include those who take antibiotics frequently, patients who are
exposed to others who commonly receive antibiotics, children younger than 6 years
(especially those in daycare facilities and their immediate family members), adults
older than 70 years, and those with underlying immunosuppression.
Penicillin resistance occurs in a stepwise fashion with irreversible mutations of the
penicillin binding proteins. In the United States, penicillin resistance decreased from
1999 to 2005. This decrease was reported in both the pediatric and the adult popula-
tion. This decline is a reflection of the introduction of the 7-valent pneumococcal
conjugate vaccine.57,58
During this same period, resistance rates to macrolides did not change, but resis-
tance to fluoroquinolones increased, likely reflecting an increase in use. The resistance
of fluoroquinolone is highest in adults older than 64 years and in patients with under-
lying COPD.
The impact of antimicrobial resistance on clinical outcome remains controversial.
Host factors such as extremes of age, immunosuppression, and comorbidity likely
also influence mortality.59
Prescribing antibiotics for respiratory infection contributes to the development of
resistance to that antibiotic. The effect seems to be greatest in the month immediately
after treatment but may persist for up to 12 months. Reduction in antibiotic use may
reduce the potential for antimicrobial resistance.60
Antibiotic resistance is a problem that can be combated at the ED level through
a combination of appropriate antibiotic selection, prescribing patterns, use of antibi-
otic resistance profiles, surveillance protocols, and an understanding of new antibiotic
treatment options.
Nonresponding Pneumonia
Nonresolving pneumonia is a clinical syndrome in which clinical symptoms of pneu-
monia do not improve or worsen despite an initial 10 days of antibiotic therapy or in
which radiographic opacities fail to resolve within 12 weeks. Mortality among nonres-
ponding patients is greatly increased compared with patients who initially respond to
treatment. Overall mortality as high as 49% has been reported for nonresponding
hospitalized patients with pneumonia.61 Nonresponse mandates either a transfer to
a higher level of care, further diagnostic testing, or a change in treatment. Inadequate
host response is the most common cause of apparent treatment failure. Patients older
than 65 years, those with COPD, diabetes, alcoholism, or those who are undergoing
immunosuppressive therapy are the most likely to be nonresponders.
Emergency physicians should be aware that as many as 10% of patients with CAP
and up to 60% of patients with HAP have inadequate responses to initial empiric
therapy. As many as 20% of these patients are diagnosed with diseases other than
pneumonia.62
antimicrobials than are the hospital-acquired MRSA strains. However, most of these
strains do contain a toxin associated with the clinical features of necrotizing pneu-
monia, shock, respiratory failure, and the formation of abscesses and empyema.
This strain should be suspected in patients with cavitary infiltrates on CXR. It is esti-
mated that 2% of CA-MRSA infections result in pneumonia.64
CA-MRSA pneumonia is associated with an influenzalike illness, occurs most
commonly in young healthy individuals, and has high mortality. The recommended
parenteral antibiotic treatment is vancomycin or linezolid. The addition of rifam-
picin may also be considered. The management of CA-MRSA should also include
culture of blood, sputum, and pleural specimens in the case of pleural effusion.
Empyema is an associated complication and should be drained. It is recommen-
ded that patients with this diagnosis be admitted to an ICU. Respiratory infection
control measures are important for the prevention of nosocomial spread of
MRSA.65
VIRAL PNEUMONIAS
Influenza
In the ambulatory setting, in uncomplicated cases of viral pneumonia caused by influ-
enza, treatment within 48 hours of symptoms with oseltamivir or zanamivir is recom-
mended. These neuraminidase inhibitors have been shown to reduce median time to
resolution of symptoms by 0.5 to 2.5 days. In this patient population, both oral oselta-
mivir and inhaled zanamivir reduce the likelihood of complications of the lower respi-
ratory tract.66
In the hospitalized patient population, it is postulated that oseltamivir may reduce
viral shedding and therefore treatment even greater than 48 hours of symptom onset
may confer some benefit. Oseltamivir has been shown to have a broad influenza spec-
trum (both influenza A and B) and a low risk of resistance.
Amantadine is effective against influenza A only. Recent circulating influenza viruses
in North America have been resistant to amantadine. Hence, treatment or chemopro-
phylaxis with amantadine is not currently recommended.67
Pandemic Influenza
Influenza A from H5N1 (Avian) and H1N1 (pandemic influenza A) have a greater
severity of infection than routine seasonal influenza. Both strains possess pandemic
potential. These strains have been associated with acute respiratory failure and
mortality greater than70%. The usual clinical presentation is fever, cough, and respi-
ratory distress progressive over 3 to 5 days. Exposure to dead or dying poultry in an
area with known or suspected H5N1 activity has been reported by most patients with
avian influenza A.68
Rapid bedside tests to detect influenza A have been used as screening tools. It is
recommended that confirmed cases be treated with oseltamivir. The current recom-
mendation is for a 5-day course of treatment at the standard dosage of 75 mg 2 times
daily. Oseltamivir has been shown to have a significant mortality reduction, especially
when started within 6 to 8 days after symptom onset. The mortality benefit seems to
affect all age groups.69 All such patients should also be placed in respiratory isolation
and droplet precautions used.
The cause of viral pneumonia is most likely unknown to the emergency physician at
initial presentation. No universal empiric therapy for viral pneumonia can be recom-
mended. Causes of viral pneumonia other than influenza A and B include RSV, adeno-
virus, rhinovirus, enteroviruses, human metapneumovirus, hantavirus, and varicella
266 Woolfrey
zoster virus. Evidence for antiviral treatment of CAP caused by viruses other than influ-
enza comes mainly from case reports and treatment of immunocompromised
patients. Ribavirin has been shown to be efficacious against RSV, human metapneu-
movirus, and parainfluenza. It can be used in intravenous form for the treatment of
severe pneumonia caused by these viruses, from experience with immunocompro-
mised patients.70 Ribavirin aerosol treatment has been shown to be less efficacious.
SUMMARY
Pneumonia is a common disease presentation to the ED. The challenge for the emer-
gency physician is to recognize the diagnosis, initiate early and appropriate empiric
antibiotic therapy, risk stratify patients with respect to severity of illness, and recognize
indications for admission. Treatment should consider not only empiric therapy guide-
lines but also the environment in which the pneumonia was contracted and the host
factors that may implicate risk for a particular microorganism.
The emergency physician should initiate antibiotic treatment in the ED for all
patients who are diagnosed with pneumonia and should be vigilant regarding respira-
tory isolation and droplet precautions. Disposition should be based not only on the
Pneumonia in Adults 267
severity of the presenting symptoms, but the underlying comorbidities of the patient,
the clinical likelihood of deterioration, and the access to outpatient follow-up.
REFERENCES
1. Heron M, Hoyert D, Murphy S, et al. Deaths: final data for 2006. Natl Vital Stat Rep
2009;57(14):1–134.
2. Trends in pneumonia and influenza morbidity and mortality. Morbidity and
Mortality Weekly Report 2010;59(14):425.
3. McCullers J. Insights into the interaction between influenza virus and pneumo-
coccus. Clin Microbiol Rev 2006;19:571–82.
4. Centre for Disease Control and Prevention Advisory Committee on Immunization
Practices (ACIP), Universal Annual Influenza Vaccination. February 24, 2010.
5. Chartbook on cardiovascuar, lung, and blood diseases, 2009. National Heart
Lung and Blood Institute; 2009.
6. Mandell LA, Bartlett JG, Dowell SF, et al. Update of practice guidelines for the
management of community-acquired pneumonia in immunocompetent adults.
Clin Infect Dis 2003;37:1405–33.
7. Mandall LA. Infectious Disease Society of America/American Thoracic Society
consensus guidelines for the management of community-acquired pneumonia
in adults. Clin Infect Dis 2007;44:S27–72.
8. Epidemiology and Prevention of Vaccine Preventable Diseases, 2006. CDC
National Immunization Program; 2006.
9. Neidermann MS, Mandell LA, Anzueto A, et al. Guidelines for the management of
community-acquired pneumonia in adults, diagnosis, assessment of severity,
antimicrobial therapy and prevention. Clin Infect Dis 2007;44(Suppl 2):527–72.
10. Vernet G. Laboratory based diagnosis of pneumococcal pneumonia–state of the
art and unmet needs. Clin Microbiol Infect 2011;17(Suppl 3):1–13.
11. Kruger S, Pletz MW, Rohde G. Biomarkers in community acquired pneumonia–
what did we learn from the CAPNETZ study? Pneumologie 2011;65(2):110–3.
12. Craven DE. Blood cultures for community acquired pneumonia–piecing together
a mosaic for doing less. Am J Respir Crit Care Med 2004;169:327–8.
13. Niederman MS, Mandell LA, Anzueto A, et al. Guidelines for the management of
adults with community-acquired pneumonia. Diagnosis, assessment of severity,
antimicrobial therapy, and prevention. Am J Respir Crit Care Med 2001;163(7):
1730–54.
14. Campbell SG, Marrie TJ, Ansey R, et al. The contribution of blood cultures to the
clinical management of adult patients admitted to the hospital with community-
acquired pneumonia: a prospective observational study. Chest 2003;123:571–82.
15. Metersky MA, Ma A, Bratzler DW, et al. Predicting bacteremia in patients with
community acquired pneumonia. Am J Respir Crit Care Med 2004;169:342–7.
16. Paganin F, Lilienthal F, Bourdin A, et al. Severe community-acquired pneumonia:
assessment of microbial activity as mortality factor. Eur Respir J 2004;24:779–85.
17. Nazarian DJ, Eddy OL, Lukens TW, et al. American College of Emergency Physi-
cian Clinical policy: critical issue in the management of adult patients presenting
to the emergency department with community-acquired pneumonia. Ann Emerg
Med 2009;54(3):704–31.
18. Reed WW, Byrd GS, Gates RH Jr, et al. Sputum gram stain in community acquired
pneumococcal pneumonia: a meta-analysis. West J Med 1996;165:197–204.
19. Metersky M. When to obtain cultures from patients with community-acquired
pneumonia. J Respir Dis 2005;26(4):143–8.
268 Woolfrey
20. Yzerman EP, den Boer JW, Lettinga KD, et al. Sensitivity of three urine antigen
tests associated with clinical severity in a large outbreak of Legionnaires’ disease
in the Netherlands. J Clin Microbiol 2002;40(9):3232–6.
21. Strålin K, Kaltoft MS, Konradsen HB, et al. Comparison of two urinary antigen
tests for establishment of pneumococcal etiology of adult CAP. J Clin Microbiol
2004;42:3620–5.
22. Kollef MH, Sherman G, Ward S, et al. Inadequate antimicrobial treatment of infec-
tions: a risk factor for hospital mortality among critically ill patients. Chest 1999;
115(46):72–4.
23. Arancibia F, Ewig S, Martinez JA, et al. Antimicrobial treatment failure in patient
with CAP. Am J Respir Crit Care Med 2000;162:154–60.
24. Sepsis and CAP: partnerships for diagnostic development. RFA no: RFA-AI-04–
043. US Department of Health and Human Service; 2004.
25. Rello J, Bodi M, Mariscal D. Microbiological testing and outcome in patients with
severe community acquired pneumonia. Chest 2003;123:174–80.
26. Wipf JE, Lipsky BA, Hirschmann HV, et al. Diagnosing pneumonia by physical
examination: relevant or relic? Arch Intern Med 1996;165:197–204.
27. Syrjala H, Broas M, Suramo I, et al. High resolution computed tomography for the
diagnosis of community-acquired pneumonia. Clin Infect Dis 1998;27:358–63.
28. Huessel CP, Kauczor HU, Ullmann AJ. Pneumonia in the neutropenic patient. Eur
Radiol 2004;14(2):256–71.
29. Reiger C, Herzog P, Fiegl M, et al. Pulmonary MRI–a new approach to the eval-
uation of the febrile neutropenic patient with malignancy. Support Care Cancer
2008;16(6):599–606.
30. Volpicelli G, Cardinale L, Berchialla P, et al. A comparison of different diagnostic
tests in the bedside evaluation of pleuritic pain in the ED. Am J Emerg Med 2012;
30(2):317–24.
31. Reissig A, Copetti R, Kroegel C. Current role of emergency ultrasound of the
chest. Crit Care Med 2011;39(4):839–45.
32. Lim WS, van der Eerden MM, Liang R, et al. Defining community acquired pneu-
monia severity on presentation to hospital: an international derivation and valida-
tion study. Thorax 2003;58:377.
33. Fine MJ, Auble TE, Yealy DM, et al. A prediction rule to identify low-risk patients
with community-acquired pneumonia. N Engl J Med 1997;336(4):243–50.
34. Marrie TJ, Lau CY, Wheeler SL, et al. A controlled trial of a critical pathway for
treatment of community-acquired pneumonia. CAPITAL Study Investigators.
Community-Acquired Pneumonia Intervention Trial Assessing Levofloxacin.
JAMA 2000;283(6):749–55.
35. Aujesky D, Auble TE, Yealy DM, et al. Prospective comparison of three validated
prediction rule for prognosis in CAP. Am J Med 2005;118:384.
36. Richard G, Levy H, Laterre PF, et al. CURB-65, PSI, APACHE II to assess mortality
rate in patients with severe sepsis and community acquired pneumonia in
PROWESS. J Intensive Care Med 2011;26(1):34–40.
37. Fang WF, Yang KY, Wu CL, et al. Application and comparison of scoring indices
to predict outcomes in patients with healthcare-associated pneumonia. Crit Care
2011;15(1):R32.
38. Moran GJ, Talan DA, Abrahamian FM. Diagnosis of pneumonia in the ED. Infect
Dis Clin North Am 2008;22:53.
39. Chen JH, Chang SS, Liu JJ, et al. Comparison of clinical characteristics and
performance of pneumonia severity score and CURB-65 among younger adults,
elderly and very old subjects. Thorax 2010;65(11):971–7.
Pneumonia in Adults 269
40. Heffelfinger JD, Dowell SF, Jorgensen JH, et al. Management of community-
acquired pneumonia in the era of pneumococcal resistance: a report from the
Drug-Resistant Streptococcus pneumoniae Therapeutic Working Group. Arch
Intern Med 2000;160:1399–408.
41. Gleason PP, Meehan TP, Fine JM, et al. Associations between initial antimicrobial
therapy and medial outcomes for hospitalized elderly patients with pneumonia.
Arch Intern Med 1999;159:2562–72.
42. Marras TK, Nopmaneejumruslers C, Chan CK. Efficacy of exclusively oral anti-
biotic therapy in patients hospitalized with non-severe community acquired
pneumonia: a retrospective study and meta-analysis. Am J Med 2004;116:
385–93.
43. Levoy O, Saux P, Bedos JP, et al. Comparison of levofloxacin and cefotaxime
combined with ofloxacin for ICU patients with community-acquired pneumonia
who do not require vasopressors. Chest 2005;128:172–83.
44. File TM. Community acquired pneumonia. Lancet 2003;362:1991–2001.
45. Houck PM, Batzler DW. Administration of first hospital antibiotics for community-
acquired pneumonia: does timeliness affect outcomes? Curr Opin Infect Dis
2005;18(2):151–6.
46. Siber SH, Garrett C, Singh R, et al. Early administration of antibiotics does not
shorten time to clinical stability in patients with moderate to severe community
acquired pneumonia. Chest 2003;124:1798–804.
47. Menendez R, Torres A, Rodriguez de Castro F, et al. Reaching stability in commu-
nity acquired pneumonia: the effects of the severity of disease, treatment, and the
characteristics of patients. Clin Infect Dis 2004;39:1783–90.
48. Confalonieri M, Potena A, Carbone G, et al. Acute respiratory failure in patients
with severe community acquired pneumonia. A prospective randomized evalua-
tion of non-invasive ventilation. Am J Respir Crit Care Med 1999;160:1585–91.
49. Antonelli M, Conti G, Moro ML, et al. Predictors of failures of non-invasive positive
pressure ventilation in patients with acute hypoxemic respiratory failure: a multi-
center study. Intensive Care Med 2001;27:1718–28.
50. Annane D, Bellissant E, Bollaert PE, et al. Corticosteroids for treating severe
sepsis and septic shock. Cochrane Database Syst Rev 2010;12. DOI: 10.1002/
14651858.CD002243.pub2.
51. Sprung CL, Annane D, Keh D, et al. CORITCUS Study Group. Hydrocortisone
therapy for patients with septic shock. N Engl J Med 2008;358(2):111–24.
52. Marti-Carcajal AJ, Salanti G, Cardina-Zorrila AF, et al. Human recombinant activated
Protein C for severe sepsis. Cochrane Database Syst Rev 2000;1:CD004388.
53. Eisner MD, Thompson T, Hudson LD, et al. Efficacy of low tidal volume ventilation
in patients with different clinical risk factors for acute lung injury and acute respi-
ratory distress syndrome. Am J Respir Crit Care Med 2001;164:231–6.
54. Petrucci N, Lacovelli W. Lung protective ventilation strategy for the acute respira-
tory syndrome. Cochrane Database Syst Rev 2007;3:CD003844.
55. Van Bembeke F, Reinert RR, Appelbaum PC, et al. Multidrug-resistant Strepto-
coccus pneumoniae infections: current and future therapeutic option. Drugs
2007;67(16):2355–82.
56. Johnson DM, Stilwell MG, Fritsche TR, et al. Emergence of multidrug-resistant
Streptococcus pneumoniae: report from the SENTRY Antimicrobial Surveillance
Program (1999-2003). Diagn Microbiol Infect Dis 2006;56(1):69–74.
57. Lynch J III, Zhanel George G. Streptococcus pneumoniae: epidemiology and risk
factors, evolution of antimicrobial resistance, and impact of vaccine. Curr Opin
Pulm Med 2010;16:217–25.
270 Woolfrey
58. Centers for Disease Control and Prevention (CDC). Pneumonia hospitalizations
among young children before and after introduction of pneumococcal conjugate
vaccine–Unites States 1997-2006. MMWR Morb Mortal Wkly Rep 2009;58:1–4.
59. Lynch JP, Zhanel GG. Streptococcus pneumoniae: does antimicrobial resistance
matter? Semin Respir Crit Care Med 2009;30:210–38.
60. Costelloe C, Metcalfe C, Lovering A, et al. Effect of antibiotic prescribing in
primary care on antimicrobial resistance in individual patients: systematic review
and meta-analysis. BMJ 2010;340:c2096.
61. Menendez R, Torres A, Zalacain R, et al. Risk factors of treatment failure in
community acquired pneumonia: implications for disease outcome. Thorax
2004;59:960–5.
62. Almirall J, Bolibar I, Vidal J, et al. Epidemiology of community acquired pneu-
monia in adults: a population based study. Eur Respir J 2000;15:757–63.
63. Deresinski S. Methicillin-resistant Staphylococcus aureus: an evolutionary, epide-
miologic, and therapeutic odyssey. Clin Infect Dis 2005;40:562–73.
64. Fridkin SK, Hageman JC, Morrison M, et al. Methicillin-resistant Staphylococcus
aureus disease in three communities. N Engl J Med 2005;352:1436–44.
65. Barton-Forbes M, Hawkes M, Moore D, et al. Guidelines for the prevention and
management of CA-MRSA: a perspective for Canadian health care practitioners.
Can J Infect Dis Med Microbiol 2006;17(Suppl C):1B–24B.
66. Treanor JJ, Hayden FG, Vrooman PS, et al. Efficacy and safety of the oral neur-
aminidase inhibitor oseltamivir in treating acute influenza: a randomized
controlled trial. US Neuramidase Study Group. JAMA 2000;283:1016–24.
67. Jefferson T, Demicheli V, Rivetti D, et al. Antivirals for influenza in healthy adults:
systematic review. Lancet 2006;367:303–13.
68. Rothberg MB, Haessler SD. Complications of seasonal and pandemic influenza.
Crit Care Med 2010;38(Suppl 4):e91–7.
69. Adisasmito W, Chan PK, Lee N, et al. Effectiveness of antiviral treatment in human
influenza A(H5N1) infections: analysis of a Global Patient Registry. J Infect Dis
2010;202(8):1154–60.
70. Hopkins P, McNeil K, Kermeen F, et al. Human metapneumovirus in lung trans-
plant recipients and comparison to respiratory syncytial virus. Am J Respir Crit
Care Med 2008;178:876–81.
71. Bozette SA, Sattler FR, Chiu J, et al. A controlled trial of early adjunctive treatment
with corticosteroids for Pneumocystis carinii pneumonia in the acquired immuno-
deficiency syndrome. N Engl J Med 1990;323:1451–7.
72. Gagnon S, Boota AM, Fischl MA, et al. Corticosteroids as adjunctive therapy for
severe Pneumocystis carinii pneumonia in the acquired immunodeficiency
syndrome. N Engl J Med 1990;323:1444–50.
73. Briel M, Bucher H, Boscacci R, et al. Adjunctive corticosteroids for Pneumocystis
jiroveci pneumonia. Cochrane Database Syst Rev 2006;3:CD006150.
74. Hirsehick RE, Glassroth J, Jordan MC, et al. Bacterial pneumonia in person in-
fected with HIV. N Engl J Med 1995;333(13):845–51.
75. Centers for Disease Control and Prevention (CDC). Trends in TB–US 2010.
MMWR Morb Mortal Wkly Rep 2011;60(11):333–7.
76. Centers for Disease Control and Prevention (CDC). Trends in tuberculosis inci-
dence–United States, 2006. MMWR Morb Mortal Wkly Rep 2007;56(11):245–50.
77. Akolo C, Adetifa I, Shepperd S, et al. Treatment of latent TB in HIV infected
patients. Cochrane Database Syst Rev 2010;1:CD000171.