INTRODUCTION
• Community-acquired pneumonia(CAP) is a
syndrome in which acute infection of the lungs
develops in persons who have not been
hospitalized recently and have not had regular
exposure to the health care system.
2.
INTRODUCTION
• Long recognizedas a major cause of death,
pneumonia has been studied intensively since
the late 1800s.
• Despite research and the development of
antimicrobial agents, pneumonia remains a
major cause of complications and death.
3.
COMMON CAUSES
Infectious
• Streptococcuspneumoniae,
• Haemophilus influenzae,
• Staphylococcus aureus,
• Influenza virus,
• Other respiratory viruses
Non Infectious
• Pulmonary edema
• Lung cancer
• Acute respiratory distress
syndrome
4.
LESS COMMON CAUSES
Infectious
•Pseudomonas aeruginosa or
other gram-negative rods
• Pneumocystis jirovecii
• Moraxella catarrhalis,
• Mixed microaerophilic and
anaerobic oral flora
Non infectious
• Pulmonary infarction
Causes of pneumoniavary according to the
– patient population
– host immune status
– geographic region.
No cause is determined in about half of patients with CAP
despite intense investigation.
Normal flora, especially streptococci from the upper airways,
may be responsible for many of these cases
7.
• Although pneumococcusremains the most
commonly identified cause of CAP, the
frequency with which it is implicated has
declined.
• In parts of the world where pneumococcal
vaccines have been used less often and
smoking rates remain high, pneumococcus
remains responsible for a higher proportion of
cases of CAP
8.
• Patients withchronic obstructive pulmonary disease (COPD)
are at increased risk for CAP caused by H. influenzae and Mor.
Catarrhalis.
• P. aeruginosa and other gram negative bacilli also cause CAP
in persons who have COPD or bronchiectasis, especially in
those taking glucocorticoids.
• Legionella pneumonia occurs in certain geographic locations
and tends to follow specific exposures.
• Mixed microaerophilic and anaerobic bacteria (so-called oral
flora) are often seen on Gram’s staining of sputum, and these
organisms may be responsible for cases in which no cause is
found.
• Mandell LA et al. Infectious Diseases Society of America/American Thoracic Society consensus
guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis
2007;44:Suppl 2:S27-S72.
• Falguera M, Carratalà et al. Risk factors and outcome of community-acquired pneumonia due to
Gram-negative bacilli. Respirology 2009; 14:105-11.
9.
APPROACH TO DIAGNOSIS
•Sputum Gram stain and cultures –
– Positive in more than 80% of cases of pneumococcal
pneumonia when a good-quality specimen (>10
inflammatory cells per epithelial cell) can be obtained.
– The yield diminishes with increasing time after antibiotics
have been initiated and with decreasing quality of the
sputum sample.
– Nebulization with hypertonic saline (so-called induced
sputum) may increase the likelihood of obtaining a valid
sample.
10.
• Blood cultures–
– Not required in routine outpatient management of CAP.
– Should be obtained in all hospitalised patients with CAP.
– Positive in about 20 to 25% of inpatients with
pneumococcal pneumonia but in fewer cases of H.
influenzae or P. aeruginosa and only rarely in cases
caused by Mor. catarrhalis.
– Positive in only about 25% of cases in which inhalation or
aspiration is responsible for the CAP.
11.
• Pneumococcal antigendetection
– Not required routinely for the management of CAP.
• Pneumococcal PCR
– Not recommended as a routine diagnostic test in
patients with CAP.
• Legionella urinary antigen test
– Desirable in patients with severe CAP.
12.
• For influenza,PCR is far more sensitive than
rapid antigen tests and has become the
standard for diagnosis, BUT, positive results on
PCR do not exclude the possibility that
bacterial pneumonia is present.
ROLES OF IMAGING
•Imaging is indispensable for the management of CAP.
• Imaging also play a complementary role for the
evaluation of treatment effects of antibiotics.
• Imaging may also be usable for differentiating
noninfectious diseases from infectious pneumonia.
• Chest radiography is usually enough to confirm the
diagnosis of pneumonia and to evaluate treatment
effects, whereas computed tomography (CT) is required
to suggest causative pathogens, to exclude
noninfectious pneumonia and to reveal underlying
diseases.
15.
LUNG ULTRASOUND
• Sensitivityof 94.0% and a Specificity of 96.0%
• Advantages
– Radiation-free
– Can be done at the bedside / on pregnant woman
– Allows for dynamic evaluations,
– Has increased accuracy in the detection of consolidation
and pleural effusion compared with chest radiograph,
– Takes less time.
• Limitations
– Learning curve,
– Repeatability,
– Operator dependency
16.
PATTERNS OF IMAGINGFINDINGS
• CAP has classically been divided into three
distinctive patterns on imaging examinations,
namely
– Consolidation (alveolar/lobar pneumonia),
– Peribronchial nodules (bronchopneumonia)
– Ground-glass opacity.
• The fourth, a unique uncommon pattern of CAP is
random nodules, suggestive of hematogenous
pulmonary infection or granulomatous infection.
17.
Consolidation predominant pattern
(alveolar/lobar pneumonia)
• Believed to be formed by the spread of
inflammation through pores of Kohn or canals
of Lambert at the periphery of the lung. Thus,
nonsegmental consolidation in the early stage
of disease.
• Most bacterial pneumonias like Streptococcus
and Klebsiella.
18.
Streptococcus pneumoniae pneumoniashowing alveolar pattern
nonsegmental consolidation in the right middle lung field, which is
demarcated by the fissure suggestive of upper lobe pneumonia
19.
Klebsiella pneumonia
Suspected whenthere is a cavitatory pneumonia, a bulging fissure
sign. Often there can be extensive lobar opacification with air
bronchogram.
20.
Mycoplasma pneumoniae pneumoniashowing alveolar pattern
Chest radiograph demonstrates ill-defined consolidation in the right
lower lung field (arrow); B: Thin-section CT reveals a non-segmental
consolidation with air bronchograms at the dorsal aspect of the
right lower lobe.
21.
Peribronchial nodules predominant
pattern(bronchopneumonia)
• Predominance of peribronchial nodules including
centrilobular nodules with or without peribronchial
consolidations.
• Consolidations are probably formed by enlargement
and coalescence of the peribronchial nodules. may
follow a chronic clinical course.
• Bronchial wall thickening is often associated.
• Hemophilus influenzae, Mycoplasma
pneumoniae,Staphylococccus aureus, Chlamydophila
pneumoniae, and viruses, MTB, NTM
22.
Staph aureus pneumonia
Chestradiograph shows extensive consolidations and peribronchovascular
consolidations of the right lung (arrows); B: Thin-section CT reveals extensive
consolidation with air bronchograms and cavities in the left upper lobe (black arrows).
Note that the bronchi in the consolidation are dilated. Dense centrilobular nodules are
seen in the left lower lobe (white arrows).
23.
Mycoplasma pneumoniae
CXR showsreticulonodular opacities and focal consolidation in the left middle to lower
lung field (arrow). The left pulmonary hilum appears enlarged; B: Thin-section
CTdemonstrates fluffy centrilobular nodules with surrounding ground-glass opacity in
the left lower lobe (arrows). Note that central bronchial wall is thickened (arrow heads).
24.
Chlamydophila pneumoniae pneumoniashowing infectious bronchiolitis
Chest radiograph shows faint reticulonodular opacities in both lower lung fields
(arrows); B: Thin-section computed tomography reveals centrilobular nodules
(arrows) with bronchiectasis (arrow heads) in the middle lobe and lingula
25.
Ground-glass opacity predominantpattern
• GGO may correspond to
– Incomplete alveolar filling by inflammatory cells or
exudate,
– Pulmonary edema secondary to infection leaving air in
the alveoli,
– Interstitial infiltrates of inflammatory cells (interstitial
pneumonia).
• Viruses, Mycoplasma pneumoniae and
Pneumocystis jirovecii are the representative
pathogens
26.
Mycoplasma pneumoniae pneumoniashowing groundglass
opacity predominant pneumonia
Chest radiograph shows patchy ground-glass opacity (GGO) with peribronchial
nodules in the right middle lung field (arrow); B: Thin-section computed
tomography reveals areas of GGO in the right upper lobe. Note that the GGO are
partly demarcated by interlobular septa (arrows).
27.
Pneumocystis jirovecii pneumonia
Chestradiograph shows bilateral reticulonodular opacities; B: Chest computed
tomography with a 5 mm slice thickness demonstrates bilateral ground-glass
opacity with reticulations.
28.
Random nodules predominant
•Probably produced by hematogenous spread
of the disease or granulomatous infection.
– Viral pneumonia (varicella-zoster),
– Miliary tuberculosis,
– Granulomatous infection, such as tuberculosis,
nontuberculous mycobacterial infection or fungal
infection
29.
Random nodules predominantpneumonia (varicella-zoster pneumonia)
Thin-section computed tomography demonstrates scattered small solid or
ground-glass opacity nodules which are unrelated to centrilobular
structures (arrows).
Pathogen Specific imagingappearances
Streptococcus pneumoniae Alveolar/lobar pneumonia
Mycoplasma pneumoniae Bronchopneumonia with bronchial wall thickening
affecting central bronchi
Chlamydophila pneumoniae Infectious bronchiolitis with bronchial dilatation
Legionella pneumophila Sharply marinated peribronchial consolidations
within ground-glass opacities
varicella-zoster Scattered nodules with a random distribution
Staph aureus Patchy unilateral or bilateral consolidation,rapid
progression,centrilobular nodules,pneumatocele in
children.
Cryptococcus neoformans Multiple nodules/masses with or without cavities in
the same pulmonary lobe
Pneumocystis jirovecii Bilateral patchy ground-glass opacities with a
geographic distribution
32.
CLINICAL CONDITIONS RELATEDTO CAP
1) Aspiration pneumonia –
– Caused by inhalation of bacteria, food, gastric acid
or other materials that provoke pulmonary
inflammation or edema.
– Commonly occurs in patients with deteriorated
consciousness, chronic debilitating disease, and
hospital settings.
• Imaging : Patchy ground-glass opacities at
dorsal parts of the lung, bronchopneumonia or
infectious bronchiolitis.
33.
CLINICAL CONDITIONS RELATEDTO CAP
• 2) Sinobronchial syndrome - Chronic and repeated
infection of the lower respiratory tract and
paranasal sinuses due to altered immune status.
• Imaging :
– Chest radiograph - Reticulonodular opacities with lower
lung field predominance.
– CT - Centrilobular or peribronchial nodules with
bronchial wall thickening and mucus filled bronchi are
seen. There are usually evidences of chronic and
repeated infection, such as bronchiectasis, parenchymal
distortion or reticular opacities.
34.
Sinobronchial syndrome ina
man . A: Chest radiograph
shows bilateral
reticulonodular opacities in
both lower lung fields
(arrows);
B:computed tomography (CT)
at the level of maxillary sinus
demonstrates opacification
of the maxillary sinuses (*)
and bone sclerosis of the sinus
walls (arrows), suggestive of
chronic paranasal sinusitis;
C: Thin-section CT reveals
bronchial wall thickening with
bronchiectasis (arrows) and
minimal centrilobular
opacities (arrow heads).
35.
CLINICAL FEATURES
• Fever
•Cough
• Shortness of breath
• Pleuritic chest pain
• Non-specific features in the elderly. May present ‘off
legs’ or with confusion, in the absence of fever.
36.
CLINICAL FEATURES ASSOCIATEDWITH
SPECIFIC CAUSES OF CAP
1) Favoring typical bacterial or legionella pneumonia
– Acute presentation
– May Present with septic shock
– Initial upper respiratory illness followed by acute
deterioration (suggesting viral infection with bacterial
superinfection)
– White-cell count, >15,000 or ≤6000 cells per cubic
millimeter with increased band forms
– Dense segmental or lobar consolidation
– Procalcitonin level, ≥0.25 μg per liter
37.
CLINICAL FEATURES ASSOCIATEDWITH
SPECIFIC CAUSES OF CAP
2) Favoring atypical bacterial (mycoplasma or
chlamydophila) pneumonia
– Absence of factors that favor typical bacterial pneumonia
– Extra pulmonary constitutional symptoms
– Cough persisting >5 days without acute deterioration
– Absence of sputum production
– Normal or minimally elevated white-cell count
– Procalcitonin level, ≤0.1 μg per liter
38.
CLINICAL FEATURES ASSOCIATEDWITH
SPECIFIC CAUSES OF CAP
3) Favoring nonbacterial (viral) pneumonia
– Acute presentation
– Exposure to sick contacts
– Upper respiratory symptoms at time of
presentation
– Patchy pulmonary infiltrates
– Normal or minimally elevated white-cell count
– Procalcitonin level, ≤0.1 μg per liter
39.
CLINICAL FEATURES ASSOCIATEDWITH
SPECIFIC CAUSES OF CAP
4) Favoring influenza pneumonia
– Absence of factors that favor typical bacterial
pneumonia
– Influenza active in the community
– Sudden onset of flulike syndrome
– Positive diagnostic test for influenza virus
SCORING OF DISEASESEVERITY
Scoring systems and assesment tools may predict the severity of disease and
help determine whether a patient with CAP requires hospitalization or
admission to an intensive care unit (ICU).
42.
Severity assessment isa crucial component in the management
of patients presenting with CAP to guide physicians in clinical
decisions. Severity assessment tools are evolving, but at present
have major limitations and should be used with caution and
only in conjunction with clinical judgment.
EMPIRICAL TREATMENT OFCAP -
Outpatient
• For syndromes suggesting typical bacterial
pneumonia: amoxicillin–clavulanate with the
addition of azithromycin if legionella species
are a consideration; levofloxacin or
moxifloxacin may be used instead.
• For syndromes suggesting influenza
pneumonia: oseltamivir with observation for
secondary bacterial infection
45.
EMPIRICAL TREATMENT OFCAP -
Outpatient
• For syndromes suggesting viral pneumonia
other than influenza: symptomatic therapy
• For syndromes suggesting mycoplasma or
chlamydophila pneumonia: azithromycin or
doxycycline
46.
EMPIRICAL TREATMENT OFCAP - Inpatient
• For initial empirical therapy: a beta-lactam
(ceftriaxone, cefotaxime, or ceftaroline) plus
azithromycin; levofloxacin or moxifloxacin may
be used instead
• If influenza is likely: oseltamivir
• If influenza is complicated by secondary
bacterial pneumonia: ceftriaxone or
cefotaxime plus either vancomycin or linezolid
in addition to oseltamivir
47.
EMPIRICAL TREATMENT OFCAP -
Inpatient
• If Staphylococcus aureus is likely: vancomycin
or linezolid in addition to the antibacterial
regimen
• If pseudomonas pneumonia is likely:
antipseudomonal beta-lactam (piperacillin–
tazobactam, cefepime, meropenem, or
imipenem– cilastatin). plus azithromycin
48.
INDICATIONS FOR EMPIRICAL
COMBINATIONTHERAPY IN CAP
• Presence of Comorbid Medical Conditions
– Chronic heart, lung, liver or renal disease
– Diabetes mellitus
– Alcoholism Malignancies
– Use of antimicrobials within the previous 3 months
• Severe CAP With or Without Comorbidities
DURATION OF THERAPY
•A meta-analysis of studies comparing treatment
durations of 7 days or less with durations of 8 days
or more showed no differences in outcomes.*
• Pneumonia that is caused by Staph. aureus or gram-
negative bacilli tends to be destructive – prolonged
therapy is used by majority.
• Cavitating pneumonia and lung abscesses are
usually treated for several weeks.
• * Li JZ, Winston LG, Moore DH, Bent S. Efficacy of short-course antibiotic regimens for community-
acquired pneumonia: a meta-analysis. Am J Med 2007;120: 783-90.
51.
REASONS FOR ALACK OF RESPONSE TO
TREATMENT OF CAP
• Correct organism but inappropriate antibiotic
choice or dose
• Resistance of organism to selected antibiotic
• Wrong dose (e.g., in a patient who is morbidly
obese or has fluid overload)
• Antibiotics not administered
• Correct organism and correct antibiotic but
infection is loculated (e.g., most commonly
empyema)
• Obstruction (e.g., lung cancer, foreign body)
52.
REASONS FOR ALACK OF RESPONSE TO
TREATMENT OF CAP
• Incorrect identification of causative organism
• No identification of causative organism and
empirical therapy directed toward wrong
organism
• Noninfectious cause
• Drug-induced fever
• Presence of an unrecognized, concurrent
infection
53.
NONINFECTIOUS COMPLICATIONS
• Influenzapneumonia and bacterial pneumonia
are each strongly associated with acute cardiac
events.
– Myocardial infarction and new major arrhythmias
(most commonly, atrial fibrillation) were each seen
in 7 to 10% of CAP patients,
– worsening of heart failure occurred in nearly 20%,
– and one or more of these complications occurred
in 25% of patients.
FUTURE DIRECTIONS
• Importantunresolved problems remain with
respect to CAP.
– Despite the most diligent efforts, no causative organism
is identified in half of patients.
– It remains to be determined whether the availability of
sensitive diagnostic tests such as PCR will increase the
use of targeted therapies and reduce dependence on
empirical antibiotic therapy.
– Increasing antibiotic resistance in bacteria may
compound the difficulty of selecting an effective regimen.
– Randomized trials are needed to determine whether the
antiinflammatory activity of macrolides or statins is
beneficial in treating CAP.