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.
INTRODUCTION
• Long recognized as 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.
COMMON CAUSES
Infectious
• Streptococcus pneumoniae,
• Haemophilus influenzae,
• Staphylococcus aureus,
• Influenza virus,
• Other respiratory viruses
Non Infectious
• Pulmonary edema
• Lung cancer
• Acute respiratory distress
syndrome
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
UNCOMMON CAUSES
Infectious
• Mycobacterium tuberculosis,
nontuberculous mycobacteria,
• Nocardia species,
• Legionella species
• Mycoplasma pneumoniae
• Chlamydophila pneumoniae
• Chlamydophila psittaci
• Coxiella burnetii
• Histoplasma capsulatum,
coccidioides species, Blastomyces
dermatitidis, cryptococcus
• Aspergillus species
Non infectious
• Cryptogenic organizing
pneumonia
• Eosinophilic pneumonia
• Acute interstitial pneumonia
• Sarcoidosis
• Vasculitis (granulomatosis with
polyangiitis)
• Pulmonary alveolar proteinosis
• Drug toxicity
• Radiation pneumonitis
Causes of pneumonia vary 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
• Although pneumococcus remains 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
• Patients with chronic 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.
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.
• 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.
• Pneumococcal antigen detection
– 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.
• 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.
MICROBIOLOGICAL INVESTIGATION
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.
LUNG ULTRASOUND
• Sensitivity of 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
PATTERNS OF IMAGING FINDINGS
• 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.
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.
Streptococcus pneumoniae pneumonia showing alveolar pattern
nonsegmental consolidation in the right middle lung field, which is
demarcated by the fissure suggestive of upper lobe pneumonia
Klebsiella pneumonia
Suspected when there is a cavitatory pneumonia, a bulging fissure
sign. Often there can be extensive lobar opacification with air
bronchogram.
Mycoplasma pneumoniae pneumonia showing 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.
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
Staph aureus pneumonia
Chest radiograph 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).
Mycoplasma pneumoniae
CXR shows reticulonodular 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).
Chlamydophila pneumoniae pneumonia showing 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
Ground-glass opacity predominant pattern
• 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
Mycoplasma pneumoniae pneumonia showing 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).
Pneumocystis jirovecii pneumonia
Chest radiograph shows bilateral reticulonodular opacities; B: Chest computed
tomography with a 5 mm slice thickness demonstrates bilateral ground-glass
opacity with reticulations.
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
Random nodules predominant pneumonia (varicella-zoster pneumonia)
Thin-section computed tomography demonstrates scattered small solid or
ground-glass opacity nodules which are unrelated to centrilobular
structures (arrows).
Miliary tuberculosis
Chest radiograph
Diffuse reticulonodular
opacities in both lungs; B:
Thin-section CT
demonstrates diffuse
military nodules with a
random distribution.
Pathogen Specific imaging appearances
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
CLINICAL CONDITIONS RELATED TO 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.
CLINICAL CONDITIONS RELATED TO 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.
Sinobronchial syndrome in a
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).
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.
CLINICAL FEATURES ASSOCIATED WITH
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
CLINICAL FEATURES ASSOCIATED WITH
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
CLINICAL FEATURES ASSOCIATED WITH
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
CLINICAL FEATURES ASSOCIATED WITH
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
POOR PROGNOSTIC FACTORS
• Age (≥65)
• Coexisting disease-cardiac
disease, diabetes, COPD,
stroke
• Respiratory rate ≥ 30/min
• Confusion
• Blood pressure
• Hypoxemia
• Urea ≥ 7 mmol/ l
• Albumin < 35 g/l
• White cell count- WCC >20 or
< 4* 109
/l
• Radiology – bilateral and
multilobar involvement.
• microbiology
SCORING OF DISEASE SEVERITY
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).
Severity assessment is a 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.
ACUTE MANAGEMENT OF CAP
EMPIRICAL TREATMENT OF CAP -
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
EMPIRICAL TREATMENT OF CAP -
Outpatient
• For syndromes suggesting viral pneumonia
other than influenza: symptomatic therapy
• For syndromes suggesting mycoplasma or
chlamydophila pneumonia: azithromycin or
doxycycline
EMPIRICAL TREATMENT OF CAP - 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
EMPIRICAL TREATMENT OF CAP -
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
INDICATIONS FOR EMPIRICAL
COMBINATION THERAPY 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
COMPARISON
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.
REASONS FOR A LACK 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)
REASONS FOR A LACK 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
NONINFECTIOUS COMPLICATIONS
• Influenza pneumonia 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.
HIGH RISK GROUPS IN WHOM VACCINATION IS
RECOMMENDED
FUTURE DIRECTIONS
• Important unresolved 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.
THANK YOU

CAP-IDSA-2019 MANAGEMENT GUIDELINES.pptx

  • 1.
    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
  • 5.
    UNCOMMON CAUSES Infectious • Mycobacteriumtuberculosis, nontuberculous mycobacteria, • Nocardia species, • Legionella species • Mycoplasma pneumoniae • Chlamydophila pneumoniae • Chlamydophila psittaci • Coxiella burnetii • Histoplasma capsulatum, coccidioides species, Blastomyces dermatitidis, cryptococcus • Aspergillus species Non infectious • Cryptogenic organizing pneumonia • Eosinophilic pneumonia • Acute interstitial pneumonia • Sarcoidosis • Vasculitis (granulomatosis with polyangiitis) • Pulmonary alveolar proteinosis • Drug toxicity • Radiation pneumonitis
  • 6.
    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.
  • 13.
  • 14.
    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).
  • 30.
    Miliary tuberculosis Chest radiograph Diffusereticulonodular opacities in both lungs; B: Thin-section CT demonstrates diffuse military nodules with a random distribution.
  • 31.
    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
  • 40.
    POOR PROGNOSTIC FACTORS •Age (≥65) • Coexisting disease-cardiac disease, diabetes, COPD, stroke • Respiratory rate ≥ 30/min • Confusion • Blood pressure • Hypoxemia • Urea ≥ 7 mmol/ l • Albumin < 35 g/l • White cell count- WCC >20 or < 4* 109 /l • Radiology – bilateral and multilobar involvement. • microbiology
  • 41.
    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.
  • 43.
  • 44.
    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
  • 49.
  • 50.
    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.
  • 54.
    HIGH RISK GROUPSIN WHOM VACCINATION IS RECOMMENDED
  • 55.
    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.
  • 56.