Pneumonia

…….
Definition

 Pneumonia is an inflammatory condition

of the lung—especially affecting the
microscopic air sacs (alveoli)—associated
with fever, chest symptoms, and a lack of
air space (consolidation) on a CXR.

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Classification:
By where or how it was acquired:
 Community-acquired (CAP), aspiration ,
 Health care–associated pneumonia (HCAP), with
subcategories of HCAP including HAP and VAP
 community-acquired , aspiration , healthcare-
associated, hospital-acquired, and ventilator-
associated pneumonia.
By the area of lung affected :
 Lobar pneumonia, bronchial pneumonia and
acute interstitial pneumonia) or
By the causative organism
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…
• Involvement may be confined to an entire lobe -
Lobar pneumonia
• A segment of a lobe-Segmental or lobular
pneumonia
• Alveoli contiguous to bronchi -
Bronchopneumonia
• Interstitial tissue - Interstitial pneumonia
These distinctions are generally based on x-ray
observations.

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Predisposing factors for pneumoniainclude:-

• Preceding respiratory viral infections

•Alcoholism
•Cigarette smoking
• Underlying diseases such as Heart failure,
COPD
•Age extremes
• Immunosuppressive therapy and disorders
• Decreased consciousness, comma , seizure etc
• Surgery and aspiration of secretions

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Epidemiology:

Affects approximately 450 million people a

year and occurrs in all parts of the world.
 It is a major cause of death among all age
groups resulting in 4 million deaths (7% of
the world's yearly total).
Death Rates are greatest in children <5, and
adults >75 years of age.
Occurs about 5X more frequently in the
developing world versus the developed world.

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PATHOPHYSIOLOGY
Pneumonia results from the proliferation of
microbial pathogens at the alveolar level and the
host’s response to those pathogens.
Microorganisms gain access to the lower respiratory
tract by:-
 Aspiration from the oropharynx- most common
 During sleep (especially in the elderly) and
 In pts with decreased levels of consciousness.
 Inhalation as contaminated droplets
 Hematogenous spread (e.g., from tricuspid
endocarditis) or
 Contiguous extension from an infected pleural or
mediastinal space
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Protective mechanisms
o Hairs and turbinates of the nares
o Branching architecture of the tracheobronchial
tree traps
o The gag reflex and the cough mechanism
o The normal flora adhering to mucosal cells of
the oropharynx
o Resident alveolar macrophages
o Local proteins (e.g., surfactant proteins A and
D) that have intrinsic opsonizing properties or
antibacterial or antiviral activity.

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Only when the capacity of the alveola macrophages
to ingest or kill the microorganisms is exceeded
does clinical pneumonia become manifest
The host inflammatory response, rather than the
proliferation of microorganisms, triggers the
clinical syndrome of pneumonia.
The release of inflammatory mediators, such as IL
1 and TNF, results in fever.
Chemokines, such as IL-8 and granulocyte
colony-stimulating factor, stimulate the release of
neutrophils and their attraction to the lung.

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Community acquired pneumonia(CAP)

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Definition
CAP
Is defined as an acute infection of the
pulmonary parenchyma in a patient who has
acquired the infection in the community.

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Etiology

Bacteria, fungi, viruses, and protozoa.

Community-acquired strains of MRSA
Typical" bacterial pathogens :
 S. pneumoniae, H. influenzae, S. aureus
(espec. Post viral infection) and gram-negative
bacilli such as K. pneumoniae and P.
aeruginosa.
“Atypical" organisms : include
 M. pneumoniae and C.pneumoniae (in
outpatients) and Legionella spp.(inpts)
Virus may be responsible for up to 18% of cases
∼10–15% of CAP cases are polymicrobial, a
combination of typical and atypical pathogens 12
Atypical pneumonia

1) Not caused by the traditional pathogens

Bacteria, viruses, fungi, and protozoa
2) Present with atypical signs & symptoms
Present with insidous onset of dry cough
No signs and symptoms of lobar consolidation
Extrapulmonary symptoms common( nausea,
vomiting, diarrhea, headache, myalgia, sore
throat)
Absence of leukocytosis
CXR=> Patchy interstitial pattern
3) Didn’t respond to common antibiotics
 such as sulphonamide, beta lactams like
penicillin
4) Not cultureable 13
Microbial Causes of CAP, by Site of Care
Outpatients Hospitalized Patients
Non-ICU ICU
Streptococcus S. pneumoniae S. pneumoniae
pneumoniae
Mycoplasma M. pneumoniae Staphylococcus
pneumoniae aureus
Haemophilus Chlamydia Legionella spp.
influenzae pneumoniae
C. pneumoniae H. influenzae Gram-negative bacilli
Respiratory virusesa Legionella spp. H. influenzae
a
Influenza A and B viruses, adenoviruses,
Respiratory virusesa respiratory
syncytial viruses, parainfluenza viruses.
Note: Pathogens are listed in descending order of frequency.
ICU, intensive care unit.
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Epidemiologic Factors Suggesting Possible Causes of
CAP
Factor Possible pathogens

Alcoholism S. pneumoniae, oral anaerobes, Klebsiella

pneumoniae, Acinetobacter spp., Mycobacterium
tuberculosis
COPD and/or H. influenzae, Pseudomonas aeruginosa, Legionella
smoking spp.,
S. pneumoniae, Moraxella catarrhalis, Chlamydia
pneumoniae

Structural lung P. aeruginosa, Burkholderia cepacia,

disease (e.g., Staphylococcus aureus
bronchiectasis
Dementia, stroke, Oral anaerobes, gram-negative enteric bacteria
decreased level of
consciousness
Lung abscess CA-MRSA, oral anaerobes, endemic fungi, M.
tuberculosis, atypical mycobacteria
Stay in hotel or on Legionella spp.
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cruise ship in
CLINICAL MANIFESTATIONS
Symptoms Signs
 Fever , chills, sweating  An ↑RR and use of
 cough(productive or non accessory muscles of
productive), respiration
 Shortness of breath  P/F may vary with
 Pleuritic chest pain underlying pathology
 Fatigue, headache,  ↑ or ↓ tactile fremitus
myalgias, and  Crackles, BBS, and
arthralgias. possibly pleural friction
 Up to 20% of patients rub may be heard
may have nausea,  New-onset or worsening
vomiting, or diarrhea. confusion.

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 Symptom frequency

Symptom Frequency
Cough 79-91%

Fatigue 90%

Fever 71-75%

Shortness of breath 67-75%

Sputum 60-65%

Chest pain 39-49%

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Diagnosis

When confronted with possible CAP, the

physician must ask two questions:
1) Is this pneumonia, and,
 answered by clinical and radiographic
methods
2) If so, what is the likely etiology?
 requires the aid of laboratory techniques.

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Clinical Diagnosis

DDX
Acute bronchitis,
Acute exacerbations of chronic bronchitis,
Heart failure,
Pulmonary embolism, and
Radiation pneumonitis.

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History
P/E
The sensitivity and specificity of the findings on P/E
are less than ideal, averaging 58% and 67%,
respectively.
CXR
A demonstrable infiltrate by CXR or other
imaging technique is required for the diagnosis
of pneumonia, (according to the 2007 consensus
guidelines from (IDSA/ATS))
Often necessary to differentiate CAP from other
conditions.
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Radiographic findings may include risk factors
for increased severity (e.g., cavitation or
multilobar involvement).
Occasionally, radiographic results suggest an
etiologic diagnosis
 Cavitation --> aspiration/anaerobic, G(-), Staph,
TB
 Pneumatoceles suggest --------S. aureus,
 Lobar consolidation, effusion, cavitation -->
bacterial
 Bilateral diffuse --> viral , PCP, Legionella
 Multiple nodular --> staphylococcal

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Interstitial
pattern
•Viral
•M. pneumonia
•Chamydophyla
psittaci
•Francisella
tularensis

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Multifocal opacities
•S. aureus
•Coxiella burnetti
•Legionella

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Miliary pattern:
•TB
•Histoplasma
•Coccidioides
•Blastomyces
•Varicella zoster

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Pneumatocoele
•S. Aureus
•S. Pyogenes
•PCP
•Legionella

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CT scan
Is not generally recommended for routine use
because the data for its use in CAP are
limited,
The cost is high, and
There is no evidence that it improves
outcome.
Reserved for further anatomical definition
(eg, detecting cavitation, adenopathy, or mass
lesions).

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Etiologic diagnosis:
 Gram Stain and Culture of Sputum
 The yield of positive cultures from sputum samples

is ≤50%
 To be adequate for culture, a sputum sample must

have >25 neutrophils and <10 squamous

epithelial cells per low-power field.
 Blood culture.(only 5-14% are positive)
 PCR- usu for research studies.

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Other microbiologic studies
Mycoplasma : PCR of throat or sputum/BAL
before first dose abx
Legionella: urine Ag (detects L.pneumophilia L1
serotype, 60-70% of clinical cases,
S. Pneumonia urinary Ag ( sen 50-80%, sp >90%)
MTb: induced sputum for AFB stain &
mycobacterium culture
Induced sputum for pcp if HIV +, or unknown
cell mediated immunity
HIV testingt
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Broncoscopy:
if Pt immunosupp.,
critically ill, failing to respond, or
Has chronic pneumonia.
Also in suspected TB if no adequate sputum
and in suspected PCP if induced sputum
unavailable or but clinical suspicion high.
Other labs: SaO2 or PaO2, CBC w/ diff, lytes,
BUN/Cr, glc, LFTs; arterial pH (if severe).

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Treatment
Objectives
- Treat the infection.
- Prevent complications.
Identify those that are at high risk and may
require hospitalization. Ther CURB-65 scoring
systems suggested to evaluate the prognosis
and determine subsequent management:

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Treatment
Decision to admit based on:-
• Severity of illness score
 The CURB-65 score

Score 30d MR

0 or 1.5%
1=home
2=admit to 9.2%
hospital
> 3= admit 22%
to ICU 32
 Pharmacologic
Community acquired ambulatory patients (Mild
Pneumonia):
First line
No recent antibiotic use:
Clarithromycin, 500mg P.O., BID for 5-7 days OR
Azitromycin, 500mg P.O., first day then 250mg P.O., for
4d. OR
Doxycycline, 100mg P.O., BID for 7-10 days.
If recent antibiotic use within 3months:
Clarithromycin, 500mg P.O. BID for 5-7 days OR
Azitromycin, 500mg P.O first day then 250mg P.O., for 4d.
PLUS
Amoxicillin, 1000mg P.O., TID for 5 to 7 days. OR
Amoxicillin-clavulanate, 625mg P.O., TID for 5-7days 33
 Community acquired hospitalized patients (Severe Pneumonia)

Non-pharmacologic
- Bed rest
- Frequent monitoring of temperature, blood
pressure and pulse rate in order to detect
complications early and to monitor response to
therapy.
- Give attention to fluid and nutritional
replacements.
- Administer Oxygen via nasal prongs or face
mask

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 Pharmacologic
The Antibiotic choice should be aimed at the most likely
causative agent.
Empiric treatment for pneumonia due to common organisms:
First line
Ceftriaxone, 1g I.V. OR I.M every 12-24 hours for 7 days.
OR
Benzyl penicillin, 2-3 million IU I.V. QID for 7-10 days.
PLUS
Azithromycin, 500mg on day 1 followed by 250mg/day
on days 2 – 5 OR
Clarithromycin, 500mg P.O., BID for 7-10 days
N.B. In a situation of beta lactam allergy, respiratory fluoroquinolones
(moxifloxacin or levofloxacin) can be used. As these medicines are second
line medicines for Tuberculosis, they should only be used when it is absolutely
important
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• Prognostic models: Pneumonia severity
index (PSI)
 PORT study: analysis of 14000 patients, validated
on >40000 patients
 Score calculator: sex, age, nursing home resident or
not, comorbid diseases, vitals, mental status, labs --
> risk class I-V
 Mortality 30% associated with class V
• Subjective assessment: ability to take po meds,
home support.

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Empirical therapy: outpatient
Considerations
Need to cover for both typical and atypicals
Rates of drug-resistance of S. pneumo
(DRSP)
No comorbidities and no risk of DRSP
 Macrolide (strong recommendation - level I)
 Doxycycline (weak - level III)

Comorbidities or antibiotics in past 3 months

 Respiratory fluoroquinolone (level I)
 B-lactam (high dose amox or amox/clavulinic
acid) + macrolide (level I)
 If high rates of high-level DRSP, consider
Cephalo 2nd or 3rd
 Suspect aspiration: clindamycin or amox-clavulinic
acid 38
Empirical therapy: Inpatient
Non-ICU:
Respiratory FQ (level I)
B-lactam (ampicillin, or 3rd gen cephalo)
+ macrolide (doxy as alternative)
ICU:
B-lactam (3rd gen Cephalo or B-lactam/blactamase
inhibitor) + FQ or azithromycin
If pen-allergy: FQ +/- clinda
If suspect CA-MRSA: add vanco or linezolid or
FQ
If suspect pseudomonas: pip-tazo or 4th gen
cephalo or carbapenem + FQ (or + AG)
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Emperical therapy

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General considerations
In addition to appropriate antimicrobial therapy,
certain general considerations apply in dealing
with either CAP or HAP.
Are critical to the success of therapy
 Adequate hydration,
 oxygen therapy for hypoxemia, and assisted
ventilation (when necessary).
 Patients with severe CAP who remain
hypotensive despite fluid resuscitation may
have adrenal insufficiency and may respond to
glucocorticoid treatment.
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Clinical follow-up
Earlier initiation (,4h after presentation) of therapy
associated with better outcome (decreased LOS)
Switch from IV to PO dependent on clinical
improvement and ability to tolerate oral intake
Criteria for clinical stability
 Temperature <37.8C
 HR < 100/min
 RR < 24 /min
 SBP> 90
 02Sat > 90% or pO2 >60
 Able to maintain oral intake
 Normal mental status

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Fever & leukocytosis usually resolve within
2–4 days.
Physical findings may persist longer.
Radiographic abnormalities may require 4–
12 wks to clear
Follow-up radiograph can be done ~4–6
weeks .
Young patients without comorbidity do well
and usually recover fully after ~2 weeks.

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Duration of therapy
Normalization of physiologic parameters and
clinical stability achieved within median 3-4d but
6 days to achieve temp<37.2 and RR<20 and
O2sat>94%
Shorter LOS not associated with adverse
outcomes
No evidence-based data on optimal duration of
antibiotic therapy
10-14 days historically
Minimum 5 days (level I recommendation) and afebrile
for 48-72h
Should not discontinue treatment if >1 criteria of
instability
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Non-response
Residual symptoms in up to 60%
Clinical non-response to therapy in 6-15% of
hospitalized patients - higher if ICU
Failure to improve or progression:
 Resistance or unusual pathogen
 Parapneumonic effusion or empyema
 Nosocomial superinfection
 Metastatic infection
 Complication from pneumonia: BOOP
 Intercurrent non-infectious illness
 Misdiagnosis: PE, CHF, alveolar hemorrhage from
vasculitis, pneumonitis (allergic, SLE), occupational
lung diseases
 Drug fever
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Complications
 common: respiratory failure, shock and
multiorgan failure, coagulopathy, and
exacerbation of comorbid illnesses.
 others: metastatic infection(brain abscess or
endocarditis) , lung abscess, and complicated
pleural effusion.
 Lung abscess may occur in association with
aspiration or with infection caused by CA-
MRSA, P. aeruginosa, or (rarely) S.
pneumoniae.
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A significant pleural effusion should be
tapped for both diagnostic and therapeutic
purposes.
 If the fluid has a pH of <7,
 a glucose level of <2.2 mmol/L, and
 a lactate dehydrogenase concentration of
>1000 U/L, or
 if bacteria are seen or cultured, then the
fluid should be drained, and a chest tube
is usually required
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49
HEALTH CARE–ASSOCIATED PNEUMONIA

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Ventilator associated pneumonia(VAP)
Definition
Is a type of hospital-acquired (or nosocomial)
pneumonia that develops after more than 48
hours of mechanical ventilation.
Etiology
If VAP develops in the first 5–7 days of the
hospital stay, similar to severe CAP.
If patients have other risk factors for HCAP, MDR
pathogens are a consideration.

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Microbiologic Causes of Ventilator-
Associated Pneumonia

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Epidemiology
Prevalence estimates vary b/n 6 and 52 cases per 100
pts.
The highest hazard ratio is in the first 5 days and a
plateau in additional cases (1% per day) after ∼2
weeks.
The cumulative rate among patients who remain
ventilated for as long as 30 days is as high as 70%.
Factors critical in the pathogenesis of VAP are :
 Colonization of the oropharynx with pathogenic
microorganisms,
 Aspiration of these organisms from the oropharynx
into the lower respiratory tract, and
 Compromise of the normal host defense mechanisms
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Clinical manifestations
Generally the same as for all other forms of
pneumonia.
 Fever, leukocytosis, increase in respiratory
secretions, and pulmonary consolidation

 A new or changing radiographic infiltrate.

 Tachypnea, tachycardia, worsening

oxygenation

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 Diagnosis
Application of clinical criteria consistently results
in over diagnosis of VAP, because of three common
findings in at-risk pts:
(1) Tracheal colonization with pathogenic bacteria in
patients with ETs,
(2) Alternative causes of radiographic infiltrates in
mechanically ventilated patients, and
(3) The high frequency of other sources of fever in
critically ill patients.
 DDX of VAP includes:-
 Atypical pulmonary edema,
 Pulmonary contusion or hemorrhage,
 Hypersensitivity pneumonitis,
 ARDS, and
 Pulmonary embolism.
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The Clinical Pulmonary Infection Score (CPIS)
 was developed by weighting of the various clinical
criteria usually used for the diagnosis of VAP
Use of the CPIS allows the selection of low-risk
patients who may need only short-course antibiotic
therapy or no treatment at all.
Initial validation of the CPIS found that a score
greater than 6 correlated with VAP .
However, subsequent studies failed to confirm this.
In a prospective cohort study, the CPIS identified
VAP with a sensitivity and specificity of only 60
and 59 percent, respectively.
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 Clinical Pulmonary Infection Score
(CPIS)

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Diagnostic approach
 VAP should be considered in any mechanically
ventilated patient
 who develops new or increased fever, alveolar
infiltrate, respiratory secretions, leukocytosis, or
respiratory abnormalities &
 Should have a CXR .
 A normal CXR excludes VAP, although ventilator-
associated tracheobronchitis may exist.
 Pts with suspected VAP and an abnormal CXR should
have their lower respiratory tract secretions
collected for microscopic analysis and culture.
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Prognosis
Crude mortality rates of 50–70%.

Many patients with VAP have

underlying diseases that would result
in death even if VAP did not occur.

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Hospital acquired pneumonia
Definition:
HAP (or nosocomial pneumonia) is pneumonia that
occurs 48 hours or more after admission.
HAP in nonintubated patients(both inside and outside the
ICU)is similar to VAP except
 Higher frequency of non-MDR pathogens
 Better underlying host immunity in nonintubated
patients.
 Anaerobes are more common in HAP(non
intubated)due to higher risk of macroaspiration .
Diagnosis is even more difficult for HAP in nonintubated
patients than for VAP
blood cultures are infrequently positive (<15% of cases)
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 Lower respiratory tract samples appropriate for culture are
considerably more difficult to obtain
 Because blood cultures are infrequently positive (<15% of
cases),
 The majority of patients with HAP do not have culture data
on which antibiotic modifications can be based.
 De-escalation of therapy is less likely in patients with risk
factors for MDR pathogens.
 Despite these difficulties, the better host defenses in non-ICU
patients result in lower mortality rates than are documented
for VAP.
 In addition, the risk of antibiotic failure is lower in those with
HAP.
 -----------------------------------//-------------------------------------------
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Empiric treatment for commonly suspected
etiologies of HAP
First line
Ceftazidime, 1gm I.V. TID for 10-14days PLUS
Vancomycin 1g I.V. BID for 10-14 days OR (particularly in
the ICU setup and in ventiltor associated pneumonia)
Imipenem-cilastatin, 500mg IV (infused slowly over 1hour)
Q6h OR
Meropenem, 1gm IV (infused slowly over 30min) Q8h
Alternatives
Ceftriaxone, 1-2g I.V. OR I.M. BID for 7 days. PLUS
Gentamicin, 3-5mg/kg I.V. QDdaily in divided doses for 7
days.
OR
Ciprofloxacin, 500mg P.O./I.V. BID every 12 hours for 7 days.
If methicillin-resistant (MRSA) suspected
Vancomycin, 1 g I.V. BID should be added to the existing
empric regimen 63