Pneumonia

Gemechu M(MD)
 Introduction
• Pneumonia is an infection of the lung parenchyma
• Despite being the cause of significant morbidity
and mortality pneumonia is often misdiagnosed,
mistreated, and underestimated.
• The development of CAP indicates either a
1. Defect in host defenses
2. Exposure to a particularly virulent
microorganism or
3. An overwhelming inoculum
Dr.Gemechu(MD) 2
 Types of pneumonia
Etiology Affected anatomy of lung
• Viral • Bronchopneumonia
• Bacterial
• Lobar pneumonia
• Parasitic
• Fungal
• Interstitial
Site of acquisition • Miliary
• community-acquired (CAP) Clinical coarse
• hospital-acquired (HAP • Atypical
• ventilator-associated (VAP). • Typical

Dr.Gemechu(MD) 3
 Cont…
• Based on affected anatomy of lung:-
• Lobar pneumonia: involvement of an entire lung lobe
• Bronchopneumonia: patchy consolidation in one or
several lobes, usually in dependent lower or posterior
portions centered around bronchi and bronchioles
• Interstitial pneumonia: inflammation of the
interstitium, including the alveolar walls and
connective tissue around the bronchovascular tree
• Miliary pneumonia: numerous discrete lesions due to
hematogenous spread

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 Cont…
Based on clinical coarse:-
A . Atypical pneumonia
- Sometimes it is called as Walking pneumonia.
– Coughing usually without sputum
– No physical findings of consolidation, only moderate elevation of
white cell count, and lack of alveolar exudate
– Caused by a variety of bacteria(mycoplasma, legionella,
chlamydia)
B. Typical or Classic Pneumonia
• Associated with - productive cough,
- chest pain,
- fever, and
- difficulty in breathing
• There is physical finding for consolidation
• Common etiologic agents are Streptococcus
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 Cont…
Based on site of acquisition:-
• Community-acquired pneumonia (CAP) is defined
as an acute infection of the pulmonary parenchyma in
a patient who has acquired the infection in the
community
• Hospital-acquired (nosocomial) pneumonia is
acquired in healthcare facilities after 48 hours of
admission or within 90 days of discharge from an
acute or chronic care facility

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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 in several ways.
• The most common is by aspiration from the
oropharynx.

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 Cont…
Mechanical factors are critically important in host
defense.
• Hairs and turbinates of the nares
• Branching architecture of air way
• Mucociliary clearance
• Gag reflex and the cough mechanism
• Normal flora in the respiratory tract

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 Cont…
• Classic pneumonia evolves through a series of four
pathologic changes
I. Edema-The initial phase with the presence of a
proteinaceous exudate—and often of bacteria—in the
alveoli.
II. Red hepatization phase- presence of erythrocytes in
the cellular intraalveolar exudate gives this second
stage its name, but neutrophil influx is more
important from the standpoint of host defense.
• Bacteria are occasionally seen in pathologic
specimens collected during this phase
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III. Gray hepatization, IV. Resolution,
• no new erythrocytes are • Final phase, the
extravasating, and those macrophage reappears
already present have been as the dominant cell
lysed and degraded. type in the alveolar
• The neutrophil is the space, and the debris of
predominant cell, fibrin neutrophils, bacteria,
deposition is abundant, and and fibrin has been
bacteria have disappeared. cleared, as has the
This phase inflammatory response.

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 Etiology

• In most cases, it is most useful to think of the

potential causes as either "typical" bacterial
pathogens or "atypical" organisms.
• Typical bacterial pathogens
– Includes S. pneumoniae(most common),
Haemophilus influenzae, and (in selected patients)
S. aureus and gram-negative bacilli such as
Klebsiella pneumoniae and Pseudomonas
aeruginosa.

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 Cont…

• Atypical organisms
– Mycoplasma pneumoniae and Chlamydia pneumoniae
(in outpatients) and Legionella spp. (in inpatients) as
well as respiratory viruses such as influenza viruses,
adenoviruses, and respiratory syncytial viruses.
– Data suggest that a virus may be responsible for up to
18% of cases of CAP that require admission to the
hospital.

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 Risk factors
• Alcoholism, asthma, immunosuppression,
institutionalization, and elderly
• smoking, cystic fibrosis, chronic obstructive
pulmonary disease (COPD), and HIV infection.
• Hospital stay
• Diabetes, hematologicmalignancy, cancer, severe
renal disease, etc

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 Clinical Features
• Productive cough
• Fever
• Pleuritic chest pain
• Dyspnea
• GI symptoms
• Mental status changes

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 Physical Findings
• Vary with the degree of pulmonary
consolidation and the presence or absence of a
significant pleural effusion
• Febrile
• RR >24 breaths/minute
• Tachycardia
• Dullness, decreased or absent air entry, criptation and
localized wheezing
• +Egophany and bronchophony

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 Diagnosis
 CBC- Leukocytosis also Leukopenia(poor prognosis)
 Blood cultures
 Sputum – gram stain and culture
 Chest X-ray with infiltrate
 AFB and Gene expert : to r/o pulmonary TB.
 U/A: to R/O drug induced pneumonia that may cause
injury in the kidney.
 ESR and C-RP to differenciete infectious causes from
inflammation.

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 Radiology
• Still a gold standard for diagnosis
• Differentiates between those that will benefit from
antibiotics from others (upper respiratory infection
and non-infectious diseases)
• Pattern of infiltrate not very helpful for etiological
diagnosis
– Lobar consolidation, effusion, cavitation --> bacterial
– Bilateral diffuse --> viral , PCP, Legionella
– Multiple nodular --> staphylococcal
– Cavitation --> aspiration/anaerobic, G(-), Staph, TB

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Consolidation with alveolar filling process

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Interstitial pattern

•Viral
•Mycoplasma pneumonia
•Chamydophyla psittaci
•Francisella tularensis
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Multifocal opacities

•S. aureus
•Coxiella burnetti
•Legionella

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 Cont…
• False negative chest radiographs are
occasionally attributed to an
 Infection very early in the course (<24 hrs),
Neutropenia

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 Differential diagnosis
Includes both infectious and noninfectious
entities such as
• Acute bronchitis,
• Acute exacerbations of chronic bronchitis,
• Heart failure,
• Pulmonary embolism, and
• Radiation pneumonitis.

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 Treatment
Management principles of pneumonia:
1) Stabilization Of Patients
2) Supportive Managements
3) Medical Treatments
• Deciding the site of care(out patient or in patient)
• There are currently two sets of criteria to decide
the site of treatment:
1) Pneumonia Severity Index (PSI
2) CURB-65 criteria
• Helps to determine severity of illness and determine
if patient should be admitted or not
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Dr.Gemechu(MD) 24
 CURB 65
• Confusion
• Urea (BUN >20mg/dL)
• Respiratory Rate > 30 breaths/minute
• Blood Pressure (systolic <90mmHg or diastolic
<60mmHg)
• Age >65 years
* 1 point for each

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 CURB65
SCORE RISK 30 DAY MANAGEMENT
MORTALITY
0 Low 0.6% Outpatient

1 Low 2.7% Outpatient

2 Moderate 6.8% Inpatient vs Outpatient

3 Severe 14% Inpatient

4 Highest 27.8% Inpatient/ICU

5 Highest 27.8% Inpatient/ICU

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 PSI
POINTS POINTS
Age in Years + 1 point per year SBP + 20 points

Gender -10 pts for women Temp not 95-104 + 15 points

F
ECF Resident + 10 points
HR >125bmp + 10 points
Cancer + 30 points
pH <7.35 + 30 points
Liver Disease + 20 points
PaO2 <60mmHg + 10 points
CHF + 10 points
Na < 130mEq/L + 20 points
CVA + 10 points BUN >64 mg/dL + 20 points
CKD + 10 points Glucose >250 + 10 points
Altered Mental Status + 20 points Hct <30% + 10 points
Respiratory Rate + 20 points Pleural Effusion + 10 points
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 PSI
CLASS POINTS MORTALITY RISK MANAGEME
NT

Class 1 0 0.1% Low Outpatient

Class 2 <70 0.6% Low Outpatient

Class 3 71-90 2.8% Low Observation

Class 4 91-130 8.2% Moderate Inpatient

Class 5 >130 29.2% High Inpatient/ICU

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Dr.Gemechu(MD) 29
 Antibiotic Management

• Initial therapy is usually empirical and is designed to cover the

most likely pathogens
• Empirical therapy for outpatient
– B-lactam (high dose amox or amox/clavulinic acid) +
macrolide
– B-lactam
– Macrolides
– Fluoroquinolone
• Empirical therapy for inpatient
– IV Fluoroquinolone
– IV B-lactam (ampicillin, or 3rd gen cephalo) + macrolide (doxy as
alternative)
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Dr.Gemechu(MD) 31
 Inpatient Treatment
 Switch to Oral Therapy
 When clinically improving, hemodynamically stable, able to take oral
meds
 Duration of Hospitalization
 Several studies support that it is not necessary to observe pt overnight
after change to PO antibiotics
 Consider discharge after no signs of clinical instability which is defined
as: Temp >40, RR>24, SBP <90, HR>100, O2 sat <90, altered mental
status, inability to take PO
 Duration of IV Treatment
 Minimum of 5 days (most treat 7-14 days)
 Before consideration of discontinuing abx need to have:
▪ Afebrile for 48-72 hours
▪ No supplemental O2
▪ No signs of clinical instabilityDr.Gemechu(MD) 32
 Failure to Improve
A number of noninfectious conditions can mimic
pneumonia, including
 Pulmonary edema,
 Pulmonary embolism,
 Lung carcinoma,
 Radiation and hypersensitivity pneumonitis,
 connective tissue disease involving the lungs.

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 Failure to Improve
• Pathogen may be resistant
• Correct diagnosis but that an unsuspected
pathogen (e.g., CA-MRSA, M. tuberculosis, or
a fungus) is the cause.
• Nosocomial superinfections.
• Either the wrong drug or the correct drug at
the wrong dose or frequency of administration
Patient must be carefully reassessed and appropriate
studies initiated.
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 Complications

• Respiratory failure
• Shock and multiorgan failure
• Coagulopathy
• Exacerbation of comorbid illnesses
• Sepsis of lung focus
• Lung abscess
• Complicated parapneumonic effusion

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 Reading
Pleural disease
• Pleural effusion
• Pneumothorax
• Hemothorax
• Empyema

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THANK U
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