Community Acquired Pneumonia

And
Hospital-Acquired Pneumonia

• CC_Contador, Everly Kay Fe B.

 Objectives
• To know the etiology, pathology and clinical
presentation of pneumonia
• To classify patients based on clinical
presentation
• To familiarize causative microorganisms
• To know how to properly managed the
patients based on the risk classification and
different categories
 Pneumonia
Pneumonia is an infection of the pulmonary
parenchyma
 Pneumonia Categories
Community –Acquired
Pneumonia (CAP)
Hospital-Acquired Pneumonia
(HAP)
Ventilator-Acquired Pneumonia
(VAP)
Healthcare-Associated
Pneumonia (HCAP)
Pneumonia Acquired outside the hospital setting
Pneumonia diagnosed >48 hours after hospital
admission
Pneumonia diagnosed with in 48-72 hours after
endotracheal intubation
Pneumonia develops inside or outside of the
hospital in the presence of risk factors for multi-
drug resistant pathogens
Diagnosed to any patient who:
• Was hospitalized in acute care hospital for 2 days
with in 90 days of the diagnosis
• Resided in a nursing home or long –term care
facility
• Received recent intravenous antibiotic therapy,
chemotherapy, or wound care with in the past 30
days of current infection
• Attended a hospital or hemodynamic clinic.
 Etiology

Pneumonia Category Most common Pathogen

CAP S. pneumoniae
VAP NMDR: S. pneumonia
MDR: P. aerogenosa

HAP Gram neg bacilli (P. aerogenosa)

S. aureus (Methicillin-sensitive
and Methicillin-resistant)

HCAP MRSA
P. aeroginosa
 Pathophysiology

Microbial pathogens in alveolar level

+
Host response to those pathogens
=PNEUMONIA
 Access Route

• Aspiration from the oropharynx – most

common
• Inhalation – as contaminant droplets
• Rarely - hematogenous spread or contiguous
extension
 Mechanical Host Defense
• Hairs and turbinates of the nares
• Branching architecture of the tracheobronchial
tree
• Gag and cough reflex
• Normal flora adhering to the mucosal cells of
the oropharynx
• Resident Alveolar macrophages
 Pathogenesis

Entry of Mechanical host Microorganisms

Microbial defense was enters the
Pathogens overcome alveolar level

Resident
Alveolar Alveolar macrophages
macrophage +
macrophages initiates inflammatory
surfactant proteins A
killing capacity response to bolster
& D engulfs
exceeds LRT defense
microbial pathogens

Release of PNEUMONIA
inflammatory SYNDROME IS
mediators MANIFESTED
 Pathology
PHASE DESCRIPTION
Edema ▪ Initial phase with the presence of proteinaceous exudate,
and often of bacteria in the alveoli

Red hepatisation ▪ Presence of erythrocytes in the cellular intra alveolar

exudate.
▪ Neutrophil influx is more important from the standpoint of
the host defense.
▪ Bacteria are occasionally seen in pathologic specimens

Gray hepatisation ▪ No erythrocytes are extravasating.

▪ Neutrophil is the predominant cell. Fibrin deposition is
abundant and bacteria have disappeared.
▪ Corresponds with successful containment of the infection
and and improvement of gas exchange.

Resolution ▪ Macrophage reappears as the dominant cell type in the

alveolar space and the debris of neutrophils, bacteria and
fibrin has been cleared, as has the inflammatory response
 Clinical Manifestations of Pneumonia
• Fever
• Tachycardia
• Hemoptysis
• Peripheral leukocytosis and increase purulent secretions
• Pleuritic chest pain
• Radiographic infiltrate and rales
• Hypoxemia
• Respiratory alkalosis
• Dyspnea
• Fatigue
 Physical examination findings
• Increased in Respiratory rate
• Percussion may vary from dull to flat
• Crackles, bronchial breath sounds, and
possibly a pleural friction rub may be
heard on auscultation.
 Radiographic Findings

The three most common

patterns are:

• Bronchopneumonia
• Lobar pneumonia
• Interstitial pneumonia
Lobar Pneumonia
• Involves single lobe
• Unilateral
• Air Bronchogram
Bronchopneumonia
• Central bronchi involved
• Patchy bilateral disease
• Asymmetrical
• Peribronchial cuffing
Interstitial Pneumonia
• Involves interstitial space
• Ground glass appearance
• Bilateral, symmetrical
 Etiologic Diagnosis

• Gram’s stain and culture of sputum

• Blood cultures
• Urinary antigen tests
• Polymerase chain reaction
• Serology
• Biomarkers
 Community Acquired Pneumonia

• Pneumonia acquired outside the hospital setting

• Leading cause of death from an infectious disease
• It is the sixth leading cause of death overall and is a
major cause of morbidity and mortality.
 Empiric Antimicrobial Therapy for CAP WITH USUAL RECOMMENDED
DOSAGES IN 50-60 KG ADULTS WITH NORMAL LIVER AND RENAL FUNCTIONS
 Management

• Pneumonia Severity Index (PSI), a prognostic

model used to identify patients at low risk of
dying
• the CURB-65 criteria, a severity-of-illness score
 CURB-65
Score
C Confusion 1
U Urea >7mmol/L 1
R Respiratory rate≥ 30 1
B SBP ≤ 90mmHg: DBP ≤60mmHg 1
65 Age > 65 yr 1

CURB-65 Score Mortality Treatment Option

0-1 1.5% Consider Home treatment
2 9.2% Hospital-supervised treatment
2-5 22% ICU admission; managed as severe
Points Mortality Treatment

I (<5o) 0.1% Outpatient

II (51-70) 0.6 % Outpatient
III (71-90) 2.8% Outpatient or
brief patient

IV (90-100 8.2% In patient

V (130) 29.2% In patient
• When should antibiotics be initiated for the empiric
treatment of community-acquired pneumonia (CAP)?

– as soon as possible after the diagnosis is

established.
• When should de-escalation of empiric antibiotic therapy be
done?

– once the patient is clinically improving, is

thermodynamically stable and has a functioning
gastrointestinal tract.
How can response to initial therapy be assessed?
– Temperature
– respiratory rate
– heart rate
– blood pressure,
– sensorium,
– oxygen saturation and inspired oxygen concentration

• Response to therapy is expected within 24-72 hours of

initiating treatment.
 Indications for streamlining of
antibiotic therapy

1. Resolution of fever for > 24 hours

2. Resolution of respiratory distress
3. Improving white blood cell count, no bacteremia.
4.Etiologic agent is not a high-risk (virulent/resistant)
5. No unstable comorbid condition or life-threatening
6. No sign of organ dysfunction
7. Patient is clinically hydrated, taking oral fluids and is
able to take oral medications
 Failure to Improve
• Complete reappraisal rather simply
selection of alternative antibiotics
• Review clinical history, physical
examination and results laboratory
investigations
• Reassess for possible resistance
• Follow up chest x-ray. CT also
provide more information.
• Obtain additional specimens for
microbial testing.
 Additional Information to Discuss with the
Patient
• 1 week- fever should have resolved
• 4 weeks- chest pain and sputum production should have
substantially reduced
• 6 weeks- cough and breathlessness should have substantially
reduced.
• 3 months- most symptoms should have resolved but fatigue
may still be present
• 6 months-most people will feel back to normal
 Prognosis

Depends on:
• Age
• Comorbidities
• Site of treatment
 Hospital-Acquired Pneumonia
– Develops >48 hours after admission

• Common in patients with severe underlying disease

• Immunosuppression
• Prolonged antibiotic therapy
• Invasive access devices such as intravascular catheters

• Most common isolates

– Gram-positive cocci - mainly S. aureus and S. pneumonia
– gram-negative rods- Enterobacteriaceae and Pseudomonas
species
CDC Criteria for Hospital Acquired Pneumonia

1. Rales or dullness to percussion on physical examination of

chest of any of the following:

– New onset of purulent sputum or change in character of

sputum
– Organism isolated from blood culture
– Isolation of pathogen from specimen obtained by
transtracheal aspire, bronchial brushing or biopsy.
2. Chest radiographic examination shows new or progressive
infiltrate, consolidation, cavitation or pleural effusion and any of
the following:

– New onset of purulent sputum or change in character of the

sputum
– Organisms isolated from blood culture
– Isolation of pathogen from specimen obtained by trans tracheal
aspirate, bronchial brushing or biopsy

– Detection of viral antigen in respiratory secretions

– Diagnostic single antibody titre (IgM) or four-fould increase in paired
serum samples (IgG) for pathogen
 Clinical Presentation
Mild to Moderate Severe
Hypotension × ✓
Sepsis syndrome × ✓
Rapid progression of ×
infiltrates ✓
End organ dysfunction × ✓
 Risk Factors for resistance
• Antimicrobial therapy in the past 90 days
• Late- onset during hospitalization (>5)
 Classification
Classification Diagnostic Features Pathogens
Group I No risk factors for Core pathogens
resistance and mild to
moderate presentation

Group 2 Risk factors for resistance Core pathogens plus

and mild to moderate MRSA and
presentation P. aeroginosa

Group 3 Severe Presentation and Core Pathogens plus

risk factors MRSA, P. aeroginosa and
Legionella species
VENTILATOR-ASSOCIATED PNEUMONIA
Health Care-Associated Pneumonia
RISK FACTORS:
– hospitalization of at least 2 days
within the recent past
– presentation from a nursing home or long-term care facility
– attending a hospital or hemodialysis clinic
– recent intravenous antibiotic therapy, chemotherapy or
wound care.

• The most common organisms isolated are methicillin-

resistant Staphylococcus aureus and P. aeruginosa.
 Prognosis
• VAP is associated with crude mortality rates as high as 50–70%

• Many patients with VAP have underlying diseases that would

result in death even if VAP did not occur which attributes to
the high mortality.

• MDR pathogens are associated with significantly greater

attributable mortality than non-MDR pathogens

• Pneumonia caused by some pathogens (e.g., S. maltophilia) is

simply a marker for a patient whose immune system is so
compromised that death is almost inevitable
Antibiotic Resistance
• Misuse of antibiotics results in increase
antibiotic selection pressure that can affects
resistance locally and globally.

• CAP- main resistance issues currently involve S.

pneumoniae and CA-MRSA
THANK YOU!
 References

• Harrison’s Principles of Internal Medicine, 20th edition

• Philippine Clinical Practice Guidelines: Diagnosis, Empiric,
Management, and Prevention or Community-Acquired
Pneumonia in
• Center for Disease Control
• Robbins and Cotran Pathologic Basis of Disease, 9th
edition
• https://www.radiologymasterclass.co.uk/search?q=m