PNEUMONIA
FOR C-I STUDENTS

PNEUMONIA
DEFINITION
• Pneumonia is an infection of the pulmonary par
enchyma.
• To the pathologist, pneumonia is an infection of t
he alveoli ,distal airways, and interstitium of the l
ung that is manifested by increased weight of th
e lungs, replacement of normal lung’s spongines
s by consolidation ,and alveoli filled with white bl
ood cells ,red blood cells and fibrin .

• To the clinician, pneumonia is a constellation of
symptoms and signs in combination with at least
one opacity on CXR.
Epidemiology
• Between 5 and 10 million cases of infectious pne
umonia occur annually in the United States and r
esult in more than 1 million hospitalizations.
• Pneumonia is a leading cause of death worldwid
e, the sixth leading cause of death in the United
States, and the most common lethal infectious di
sease.

CLASSIFICATION
• ETIOLOGIC
1.Infections 2.Inhala
tion of gastric contents 3.Immunological reactio
ns 4.Inhalation of other toxic substanc
es
• ANATOMIC
1.Lobar or segmental : process is confined to th
ese division of the lung
2.Bronchopneumonia : small areas of the lung al
veoli and lobule around small terminal bronchi ar
e affected

• Revised classification system
1.Community-acquired pneumonia (CAP)
–includes
- Cases of infectious pneumonia in patients l
iving independently in the community
- Patients who have been hospitalized for ot
her reasons for less than 48 hours before t
he development of respiratory symptoms

2.Health care–associated pneumonia (HCAP)
-Patients who have previously been hospitalized
for at least 2 days within the 90 days before infe
ction
-Patients from nursing homes who received intrav
enous antibiotic therapy, chemotherapy, or woun
d care within the past 30 days
-Patients from hemodialysis centers
-Patients contracting pneumonia greater than 48
hours after the institution of endotracheal intubat
ion and mechanical ventilation
a. Hospital-acquired pneumonia (HAP)
b. Ventilator-associated pneumonia (VAP).

PATHOPHISIOLOGY
• Pneumonia results from the proliferation of microbial pat
hogens at the alveolar level and the host's response to t
hose pathogens.
1.Microorganism
• How do micro organisms gain access to the lower respir
atory tract ?
a .Aspiration from the oropharynx or nasopharynx
b .Direct inhalation from ambient air
c .Haematogenous dissemination
d .Penetrating chest trauma
e .Local spread from contagious site

2 . Host defence
• What are the host defence mechanisms?
A. mechanical factors
- Hairs and turbinates of the nares & airway cilia
-The gag reflex and
-The cough mechanism
B. Cellular immunity
- Alveolar macrophage and neutrophils
C. Humoral immunity
- IgG and IgA

PATHOLOGY
• Classic pneumonia evolves through a series of p
athologic changes.
A. Congestion or Edema
B. Red hepatization
C. Gray hepatization
D. Resolution
* This pattern has been described best for pneum
ococcal pneumonia and may not apply to pneum
onias of all etiologies, especially viral or Pneumo
cystis pneumonia.

CLINICAL MANIFESTATION
-Cough that is either non-productive or prod
uctive of mucoid, purulent, or blood-tinged
sputum
-Fever
-Pleuritic chest pain
-Shortness of breath
-Gastrointestinal symptoms (20%)
-Other symptoms may include fatigue, head
ache, myalgias, and arthralgias.

PHYSICAL FINDINGS
• Findings on physical examination vary with
the degree of pulmonary consolidation and
the presence or absence of a significant pl
eural effusion.
-Increased respiratory rate and use of ac
cessory muscles of respiration -In
creased or decreased tactile fremitus -
Relative or stony dullness -
Crackles, bronchial breath sounds

INVESTIGATION
• Clinical diagnosis
-Chest radiography
• Etiologic diagnosis
-Gram stain and culture of sputum
-Blood culture
-Antigen tests
-PCR
-Serology
-Bronchoscopy

DIFFERENTIAL DIAGNOSIS
• Acute bronchitis
• Acute exacerbations of chronic bronchitis,
• Heart failure
• Pulmonary embolism

COMPLICATIONS
• Respiratory failure
• Shock and multiorgan failure
• Exacerbation of comorbid illnesses
• Metastatic infection (e.g., brain abscess or
endocarditis)
• Lung abscess
• Complicated pleural effusion (Empyema)

MANAGEMENT
• The principles of treatments are
1.To treat non complicated pneumonia as
outpatient and complicated pneumonia an
d severely ill patients as inpatients
2.To kill the organism with appropriate anti
biotics
3.To recognize and treat complications

Criteria for hospitalization
• Age >65
• Co morbidity
• Leukopenia (<5000/ul) not attributable to a known conditi
ons
• S.aures ,G-ve bacilli, anaerobes suspected causes of p
neumonia
• Suppurative complications
• Failure of PO treatment
• RR >30’ ,PR >120’ ,SBP<90/mmhg
• Po2 < 60mmhg , acute alteration in mental status
• Multiple lobe involvement

FOLLOW UP
• Fever and leukocytosis usually resolve wit
hin 2 and 4 days, respectively .
• Physical findings may persist longer.
• Chest radiographic abnormalities are slow
est to resolve and may require 4–12 week
s to clear.

Failure to improve
• Noninfectious conditions
• Correct diagnosis but that a different patho
gen
• The pathogen may be resistant to the drug
selected
• Wrong drug or the correct drug at the wron
g dose or frequency of administration
• Nosocomial superinfections

Suppurative Lung diseases
• Lung Abscess
• Bronchectasis
• Empyema

LUNG ABCESS
• Is defined as pulmonary parenchymal necrosis and cavit
ation resulting from infection.
Conditions that predispose to lung abscess
• any cause of aspiration or decreased ciliary action
reduced levels of consciousness
alcoholism
seizure disorders
general anesthesia
cerebrovascular accidents
drug addiction

• Periodontal disease, gingivitis, sinus infecti
on, and bronchiectasis
• septic pulmonary embolism
• Bronchial obstruction – neoplasm , foreign
bodies
• Lung infarction
• Fluid-filled cysts or bullae
• Pulmonary contusion

MICROBIOLOGY
• Anaerobic bacteria ( most common )-strept
occoci, H.influenza
• Aerobic or facultative bacteria - S. aureus,
Klebsiella pneumoniae, Nocardia sp., and
gram-negative organisms
• Fungi
• parasites

CLINICAL MANIFESTATION
• Clinical course
-acute presentations - aerobic bacteria
-evolve over an extended period of time -
anaerobic infection
• Presentation
-Asymptomatic
-Symptomatic - cough, copious foul smelli
ng purulent sputum production, pleuritic ch
est pain, fever, and hemoptysis

PHYSICAL EXAMINATION
• Unrevealing
• Fetid breath and poor dentition
• Dullness to percussion
• Reduced breath sounds or criptation
• Clubbing or hypertrophic pulmonary osteo
arthropathy

INVESTIGATION
• Chest radiograph - cavity with an air-fluid level, with or wi
thout surrounding infiltrate
-Lung abscess occur commonly in dependent segment
s of the lung
.The posterior segments of the upper lobes and
.The superior segments of the lower lobes
• CT of the chest - to define the size and location of the ab
scess
• Gram stain and culture of sputum
• Blood culture
• Pleural fluid cultures
• Bronchoscopy

complications
• Empyema, with or without bronchopleural f
istula
• Massive hemoptysis
• Septicemia

MANAGEMENT
The principles of treatments are
1.To kill the organism with appropriate antibiotics
- Clindamycin (150 mg–300 mg every 6 h) 4-8wks
- Metronidazole 400mg tid plus penicillin
2. To drain the pus -Postural
-Bronchoscopical
3.Surgical resection of affected segment
Indications
-refractory hemoptysis
-inadequate response to medical therapy
-Empyema or bronchopleural fistula
-the need for a tissue diagnosis when there is concern fo
r a noninfectious etiology (lung ca).

BRONCHECTASIS
• is an abnormal and permanent dilatation of
bronchi.
• It may be either focal, involving airways su
pplying a limited region of pulmonary pare
nchyma, or diffuse, involving airways in a
more widespread distribution .

PATHOLOGY
• Three different patterns of bronchiectasis
have been described
1. Cylindrical bronchiectasis
2. Varicose bronchiectasis
3. Saccular (cystic) bronchiectasis

PATHOGENESIS
• Bronchiectasis is a consequence of inflammation
and destruction of the structural components of t
he bronchial wall.
• The induction of bronchiectasis requires several
factors:
(1) an infectious insult
(2) airway obstruction
(3) reduced clearance of mucus and other mate
rial from the airways
(4) a defect in host defense

CLINICAL MANIFESTATION
• Persistent or recurrent cough and purulent
sputum production
• Hemoptysis
• Asymptomatic or nonproductive cough ("dr
y" bronchiectasis )
• Systemic symptoms (fatigue, weight loss,
myalgias,fever)
• Dyspnea or wheezing

PHYSICAL EXAMINATION
• Crackles, rhonchi, and wheezes
• Clubbing

MANAGEMENT
• The principles of treatment
(1) treatment of infection, particularly during
acute exacerbations
• empiric coverage (e.g., with amoxicillin, t
rimethoprim-sulfamethoxazole, or levoflox
acin)
(2) improved clearance of tracheobronchial s
ecretions

(3) reduction of inflammation; and
(4) treatment of an identifiable underlying pr
oblem

Empyema
• Is defined as grossly purulent pleural effusion.
• Causes
Extension of infection from infected lung (
pnemonia,lung abcess)
Subphrenic abcess
Chest trauma
Esophageal perforation
Iatrogenic

MANAGEMENT
• Principles of treatment
1.Removal of pus – chest tube drainage
2.Antibiotic
3.Decortication