For Medical students.

2.  Pneumonia is defined as acute inflammation
of the lung parenchyma distal to the terminal
bronchioles (consisting of the respiratory
bronchiole, alveolar ducts, alveolar sacs and
alveoli). The terms ‘pneumonia’ and
‘pneumonitis’ are often used synonymously
for inflammation of the lungs, while
‘consolidation’ (meaning solidification) is the
term used for gross and radiologic
appearance of the lungs in pneumonia

3.  The microorganisms gain entry into the lungs
by one of the following four routes:
1. Inhalation of the microbes present in the air.
2.Aspiration of organisms from the
nasopharynx or oropharynx.
3. Haematogenous spread from a distant focus
of infection.
4. Direct spread from an adjoining site of
infection.

4.  The normal lung is free of bacteria because of
the presence of a number of lung defense
mechanisms at different levels such as
nasopharyngeal filtering action, mucociliary
action of the lower respiratory airways, the
presence of phagocytosing alveolar
macrophages and immunoglobulins.
 Failure of these defense mechanisms and
presence of certain predisposing factors
result in pneumonias

5. These conditions are as under:
1. Altered consciousness. The oropharyngeal
contents may be aspirated in states causing
unconsciousness e.g. in coma,cranial trauma,
seizures, cerebrovascular accidents, drug
overdose, alcoholism etc.
2. Depressed cough and glottic reflexes.
Depression of effective cough may allow aspiration
of gastric contents e.g.in old age, pain from
trauma or thoracoabdominal surgery,
neuromuscular disease, weakness due to
malnutrition,kyphoscoliosis, severe obstructive
pulmonary diseases, endotracheal intubation and
tracheostomy.

6. 3.Impaired mucociliary transport. The normal protection
offered by mucus-covered ciliated epithelium in the airways
from the larynx to the terminal bronchioles is impaired or
destroyed in many conditions favouring passage of bacteria
into the lung parenchyma. These conditions are cigarette
smoking, viral respiratory infections, immotile cilia
syndrome, inhalation of hot or corrosive gases and old age.
4. Impaired alveolar macrophage function. Pneumonias may
occur when alveolar macrophage function is impaired e.g. by
cigarette smoke, hypoxia, starvation, anaemia, pulmonary
oedema and viral respiratory infections

7. 5.Endobronchial obstruction. The effective
clearance mechanism is interfered in
endobronchial obstruction from tumour,
foreign body, cystic fibrosis and chronic
bronchitis.
6.Leucocyte dysfunctions. Disorders of
lymphocytes including congenital and acquired
immunodeficiencies (e.g. AIDS,
immunosuppressive therapy) and granulocyte
abnormalities may predispose to pneumonia.

8. MORPHOLOGIC FEATURES. Laennec’s original
description divides lobar pneumonia into 4 sequential
pathologic phases: stage of congestion (initial phase),
red hepatisation (early consolidation), grey hepatisation
(late consolidation) and resolution. However, these
classic stages seen in untreated cases are found much
less often nowadays due to early institution of
antibiotic therapy and improved medical care. In lobar
pneumonia, as the name suggests, part of lobe, a
whole lobe, or two lobes are involved, sometimes
bilaterally. The lower lobes are affected most
commonly.
The sequence of pathologic changes described below
represents the inflammatory response of lungs in
bacterial infection

9. 1. STAGE OF CONGESTION: INITIAL PHASE:The initial
phase represents the early acute inflammatory
response to bacterial infection and lasts for 1 to 2
days. Grossly, the affected lobe is enlarged, heavy,
dark red and congested. Cut surface exudes blood-
stained frothy fluid.Histologically, typical features
of acute inflammatory response to the organisms
are seen. These are as under:
I.Dilatation and congestion of the capillaries in the
alveolar walls.
ii) Pale eosinophilic oedema fluid in the air spaces.
iii) A few red cells and neutrophils in the intra-
alveolar fluid.
iv) Numerous bacteria demonstrated in the alveolar
fluid by Gram’s staining.

10. RED HEPATISATION: EARLY CONSOLIDATION
This phase lasts for 2 to 4 days. The term hepatisation in
pneumonia refers to liver-like consistency of the affected
lobe on cut section. Grossly, the affected lobe is red, firm
and consolidated. The cut surface of the involved lobe is
airless, red-pink, dry, granular and has liver-like
consistency. The stage of red hepatisation is accompanied
by serofibrinous pleurisy. Histologically, the following
features are observed:
i) The oedema fluid of the preceding stage is replaced by
strands of fibrin.
ii) There is marked cellular exudate of neutrophils and
extravasation of red cells.
iii) Many neutrophils show ingested bacteria.
iv) The alveolar septa are less prominent than in the first
stage due to cellular exudation.

11. GREY HEPATISATION: LATE CONSOLIDATION:This phase lasts
for 4 to 8 days. Grossly, the affected lobe is firm and heavy.
The cut surface is dry, granular and grey in appearance with
liverlike consistency The change in colour from red to grey
begins at the hilum and spreads towards the periphery.
Fibrinous pleurisy is prominent.Histologically, the following
changes are present:
i) The fibrin strands are dense and more numerous.
ii) The cellular exudate of neutrophils is reduced due to
disintegration of many inflammatory cells as evidenced by
their pyknotic nuclei. The red cells are also fewer. The
macrophages begin to appear in the exudate.
iii) The cellular exudate is often separated from the septal
walls by a thin clear space.
iv) The organisms are less numerous and appear as
degenerated forms.

12.  RESOLUTION :This stage begins by 8th to 9th day if no chemotherapy is
administered and is completed in 1 to 3 weeks. However, antibiotic therapy
induces resolution on about 3rd day. Resolution proceeds in a progressive
manner.
 Grossly, the previously solid fibrinous constituent is liquefied by enzymatic action,
eventually restoring the normal aeration in the affected lobe. The process of
softening begins centrally and spreads to the periphery. The cut surface is grey-
red or dirty brown and frothy, yellow, creamy fluid can be expressed on pressing.
The pleural reaction may also show resolution but may undergo organisation
leading to fibrous obliteration of pleural cavity.
Histologically, the following features are noted:
i) Macrophages are the predominant cells in the alveolar spaces, while neutrophils
diminish in number. Many of the macrophages contain engulfed neutrophils and
debris.
ii) Granular and fragmented strands of fibrin in the alveolar spaces are seen due to
progressive enzymatic digestion.
iii) Alveolar capillaries are engorged.
iv) There is progressive removal of fluid content as well as cellular exudate from the
air spaces, partly by expectoration but mainly by lymphatics, resulting in restoration
of normal lung parenchyma with aeration.

14. COMPLICATIONS. Since the advent of antibiotics, serious
complications of lobar pneumonia are uncommon. However,
they may develop in neglected cases and in patients with
impaired immunologic defenses. These are as under:
1. Organisation. In about 3% of cases, resolution of the
exudate does not occur but instead it undergoes
organisation. There is ingrowth of fibroblasts from the
alveolar septa resulting in fibrosed, tough, airless leathery
lung tissue. This type of post-pneumonic fibrosis is called
carnification.
2. Pleural effusion. About 5% of treated cases of lobar
pneumonia develop inflammation of the pleura with
effusion. The pleural effusion usually resolves but
sometimes may undergo organisation with fibrous
adhesions between visceral and parietal pleura.

15. 3. Empyema. Less than 1% of treated cases of lobar
pneumonia develop encysted pus in the pleural
cavity termed empyema.
4. Lung abscess. A rare complication of lobar
pneumonia is formation of lung abscess, especially
when there is secondary infection by other
organisms.
5. Metastatic infection. Occasionally, infection in
the lungs and pleural cavity in lobar pneumonia
may extend into the pericardium and the heart
causing purulent pericarditis, bacterial
endocarditis and myocarditis.

16. Thank You