Page 486 - Textbook of Pathology, 6th Edition

470 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.
4. RESOLUTION (Fig. 17.6,D). 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:
Figure 17.7 Lobar pneumonia, acute congestion stage. There is i) Macrophages are the predominant cells in the alveolar
congestion of septal walls while the air spaces contain pale oedema spaces, while neutrophils diminish in number. Many of
fluid and a few red cells.
the macrophages contain engulfed neutrophils and debris.
Grossly, the affected lobe is firm and heavy. The cut ii) Granular and fragmented strands of fibrin in the
surface is dry, granular and grey in appearance with liver- alveolar spaces are seen due to progressive enzymatic
like consistency (Fig. 17.9, A). The change in colour from digestion.
red to grey begins at the hilum and spreads towards the iii) Alveolar capillaries are engorged.
SECTION III
periphery. Fibrinous pleurisy is prominent. iv) There is progressive removal of fluid content as well
Histologically, the following changes are present as cellular exudate from the air spaces, partly by
(Fig. 17.9,B): expectoration but mainly by lymphatics, resulting in
i) The fibrin strands are dense and more numerous. restoration of normal lung parenchyma with aeration.
ii) The cellular exudate of neutrophils is reduced due to COMPLICATIONS. Since the advent of antibiotics, serious
disintegration of many inflammatory cells as evidenced
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 resul-
Systemic Pathology
ting 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.
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,
Figure 17.8 Lobar pneumonia, red hepatisation stage. The alveoli
are filled with cellular exudates composed of neutrophils admixed with bacterial endocarditis and myocarditis. Other forms of
some red cells. metastatic infection encountered rarely in lobar pneumonias