1.

Pneumonia is an infection of the pulmonary parenchyma,

defined as lung inflammation in which air sacs are filled
with inflammatory cells, resulting in consolidation. It
results from the proliferation of microbial pathogens at
the alveolar level and the host's response to those
pathogens.

10. The congestion phase is rapidly followed by a red

hepatization phase. The presence of erythrocytes in the
cellular intraalveolar exudate gives this second stage its
name. Bacteria are occasionally seen in pathologic
specimens collected during this phase. Indicated here are
the findings associated with this stage.

2.

as seen here, it is imperative to describe the pneumonia in

terms of etiology, morphology, duration, and its clinical
manifestations.

11. Seen here is the histology of the congestion and red

hepatization phase.

3.

Pneumonia, in terms of mode of acquisition, is classified as

community-acquired, hospital-acquired, or atypical. The
most common of these is community-acquired.

4.

In terms of etiologic agent, pneumonia may arise from

bacterial, viral, protozoal, or fungal infection. They differ
from one another in terms of clinical and laboratory
presentation.

5.

6.

In terms of morphology, pneumonia may be lobar,

broncho, or interstitial pneumonia. As will be discussed
later on, the case at hand presents with manifestations of
the lobar type.
lobar pneumonia evolves in four stages : Congestion (first
2 days), Red hepatisation (fibrinous alveolitis) (2nd to 4th
day), Grey hepatisation (leukocytic alveolitis) (4th to 8th
day), Resolution (after 8th day)

7.

First, microorganisms gain access to the lower respiratory

tract, the most common of which is by aspiration from the
oropharynx. Normally, the branching architecture of the
tracheobronchial tree traps particles on the airway lining,
where mucus and local antibacterial factors prevent entry.
Resident alveolar macrophages are also extremely efficient
at clearing and killing pathogens. When the microbes
bypass the mechanical barriers and exceed the capacity of
the alveolar macrophages to ingest or kill, clinical
pneumonia becomes manifest. In that situation, the
alveolar macrophages initiate the inflammatory response
to bolster lower respiratory tract defenses. The host
inflammatory response, rather than the proliferation of
microorganisms, triggers the clinical syndrome of
pneumonia.

8.

This inflammatory response presents in the patient as

fever, an increase in mucus production, and airway
constriction resulting in wheezes. It also triggers the
release and accumulation of macrophages and
neutrophils. The initial phase is, thus, one of edema, with
the presence of a proteinaceous exudateand often of
bacteriain the alveoli. Consequent leukocytosis and
capillary leak cause both a decrease in compliance and the
ability of gas to diffuse, leading to hypoxemia. Hypoxemia
presents as increased respiratory rate, intercostal
retractions, and increased PR. The resulting manifestation
of these is dyspnea.

9.

The occurrence of pleurisy also arises dues to the invading

inflammatory exudates coating the pleural surfaces
causing three Rs: roughening, rubbing, and receptor
irritation.

12. In the third phase, gray hepatization, no new erythrocytes

are extravasating, and those already present have been
lysed and degraded. The neutrophil is the predominant
cell, fibrin deposition is abundant, and bacteria have
disappeared. This phase corresponds with successful
containment of the infection and improvement in gas
exchange.
13. Seen here is the gray hepatization stage, evidencing the
continuous predominance of neutrophils and the fibrin
deposition mentioned earlier.
14. In the final phase, resolution, the macrophage reappears
as the dominant cell type in the alveolar space. Enzymatic
digestion may eliminate the debris of neutrophils and
bacteria, or reabsorb certain components, or may lead to
fibrosis.
15. Seen here is the resolution stage.