Lung Abscess

Defn :-Localised destruction and necrosis of lung tissues with pus

formation is called lung abscess. It is a type of liquefactive necrosis of
the lung tissue.
What is abscess ?Ans :-Abscess is a localised collection of pus within
the substance of an organ, a tissue or a confined space. It is commonly
found in solid organs like brain, liver, kidneys, lungs & bones.
What is Pus ?Ans :-It is the mixture of dead & degenerated
neutrophils, bacteria, fragments of necrotic tissues, cell debris and
fibrin.
If abscess is acute and pyogenic - it is surrounded by a zone of
hyperaemia (inflammatory zone).
If abscess is chronic – Then it may be walled off by connective tissue
(fibrosis) that limits further spread.
Aetiology and Pathogenesis :-Organisms most commonly isolated
from the lung abscess are :-
(i) Aerobic and anaerobic streptococci.
(ii)Staphylococcus aureus.
(iii)Various gram-ve organisms e.gklebsiella pseudomonas etc.
(iv)Anaerobic organisms normally found in the oral cavity like
Bacteroids, fusobacterium and peptococcus species – enter into
the lungs with inhaled foreign material.
The causative organisms are introduced into the lungs by the
following mechanisms :-
(a)Aspiration of infective material :-Here the abscesses formed are
more frequent in the right lung because the right main bronchus is
anatomically more in line with the trachea than the left. Aspiration is
more common in acute alcoholism, coma, deepanesthesia, sinusitis,
gingivodental sepsis and debilitating pt.
(b)Following (orcomplication of)primary bacterial infection :- e.g.

-Post pneumonic abscesses formation are usually associated with

staph. aureas, klebsiellapneumoniae, & type 3 streptocoecus
pneumoniae.
- Other infective conditions are – tuberculosis, bronchiectasis and
fungal infections.

(c)Septicembolism :-Infected emboli from thrombophlebitis in any

portion of the systemic venous circulation or from the vegetation
of infective bacterial endocarditis on the right side of the heart
trapped in the lung and formed multiple lung abscesses.

(d) Neoplasia :-Secondary bacterial infection, due to bronchial

obstruction by primary or metastatic tumours, causes lung abscess
distal to obstruction.

(e) Miscellaneous :-
(i) Direct traumatic penetration of bacteria into the lungs.
(ii) Spread of infections from the surroundings organs like
oesophagus, spine, pleural cavity etc.
(iii)Septic infarct of lung.

(f) Primary cryptogenic lung abscess :-Still the causes of the lung
abscesses are not known. (Still the source of infection is unknown).
If no etiological factor for abscess is identified then it is termed as
primary cryptogenic lung abscess.

Marphology :- Gross Appearance :-

(i) Lung abscess may be single or multiple. Their size may vary from
few mm to large cavities of 5 to 6 cm.
(ii) Pulmonary abscess due to aspiration are more common on right
lung and are most often single.
(iii) The abscesses that develop in the course of pneumonia,
Bronchiectasis& septic emboli are usually multiple, basal and
diffusely scattered in the lung.

(iv) In initial state – Cut section of lung showing:- The wall of abscess
is poorly defined and ragged and it is surrounded by a zone of
inflammation. In late state- it develops a fibrous wall.

Microscopic Appearance :-

(a) The cavity may or may not be filled with pus. If a cavity is
connected with a bronchus then all the contained are drained
with sputum and there is left an air containing cavity.

(b) In all abscesses there is suppurative destruction of the lung

parenchyma within the central area of cavitation.

(c) Continued abscess cavity infection leads to large, fetid, green-

black, multilocular cavities with poor demarcation of their margins
– This is called “gangrene of the lung.”

(d)In chronic cases – There is considerable fibroblastic proliferation

forming a fibrous wall.

Complications :-In most cases with good antibiotic treatment, they

completely resolve. But few complications are :-

(i) Communication with bronchus and produces copious purulent

sputum.

(ii) Empyema

(iii) Bronchopleural fistula.

(iv) Hemorrhage with hemoptysis

(v) Metastatic abscess to brain, bones, meningitis etc.

(vi) In chr. Long standing cases- 2ndary amyloidosis may develop.

Investigations :-x-ray chest, CT Scan, microscopic examination- gram

stain, c/s. etc

Community- Acquired Acute Pneumonia (CAP).

This inflammatory consolidation of lung is acquired from the normal
environment i.e from community. It usually occurs in healthy
individuals.
Again, the CAP is divided into two types :-
Typical Pneumonia Atypical Pneumonia
-Inflammation of lung -Inflammation of alveolar septa and
parenchyma with alveolar pulmonary interstitium without any
exudate. alveolar exudate (atypical denotes the
lack of alveolar exudate)
-That means alveoli -It is most commonly caused by
contain exudate. viruses, so it is also called “C.A. viral
pneumonia.”
-It is mainly caused by -Sometimes, it is also caused by
bacteria. So it is also called Mycoplasma
“community acquired pneumoniae&chlamydiapneumoniae.”
bacterial pneumonia.”

Community acquired bacterial Pneumonias:-

Here the bacterial infection of the lung is often follows the viral
infection of an URT. Bacterial inflammation of the lung parenchyma
causes the alveoli to be filled with an inflammatory exudate, thus
causing consolidation (Solidification) of the pulmonary tissue.

Risk factors are :- Extremes of age (infant & old age) but it can occur
in any age group, chronic diseases like ccf, COPD and diabetes,
congenital or acquired immune deficiencies, and decreased or absent
splenic function (Sickle cell disease or possplenectomy, which puts the
pt. at risk for infection with encapsulated bacteria like pneumococcus)

Causative microorganisms are :-

-Streptococcuspneumoniae or pneumococci→ 90 to 95 % bacterial
pneumonias are caused by this organism. It is gram +ve lancet shaped
encapsulated diplococcic.
Most common types involved in pneumonia are type 1,3,7and 2. Type
3 usually causes virulent form of pneumonia. Sometimes, it causes
lung abscess.
Others are :-H.influenzae, staphylococcus aureus, legionella
pneumophila, klebsiellapneumoniae, pseudomonas aeruginosa,
mycoplasma pneumoniae, chlamydia pneumoniae etc.

Pathogenesis :- (Previously I have told you)

Pathology/Morphology :-On the basis of anatomic parts of the lung

involved, the bacterial pneumonia has two histological patterns :-
(i) Lobar pneumonia.
(ii) Lobular or bronchopneumonia.

Lobar pneumonia :-Inflammatory consolidation of a segment of a lobe

or of an entire lobe is called lobar pneumonia.
The inflammatory response of a classical lobar pneumonia is classified
into 4 stages :-
(i) Stage of congestion – last for 1-2 days.
(ii) Stage of Red hepatization – last for 2-4 days.
(iii) Stage of Grey hepatization – last for 4-8 days.
(iv) Stage of Resolution – last for 8-21 days.

Stage of congestion :- Macroscopic or Gross pathology – The affected

lobe is enlarged, heavy (↑ wt.), dark-red and pulmonary blood vessels
are dilated and congested (hyperemic).

Cut Section :-On squeezing, the redish frothy fluid can be expressed
from the cut surface.

Microscopic pathology :-
(i) In the alveolar wall, the pulmonary capillaries are dilated and
congested.

(ii) The alveolar septa are stretched & thin.

(iii) The alveolar spaces are completely filled with pale eosinophilic
exudate.

(iv) Alveolar exudate contains a few red blood cells, small number of
neutrophils and a large number of bacteria. (i.e the fluid is highly
infectious)

Stage of Red hepatization :-

Hepatization- means the affected lobe of lung looks like liver. The lung
feels like liver in consistency so called hepatisation and it sinks in
water.
On Gross examination :-The affected lobe appears bright red, firm,
dry granular and airless with a liver like consistency, hence the term
Red hepatisation.
Microscopic examination :-
(i) Still the blood vessels of the alveolar walls are dilated and
congested.
(ii)The alveolar walls are heavily infiltrated with neutrophils and
RBC. It is oedematous due to exudate. The septa are not clearly
visible due to cellular exudate.

(iii) The alveolar spaces are filled with numerable polymorphs. RBC
and fine fibrin threads.

(iv) Many neutrophils show ingested bacteria.

Stage of Grey hepatisation :-From here the healing process starts. The
blood vessels are less dilated and congested, therefore, the area is less
red in colour.
The affected area is greyish brown in colour due to the presence of
large number of coarse fibrin threads & pus cells.

Gross appearance :-The affected lobe becomes grey in colour due to

the presence of fibrinosuppurative exudate in the alveoli and still the
area has liver like consistency, hence the term grey hepatisation.

(i) The alveolar septa are thickened (due to accumulation of

fibroblast) and clearly visible (due to less cellular exudate) due to
inflammatory reaction.

(ii) Degree of dilatation and congestion of blood vessels is gradually

decreased.

(iii) There is progressive disintegration of RBC and neutrophils in the

alveoli. The RBC are lysed & neutrophils are changed into pus
cells.
(iv) Large number of macrophages begin to appear in the exudate.

(v) Large number of coarse fibrin threads are present in the alveoli.

(vi) Due to presence of large number of coarse fibrin thread, the

exudate retract towards the centre of alveolar space and create a clear
space between alveolar septa & cellular exudate.

Stage of Resolution :-“Resolution” means “complete return to normal

tissue following acute inflammation.” This occur when-

(a) The tissue damage is slight

(b)The architectural frame work should be maintained.
(c)The cellular changes should be reversible.
(d)The host should be well nourished and immunized.
(e)The pathogens should be less virulent.
Gross Appearance :- (i) The solid exudate is liquefied or digested by
enzymatic activity.(Protecolytic enzymes are secreted by
macrophages) and these liquefied debris are cleared by macrophages
or cough mechanism (in the form of sputum).

Microscopic Appearance :-

(i) Alveolar capillaries are again dilated due to resorption of the

semisolid fluid and debris.

(ii) Alveoli contain few macrophages and many of them contain

engulfed neutrophils and debris. These alveoli also contain
fragments of fibrin bands.

(iii) Some of the alveoli contain air due to healing. Usually after 21
days (3 wks) the normal architecture of lung is achieved.

Bronchopneumonia :-It is acute inflammation of bronchi, bronchioles

and pulmonary interstitium of lobules resulting in patchy
consolidation of the lung. These patchy necrotic areas are common at
the base of the lungs because the secretions gravitate to lower lobe.
These patchy consolidation may be monolobar but is more often
multilobar and frequently bilateral. Well developed lesions are 3 - 4
cm is dia, slightly elevated, dry granular, grey-red to yellow, and
margins are poorly demarcated.

On cut section :-These patchy consolidations are often centred

around a bronchiole.

Microscopic Appearance :-

(i) The bronchi, the bronchioles as well as the adjacent alveoli are
filled with neutrophil rich exudate.

(ii) The alveolar septa are thickened due to congested capillaries and
neutrophilic infiltrate.

(iii) All four stages are also in bronchopneumonia, but they are not
clearly distinguished to each other due to small area involved.

Complications :-Of both lobar pneumonia and bronchopneumonia.

(i)Organization :-In about 3 % cases of pneumonia there is no

complete resolution of exudate take place. It is organized. Then
the fibroblast which are present in the alveolar septa grow into the
alveolar space and begin to proliferate leading to fibrosis. This
type of post pneumonic fibrosis is called carnification.

(ii) Pleural effusion :-Excessive accumulation of fluid in the pleural

cavity is called pleural effusion.

(iii) Empyema :-Accumulation of pus in the pleural cavity is called

empyema. Sometimes the pus forming organisms involve the
pleura& causes empyema.

(iv) Lung Abscess :-Massive tissue destruction and necrosis causing

abscess formation. Lung abscess is common with type 3
pneumococci or klebsiella infections.

(v) Metastatic infection :-Sometimes the bacteria enter into the

blood circulation (dissemination) and go to the distant organs like
heart valves, pericardium, brain, kidneys, spleen or joints, causing
metastatic abscesses, endocarditis, meningitis or suppurative
arthritis.

Diagnosis of CAP :-
Symptoms in infant and children
- Fever with chill, cough, unusually rapid breathing.
- Breathing with grunting or wheezing sounds.
- Laboredbreathing that makes achild’s rib muscles retract (When
muscles under the rib cage or bet. ribs draw in ward with each
breath.
- Vomiting
- Chest pain (if pleura is inflammed)
- Loss of appetite (in old kids) or poor feeding (in infants)
- In extreme cases, bluish colour of lips & fingernails.

Symptoms in Adult :-

- Abrupt onset of high fever with shaking chills.

- Cough which at first is short, painful & dry, but later it is
productive with muco-purulent sputum.
- - Rusty coloured sputum→in strep. pneumoniae
- -Thick, nucoid, blood tinged→inklebsiella infection
- -Green coloured sputim→in pseudomonas.
- Chest pain(Pleuritic pain)→if pleura is inflammed.
- Hemoptysis→rare.
- Upper abdominal tenderness is sometimes apparent in pts. with
lower lobe pneumonia.
(b) Investigations :-
(i) X-ray chest :-

- Whole lobe is radiopaque in lobar pneumonia.

- Focal opacities in bronchopneumonia.
- Costophrenic angle is obliterated in pleural effusion and
empyema.

(ii) Lab. Investigations :-

(a) General blood Tests :-

TLC = ↑↑ed.

DLC = Neutrophilic leucocytosis (˃90% neutrophils)

ESR = ↑↑

C – Reactive protein – is elevated.

(b) Microbiological exam :-

- Blood of culture – Frequently positive in pneumococcal pneumonia.

- Serology :-Ab. titre for diagnosis of mycoplasma, chlarydia,

legionella and viral infection.

- Pneumococcal Ag detected in serum.

- Throat swab/Nasopharyngeal swab :-Help in children or during

influenza epidemic.

Difference between lobar pn.andBronchopn.

(1) Defn. – Consolidation of -Patchy pneumonic

segment or whole lobe of lung. consolidations
-Usually middle and lower lobes -Usually lower lobes.
are involved.
-Usually unilateral -Usually bilateral.
-Margin of lesions are well -Margins are poorly demarcated.
demarcated.
-Occurs in all age group even -Occurs in extreme of age &
healthy individual can also usually debilitating pt.
involved.
(ii)Stages of pathology :-All four -All four stages are present but
stages are clearly distinguished not clearly separated to each
to each other.
 other due to small area
involved.
(iii)Complications :-Bacterimia, -Fibrosis, Bronchiectasis, lung
meningitis, endocarditis, septic abscess are common.
arthritis are common.
(iv)C.F. :- Its onset is sudden or -Its onset is insidious with low
abrupt with high grade fever grade fever and productive
shaking chill & bloody or rusly cough of puruleut sputum.
sputum.
(v)In X-ray :- Whole lobe is radio -Multiple focal/patehy opacities.
opaque.
(vi)T/t :-By serum or vaccine is -By serum or vaccines is not so
so successful. successful.