CHRONIC LOWER

RESPIRATORY TRACT
INFECTIONS
 BRONCHIECTASIS

 LUNG ABSCESS
 Bronchiectasis
 Definition
Dilation of bronchi.

 Epidemiology
Incidence low(<0.5%) in the developed countries:
a) Availability of vaccines against measles and
pertussis
b) Advances in antimicrobial therapy
 Bronchiectasis contd.
 Pathogenesis
Exact process obscure. Most likely
multifactorial, with the different factors
taking on different degrees of importance in
each patient.
 Bronchiectasis contd.
 Mechanistic Theories
There are 4:

i) Pressure of secretion theory

ii) Atelectasis theory

iii)Traction theory

iv)Infection theory
 Pressure of secretion theory
Thick secretions obstruct, then mechanically
distend the airway and the dilation persists
even after clearance of the obstruction.
 Atelectasis theory
Collapse of lung parenchyma leads to
increasingly negative intrapleural pressure
and later dilation of the bronchus in
question.
 Traction theory
Fibrosis and scarring from parenchymal
disease exert traction on the bronchial walls.
 Infection theory
Infection and the inflammatory response
damage the supportive structures of the
bronchial wall and subsequent
bronchiectasis.
Summary
Only the Infection Theory is supported by animal models of
this disease. Atelectasis and traction play minimal, if any
roles, in the pathogenesis of bronchiectasis.

Bronchial obstruction and poor drainage i.e. retention of

secretions (from such cases as foreign bodies) along with
infection appear to be the major factors in most cases.

Infection or obstruction occurring alone is unlikely to lead to

the more severe forms of bronchiectasis.
Classification
a) Cylindrical bronchiectasis (Group I)
Dilation regular, with the airway continuing to have a
regular outline.

b) Varicose bronchiectasis (Group II)

Dilation irregular, with areas of dilation and constriction.

c) Saccular bronchiectasis (Group III)

Dilation marked, with destruction of structural components
of the airway wall.
 Practice point
MEDICAL TREATMENT CAN HALT THE
PROGRESSION OF THE POTENTIALLY
REVERSIBLE CYLINDRICAL FORM TO
THE IRREVERSIBLY DESTRUCTIVE
SACCULAR BRONCHIECTASIS
AETIOLOGY
a) Infection
The most common:
i)Tuberculosis
ii)Histoplasmosis
iii)Pertussis, measles(complicated by pneumonia)
iv)Adenovirus (types 1,3,4,7, and 21) – 20 to 64 per cent
develop bronchiectasis
v) Herpesvirus
vi) Aspergillus fumigatus
vii) Mycoplasma pneumoniae
b) Congenital and genetic disorders
 i) Cystic fibrosis
 ii) Williams-Campbell syndrome
 iii) Tracheobronchomegaly
 iv) Marfan syndrome
 v)Alpha-1-antiproteinase deficiency[α-1-
antitrypsin deficiency]
 vi) Congenital bronchiectasis
c) Ciliary Abnormalities
 i) Congenital : Kartagener syndrome [triad of
situs inversus,sinusitis & bronchiectasis].
There is an underlying congenital abnormal
ciliary function.

 ii)Acquired : occurs as a result of infection.

d) Immunodeficiency
e) Foreign body aspiration
g) Right middle lobe syndrome
h) Asthma
i) Others:
-heroin intoxication
-intralobar pulmonary sequestration
-bronchogenic cyst
-chronic sinusitis
 -recurrent aspiration e.g. tracheo-
oesophageal fistula, cerebral palsy
 -inhaltion of noxious gases
 -racial predilections
Presentation
 Age: mainly preschool and early school age
years.
 Symptoms: manifestations range from
chronic cough with early morning sputum
production in an overtly healthy child to
recurrent pneumonia with or without
haemoptysis in a chronically ill one.
 Chronic cough worse in the morning.
Purulent , foul smelling sputum. Halithosis.
Haemoptysis
Others: weight loss, intermittent fever,
wheezing, dyspnoea, chest pain.
Clinical signs
Harrison’s sulci
Finger clubbing
Cyanosis
Dullness to percussion, crepitations
(crackles), rhonchi, decreased air entry,
bronchial breath sounds- usually localized
over the bronchiectatic area when saccular
changes are present except in diffuse
disease.
Diagnosis
 CXray findings not diagnostic but can be
suggestive
 In mild cases: segmental accentuation, loss
of definition of lung markings.
 In severe cases: ‘honeycomb’ pattern of
cystic changes.
 Bronchography
 Flexible fibreoptic bronchoscopy
 CT Scan
 Magnetic resonance imaging
 Lung scintigraphy
Differential diagnoses
All underlying causes
 Evaluation of patients with
bronchiectasis
Identify cause and predisposing factors
Infection: Sputum or BALF for M/C/S
Mycobacterial/fungal cultures
Viral culture
Skin tests (PPD, fungal)
Serological studies
 Immunodeficiency
FBC
Quantitative immunoglobulins
IgG subclasses
WBC function (nitroblue tetrazolium dye
test, chemotactic assays,
etc.)
Total haemolytic complement
 Aspiration
Barium swallow
Extended oesophageal pH monitoring
 Ciliary dysfunction
Nasal/tracheal epithelium: light and electron
microscopy

Cystic fibrosis
Sweat test
 Complications
Brain and lung abscess
Empyema & pyopneumothorax
Bronchopleural fistula
Severe atypical pneumonia
Haemoptysis
Amyloidisis
Cor pulmonale in advanced disease
 Treatment
Medical
 Chest physiotherapy
 Antibiotics
 Bronchodilator
 Good nutrition
 Bronchoscopy: to remove foreign body or
thick secretion
 Treatment (contd.)
Surgical
Failure of medical treatment, if disease is
localized

Prognosis
Depends on causative factors