BRONCHIECTASIS

 Broncos- Airways; Ectasia -Dilation

 Defn: “It refers to an abnormal irreversible airway
dilation that involves the lung in either a focal or a
diffuse manner”.
 Etiology: it can arise from infectious or noninfectious
causes
 Based on pattern of lung involvement
a) Focal Brochiectasis
b) Diffuse Brochiectasis
PATTERN OF LUNG ETIOLOGY
INVOVEMENT
Focal Mechanical Bronchial Obstruction
1. Foreign Body
2. Endobrochial Growth (Tumor Mass, Endobrochial TB)
3. Extrinsic compression Of bronchus By Lymph node or
Tumor
Diffuse 1. Post Infective Bronchial Damage (Bacterial and Viral
Pneumonias - Pertussis, Measles, Aspiration
Pneumonia
2. Immune Deficiency (Hypogammaglobulinemia，HIV,
bronchiolitis Obliterans After Lung Transplantation)
3. Genetic causes (cystic fibrosis, Kartagener's syndrome
, α1- AT deficiency)
4. Immunological Overresponse (ABPA, Post Lung
Transplant
PATTERN OF LUNG ETIOLOGY
INVOVEMENT

Diffuse 5. Autoimmune or rheumatologic causes (Rheumatoid

Arthritis, Sjögren's syndrome, inflammatory bowel
disease)
6. Tractional Bronchiectasis ( Post Radiation Fibrosis,
Idiopathic Pulmonary Fibrosis)
Pathogenesis
 Primary Necrotising pneumonia due to S. Aureaus, K.
Pneumoniae and P. Aerogenosa – destruction of bronchial
wall - Bronchiectasis
 Necrotizing anerobic Pneumonias secondary to aspiration
or bronchial obstruction – Parenchymal destruction and
Bronchiectasis
 Vicious Cycle Hypothesis:
 Environmental insult often on a backround of Genetic
Susceptibility (Ex: Impaired Mucociliary clearence) 
Resulting in persistance of Microbes in the sinobronchial
tree and Microbial colonisation  chronic inflamation in
bronnchi  Bronchiectasis
Pathogic process in right midle
lobe Mycobacterium infection
 Infection causes enlargement of peribronchial Lymph
nodes resulting obstruction.
 The obstruction results in brochiectasis that persists
when the nodes return to normal size.
Clinical features
 Cough with Mucupurulent Sputum Production
(Purulent, Tenacious, frequently worse in the morning
– having accumulated during recumbency in sleep)
 Hemoptysis (may vary from blood streaks to Large clot
 Dyspnea
 Features of Acute exacerbation – Increasing cough,
dyspnea, volume of sputum production, fever
hemoptysis, chest pain
 Halitosis
 Clubbing and hypertrophic pulmonary
osteoarthropathy
 On auscultation – early & mid inspiratory crepitation
as well as diffuse ronchi and prolonged expiration ,
Bronchial breath sound may be heared in severe cases
or in complicating pneumonia
Treatment
 Controlling infection
 Reducing inflammation
 Improving bronchial hygiene
Control of infection
1. Since infection plays major role in the causation and
progression of bronchiectasis – reducing microbial load
and associated inflammatory mediators remains
cornerstone of therapy.
2. Antibiotics are directed at commonly isolated pathogens
– H. influenzae, S. pneumonia & P. Aerogenosa
3. Oral /IV Fluroquinolones  10- 14 days
4. Oral /IV penicillin or cephalosporin
5. Administration of antipseudomonal antibiotics
6. Administration of antibiotic aerosols (Tobramycin 300
mg nebulized 2 times daily against pseudomonas)
 Other aerosolized antibiotics – aztreonam, colistin,
gentamycin
5. Bronchial hygiene
 Chest percussion & postural drainage – facilitate
mucus clearance
6. Mucus clearance
– maintenance of hydration (oral/ IV) – prevent
inspissated sputum retention,
7. Humidification of Inhaled Air or Oxygen as an
adjunct to chest physical therapy
8. Use of nebulized normal or Hypertonic saline and
acetylcysteine
9. Bronchodilator ;
 Beta agonist , Anticholinergics, or theophyllines
10. Anti- inflammatory: ICS (Fluticasone)
 Surgery: in selected cases surgical resection of most
severely affected segment, Bleeding segment, or areas
of harboring resistant tuberculosis or atypical
mycobacteria may confer significant benefit,
 Lung transplantation – In advanced cases
Vaccination : vaccination against S.pneumonia and H.
Influenza