Chronic Lower Respiratory Tract Infections

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-1antitrypsin 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. tracheooesophageal 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.

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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