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Types of Bronchiectasis Explained

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0% found this document useful (0 votes)
10 views26 pages

Types of Bronchiectasis Explained

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Bronchiectasis

outline
Definition
Causes
Clinical
manifestation
Diagnosis
treatment
Definition:
 is an abnormal and permanent dilatation of
bronchi with destruction of the muscle tissue.
 It may be either focal, involving airways
supplying a limited region of pulmonary
parenchyma, or diffuse, involving airways in
a more widespread distribution.
epidemiology:
 Recent studies have estimated there to
be about 110,000 patients with
bronchiectasis in the US.
 typically affects older individuals.
 approximately two-thirds of patients are
women.
Pathology:
 Airway inflammation is primarily
mediated by neutrophils⇒activation of
enzymes – elastase and matrix
metalloproteinases.
 bronchial wall components including
cartilage, muscle, and elastic tissue, are
destroyed and may be replaced by
fibrous tissue.
 The dilated airways frequently contain
pools of thick, purulent material.
---pathology.
 The distal parenchyma; fibrosis,
emphysema, bronchopneumonia, and
atelectasis.
 As a result of the inflammation, vascularity
of the bronchial wall increases.
Three patterns:
 cylindrical bronchiectasis:
uniformly dilated and end abruptly .
 varicose bronchiectasis: irregular
or beaded pattern of dilatation
resembling varicose veins.
 saccular (cystic) bronchiectasis:
ballooned appearance at the periphery,
ending in blind sacs without
recognizable bronchial structures distal
to the sacs.
aetiology
1. Infectious Causes:
a. Viruses - Adenovirus and influenza
b. -Virulent bacterial infections- Staphylococcus
aureus, Klebsiella, and anaerobes.
- Infection with Bordetella pertussis, particularly in
childhood
- Bronchiectasis has been reported in patients with HIV
infection( recurrent bacterial infection)
- Tuberculosis,(a major cause of bronchiectasis
worldwide),can produce airway dilatation by a
necrotizing effect on pulmonary parenchyma and
airways and indirectly as a consequence of airway
obstruction from bronchostenosis or extrinsic
bronchial stenosis or secondary traction from fibrosis
compression by lymph nodes
- CF ⇒ tenacious secretions in the
bronchi ⇒impaired bacterial clearance
⇒ colonization and recurrent infection
with P. aeruginosa,S. aureus, H.
influenzae, Escherichia coli.
2. Noninfectious Causes
 inhalation of a toxic gas such as ammonia or
aspiration of acidic gastric
contents⇒inflammation, destructive changes, and
bronchial dilatation.

 alpha1-antitrypsin deficiency ⇒ panacinar


emphysema,,bronchiectasis.
 Foreign-body aspiration .
 Hilar adenopathy
 COPD
Clinical Manifestations
 persistent or recurrent cough and purulent sputum
production.
 Hemoptysis occurs in 50–70% (bleeding from
hypertrophied bronchial arteries.)
 Dyspnea, rhinosinusitis, recurrent pleurisy.
 Systemic symptoms such as fatigue, weight loss, and
myalgias can also occur.
Physical examination
 combination of crackles, rhonchi, and
wheezes may be heard, all of which reflect the
damaged airways containing significant
secretions.
 clubbing may be present.
 particularly those with chronic hypoxemia,
may have cor pulmonale and RV failure.
Diagnosis
 laboratory testing
radiographic imaging
pulmonary function
testing.
Laboratory tests
 CBC with differential
 levels of the immunoglobulins IgG, IgM,
and IgA
 Sputum culture and smear for bacteria,
mycobacteria, and fungi
 CxR
 often nonspecific.
 may be normal with mild disease.
 saccular bronchiectasis may have prominent
cystic spaces, either with or without air-liquid
 dilated airways with thickened walls often crowded
together in parallel :
-longitudinally, the airways appear as "tram tracks"
-when seen in cross-section, they produce "ring
shadows."
HRCT
 provides an excellent view of dilated airways
 it is now the standard technique for
detecting or confirming the diagnosis of
bronchiectasis.
Lung function tests:
 reduced or normal forced vital
capacity (FVC)
 low forced expiratory volume (FEV1),
and
 low FEV1/FVC) is the most frequent
finding.
Treatment
Goals
(1) treatment of infection, particularly
during acute exacerbations.
(2) improved clearance of
tracheobronchial secretions.
(3) reduction of inflammation, and
(4) treatment of an identifiable
underlying problem.
Antibiotics
 during acute episodes.
 guided by Gram's stain and culture of sputum
 Empiric; amoxicillin, TMP-SMXor levofloxacin.
 When Pseudomonas is present, oral quinolone or
parenteral aminoglycoside, carbapenem, or third-
generation cephalosporin .
 Duration is 10-14 days or longer.
 Oral
prednisone (0.5-1.0 mg/kg/day)
decreases inflammation in ABPA; prolonged
course of itraconazole (400 mg/day) can be
added.
Bronchial hygiene
 Hydration to euvolemia.
 Mucolytic agents like Aerosolized
recombinant Dnase –CF.
 Bronchodilators in reversible airflow obstruction.
 chest physiotherapy.
surgical resection-indications:
 massive hemoptysis.
 Reduction in acute infective episodes
 Reduction in massive purulent and viscid
sputum
 Removal of destroyed lung obstructed by a
tumor or FB.
 Removal of an area suspected of harboring
resistant organisms such as MAC,MDR-TB
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