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- IRREVERSIBLE airway dilation that involves the lung either: FOCAL OR DIFFUSE
- A Chronic disease
- 25-50% idiopathic in origin
- Loss of airway tone results in air trapping
- Na compare siya between straw and a big pipe. If I ask you to blow a straw and nilagay ko yung
daliri ko sa kabilang side I can feel the air. Pero pag hinarap kita sa big pipe and sabi koi blow mo
I wont be able to feel the air kasi yung air paikot ikot nalang sa loob nang tude so hirap kang
ilabas ( air will acelarated and roll against the wall of the dilated bronchi.
Focal bronchiectasis: bronchiectatic changes in a localized area of the lung and can be consequence of
obstruction.
Diffuse bronchiectasis: wide spread bronchiectasis changes throughout the lung often arises from an
underlying systemic or inf disease
Categories:
1. Cylindrical or tubular bronchiectasis - most common, the bronchi appear as uniformly dilated
tubes that end abruptly at the point that smaller airways are obstructed by secretion
2. Varicose bronchiectasis – the affected bronchi have irregular or beaded pattern of dilation
resembling varicose veins.
3. Saccular or cystic bronchiectasis - the bronchi have a ballooned appearance at the periphery,
ending in blind sac without recognizable bronchia structure distal to the sacrs
1. Upper lung field involvement: common in cystic fibrosis, observed in post radiation fibrosis
corresponding to the lung region encompassed by radiation port
2. Lower lung field involvement: source chronic recurrent aspiration ( esophageal motility)
- End stage fibrotic lung disease
- Recurrent immunodeficiency associated infection ( hypogammaglobulinemia
3. Mid lung field involvement: infection by non- tuberculosis mycobacteria ( MAC) –
mycobacterium avium complex.
4. Congenital + midlung involvement: dyskinetic, immotile cilia syndrome.
5. Central airway involevement: assoc. with allergic bronchopulmonary aspergilosis in which
immune mediated reaction to aspergillus damage the bronchial wall
6. Congenital + central airway: cartilage efficiency include tracheobronchomegaly
- Mounier- kuhn syndrome and Williams-campbell syndrome)
Etiology and proposed workup
1. Focal di ba sabi ko kanina pag focal isang area lang pero its either intrinsic which is yunf mga
airway tumor, aspirated foreign body or stenosis or pwede din extrinsic na dahil nacompress
dahil sa lymphadenopathy. So inshort more OBSTRUCTION ANG ETIOLOGY you do:
a. Bronchoscopy
b. Chest imaging ( xray or ct scan)
2. Diffuse
a. Infection in origin sputum g/s , c/s and AFB if no pathogen seen bronchoscopy with
bronchoalveolar lavage
b. Immunodeficiency ( hypogamma,HIV, bronchiolitis) CBC with diff count, immune
globulin measurement and hiv testing
c. Genetic cause (CF, kartageners) chloride test for cf, respitract biopsy, alpaha 1 trypsin
testing and genetic testing
d. Autoimmune or rheumatologic cause, immune mediated and recurrent aspergillosis
joint examination, serologic testing, aspergillosis work up and swallowing finction for
recurrent aspiration
PATHOLOGY:
- In bronchiectasis the affected airway is the BRONCHI which is a relatively large airways with
affected supporting structures.
- Bronchiectasis is sometimes preceded by pneumonia which was not treated early
Gross microscopic
- Airway affected are the medium sized - bronchial and peri bronchial
airways, often at the level of the inflammation and fibrosis
segmental and subsegmental - ulceration of the bronchial wall
- Cartilage and muscles and elastic tissues - squamous metaplasia
are destroyed and replaced by fibrous - mucus gland hyperplasia
tissue - fibrosis, emphysema, bronchopneumonia
- Pools of thick purulent material in the and atelectasis of the lung parenchyma
dilated airways - inc vascularity of the bronchial wall with
- Peripheral airways are obstructed by enlargement and anastomoses between
secretion or obliterated and replaced by the bronchial and pulmo arterial
fibrous tissue circulation
PATHOGENESIS:
2. Mucociliary clearance mechanism- it is the most important defense mechanism of the airways,
so if this is impaired microbes will undergo STASIS more susceptible for bacteria.
3. Pool of thick secretion in the airways- good medium for the microorganism to grow
4. Anti- proteases such as alpha 1 antitrypsin – play an important role in neutralizing the
damaging effects of neutrophil elastase and in enhancing bacterial killing. Which bronchiectasis
and emphysema have been observed antitrypsin deficiency
5. Immune mediated reaction – damage the bronchial wall assoc with systemic autoimmune
condition ( sjogren syndrome and rheumatoid arthritis)
Traction bronchiectasis – refers to dilated airways arising from PARENCHYMAL DISTRUCTION as a result
of lung fibrosis.
Infection causes:
- Patients w/ large lymph nodes – usually located at the mediastinal or hilar area leading to
airway obstruction
*** acute exacerbation of bronchiectasis are usually characterized by changes in the nature of sputum
production, with inc volume and purulent
*** dry type of bronchiectasis : no building up of secretions since there is normal drainage in the upper
lobe assuming an upright position
DIAGNOSTICS:
-no consult by this time, will only seek consult after a year of coughing or when worst : hemoptysis.
1. Chest Radiograph
2. Bronchography
3. CT Scan
4. Bronchoscopy
1. Chest Radiograph
CT Findings:
Airway dilatation (detected as parallel “tram tracks”)
Bronchial wall thickening in dilated airways, inspissated reactions ( e.g. the “tree-in-bud”
pattern)
Cysts emanating from the bronchial wall (especially pronounced in cystic bronchiectasis)
4. Sputum Exam
- May reveal abundant neutros & colonization of infection with variety of possible organisms
- Appropriate staining & culture often provide a guide to antibiotic therapy
5. Bronchoscopy
- Reveal underlying endobronchial obstruction in focal bronchiectasis
- Done if with hemoptysis, will administer agent to stop the bleeding
Other tests:
Measurement of sweat chloride levels for cystic fibrosis
Structural or functional assessment of nasal or bronchial cilia or sperm for PCD
Quantitative assessment of immunoglobulins may explain
the recurrent airway infection
Skin testing, serology & sputum culture for Aspergillus in
ABPA-related bronchiectasis
PFT may demonstrate airflow obstruction as a consequence
of diffuse bronchiectasis or associated COPD
o PFT:
FEV1:FVC ratio
RV, FRC
Normal FVC
↓ FEV1: ↓ FVC ratio
* ↓ FVC – not as low as restrictive pattern
*Obstructive type – bronchiectasis, COPD, asthma,
bronchiolitis
Serologic evaluation – fungal infection and viral infection
GERD test – causing aspiration upon backflow of acid
TREATMENT:
4 Major Goals:
1. Elimination of an identifiable underlying problem
2. Improve clearance of tracheobronchial secretions
3. Control of infection, particularly during acute exacerbations
4. Reversal of airflow obstruction
1. Elimination
Treatment of hypogammaglobulinemia with Ig treatment
*Massive hemoptysis
Complete bedrest and antibiotics
If it still persists, surgical resection and bronchial arterial embolization
*Lung transplant
For selected patients who are disabled despite maximal therapy
I. Antibiotic treatment:
- Antibiotic targeting causative or presumptive pathogen ( with H. influenza and P aeruginosa
commony isolated) should be administered in acute exacerbation usually for a minimum of 7-10
days and perhaps for as long as 14 days.
- Consensus guidelines have advised that diagnostic criteria for true clinical infection with NTM
should be considered
o in patient with symptoms and radiographic findings of lung disease
o who have at least 2 sputum samples positive in culture
o at least one bronchoalveolar lavage BAL fluid sample positive on culture
o biopsy sample displaying histopathologic features in NTM infection along with one
positive sputum culture or a pleural fluid sample positive on culture
- MAC strain are the most common NTM pathogens and the recommended regimen for HIV
negative patients include MACROLIDE COMBINED WITH RIFAMPIN AND ETHAMBUTOL
- IF P. AERUGINOS --. QUINOLONE OR AMINOGLYCOSIDES 3RD GEN CEPAHLOSPHORIN
COMPLICATIONS
Decrease ability to mobilize secretions → recurrent infection → increase sputum production
Eventually, RV may fail
Prognosis:
Bronchiectasis is not curable
Early recognition & adequate treatment can help control bronchiectasis & ↓ symptoms
Lifelong awareness of the need for treatment