BRONCHIECTASIS & LUNG ABSCESS
Dr. constantino
Bronchiectasis
Irreversible airway dilatation, focal or diffuse
Affects older individual, 2/3 women
 Focal
- Localized, extrinsic/intrinsic obstruction
 Localized depends on one segmental of
the lung or one lobe and secondary to
extrinsic or intrinsic obstruction
 Intrinsic – obstruction by an enlarged
lymph node or parenchymal masses
 Extrinsic – foreign body, bronchial
tumor or tuberculosis and bronchitis
 Diffused
- Widespread, systemic infectious process III.
I. Pathology
 Destructive inflammatory changes in medium sized airway
walls (segmental/subsegmental)
 Mediated by neutrophils, elastase and MMO
 Inflammatory changes mediated by neutrophils
and the inflammatory changes they produced like
elastase and matrix metalloproteinase
 Structural components destroyed, fibrosis
 Structural components include cartilage, muscle
and elastic tissue and they undergo fibrosis
 Dilated airways with thick purulent material
 Peripheral airways occluded by secretion or obliterated
 Traction bronchiectasis
 Dilated airways caused by parenchymal distortion
due to fibrosis so the airways are pulled apart
because of the fibrosis
II. Histology
 Bronchial and peribronchial inflammation and fibrosis
 ulceration of bronchial wall
 squamous metaplasia
 Mucous gland hyperplasia
 You have a lot of changes in the wall with variant
degrees of injury
 Involved area: combination of fibrosis, emphysema,
bronchopneumonia, atelectasis
 Involved area supplied by the affected bronchus
 Increased vascularity, enlargement of bronchial artery and IV.
anastomosis of the bronchial and pulmonary circulation
 Reason why bleeding is the common problem in
bronchiectasis
 Patterns:
A. Cylindrical or tubular pattern
 Uniform dilatation and ends disruption
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Pulmonology
B. Vascular
 Irregular or beaded pattern
 Similar to varicose veins
C. Saccular (cystic)
 Ballooned, end in blind sac
 In xray, it is very difficult to see the cylindrical or
tubular pattern, what would be very visible are
“tram tracts” appearance  bronchiectatic
structures of the lung which are closed together
because of the atelectasis, they are parallel to each
other  similar to “train” tracts
Etiogenesis
 Consequence of inflammation and destruction of
structural components of bronchial wall
 Infection is the usual cause – offending agents:
pigments, protease and toxins injure epithelium
and impair mucociliary clearance
 Inflammatory response induces epithelial injury due
to mediators
 Allow colonization of the mucosa by bacteria and
subsequently produces another bout or infection
 The inflammatory produces epithelial injury
because of the elucidation of the mediators
 Compromised protection susceptible to
colonization by microorganism and bacterial growth
 Cycle: Inflammation  airway damage  impaired
clearance  INFECTION
 “VICIOUS CYCLE HYPOTHESIS
 Infection  inflammation  subsequent
airway damage with empiric clearance of
secretions  susceptible again to infection
which develops another bout of infection
 This is a cycle that goes on and on, and that
is the reason why there is CHRONIC
INFLAMMATION IN BRONCHIECTASIS
 As time goes on, it progresses involving
more areas of the lung which subsequent
changes also in pulmonary function
resulting to symptoms
Etiology
A. Infectious
 Primary
 Most important – VIRUSES AND BACTERIA
 Viruses – adenoviruses and inflammatory virus
 Adenoviruses and influenza virus were the
most implicated in the development of
bronchial inflammation and destruction and
subsequent bronchiectasis formation
 Bacteria
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BRONCHIECTASIS & LUNG ABSCESS
Dr. constantino
 Especially with necrotizing organism like
staph and klebsiella would lead to
bronchiectasis especially is treatment is not
given or delayed
 Staph
 Klebsiella delayed treatment
 Bordetella  childhood
 Common bronchiectasis in childhood
 TB  direct/indirect
 Common cause of bronchiectasis in the
Philippines
 Direct: due to parenchymal destruction due
to the TB infection
 Indirect: either by extrinsic compression of
the bronchus by enlarged lymph nodes or
endobronchial obstruction because of
bronchostenosis
 MOTT: 1 or 2 infection
 HIV  recurrent bacterial infection
 Due to immunodeficient status of
the patient
 Secondary
 Localized impairment of host defenses
 Endobrochial obstruction  chronic
infection
 Most common
 Endobronchial obstruction – cannot clear
organism or secretions involved in lung
segments  bacterial colonization 
CHRONIC INFECTION  bronchial mucosal
injury
 Generalized impairment of pulmonary defense
 Immunoglobulin deficiency state
 IgG (IgG2)
 Panhypogammaglobulinemia: skin/sinus
infection
 These two are the most common
 PCD: 5-10% causes recurrent upper/lower RT,
abnormal radial spokes, dysnein arms,
microtubules
 PCD – primary ciliary dyskinesia
 Recurrent upper/lower RT – remember
cilia is needed in the mucociliary
movement so if you have dyskinetic
cilia, you will have impaired mucociliary
clearance
 Abnormal radial spokes, dynein arms
and microtubules – part of the ciliary
apparatus
 Males – infertile
 Because ciliary movement is also
needed for sperm motility
 50% kartagener’s syndrome
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Pulmonology
 Kartganer’s Syndrome Triad:
bronchiectasis, situs inversus, sinusitis
 Ciliary movement is also needed for
proper location of the viscera during
embryonic development, so if you have
impaired ciliary movement  abnormal
location  SITUS INVERSUS in
Kartagener’s syndrome
 CF (Cystic Fibrosis) : thick tenacious secretions 
impair mucocilary clearance  subsequent
bacterial colonization  chronic infection
B. Non Infectious
 Toxic exposure
 More common
 Leads to a severe inflammatory response that
would subsequently injured the bronchial
mucosa
 Gas inhalation (ammonia), acid aspiration
 In gastric acid aspiration – lungs don not only
exposed to gastric acid but also the bacteria 
secondary bacterial infection
 Immune response trigger inflammation and
subsequent destruction of tissue
 Example: allergic bronchopulmonary
aspergillosis (ABPA)
 Syndrome wherein there is aspergillosis in the
lungs and asthma like manifestations
 α -1 antitrypsin deficiency – occ. Bronchiectasis
 Yellow nail syndrome – hypoplastic lymphatics
 Pleural effusion and yellowish discoloration of
the nails
Table 258-1 Major etiologies of Bronchiectasis and
Proposed work up
 Focal : Obstruction  Bronchoscopy – if suspecting
obstruction in bronchiectasis
 Diffused:
 Infection
 Gram’s stain/culture
 If difficult to identify  Bronhoscopy
with bronchoalveolar lavage
 Immunodeficency syndromes
 Immunoglobulin methods to test for HIV
 Genetic causes
 CF  measurement of swear chloride
levels
 Kartagener’s syndrome  biopsy of th
bronchial and submucosal and look at
the cilia if it’s abnormal
 Autoimmune causes
 Workup for connective tissue diseases
 Recurrent aspiration
 Test for swallowing if there is impaired
swallowing
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Dr. constantino
V. Clinical Manifestation:
 Persistent productive cough, thick, tenacious sputum
and history of purulent respiratory cough infection
 Reason why patient come back a lot of
times because of chronic productive
cough
 Different from chronic bronchitis, in the
sense of usually a patient has a lot of
sputum upon waking up in the morning.
Reason is that when they sleep the
secretion pooled in the lungs so when
they wake up they cough out and
produce copious amount of sputum In
the morning
 Dry type bronchiectasis – upper lobes
 Usually involves upper lobes especially in
tuberculosis
 Dry – cough is non-productive
 Hemoptysis – 50-70% due to friable mucosa,
hypertrophied bronchial artery VII.
 Remember in BE, you have
hypervascularization and enlargement of
the bronchial arteries with anastomosis to
the bronchial and pulmonary aterial
circulation
 Bleeding may be arterial – massive
hemoptysis >200ml of blood
 PE: crackles, rhonchi, wheezing, clubbing
 Clubbing because of the presence of chronic
inflammation in the lungs
 PFT: mild to moderate airway obstruction
 Pulmonary function testing like spirometry
 Mild to moderate obstruction – means that
BE is an obstructive disease
VI. Diagnosis
 CXR: “tram tracks” indicate dilated airways and
sometime cystic lucencies
 One feature would be the prominent
bronchial markings because of the
peripheral inflammation and they would
reach up to periphery of the lungs
 Normally, there is tapering of the
pulmonary marking, but once they reach
the 2/3 of the lng zone, it is not seen
anymore
 “tram tracks appearance – 2 enlarged
bronchi parallel to each other
 Typical appearance: combination of tubular
and cystic BE
 CXR (varicose type of BE): irregular beaded
pattern, parang beads
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Pulmonology
 CXR (tubular): behind the cardiac shadow,
you will see the prominent bronchial
markings close to each other due to
atelectasis
 Chest CT Scan
 Modality of choice
 Especially the high resolution CT Scan
 In ordinary CT scan, you cannot see the
tubular pattern of BE but with HRCT you
can see all types of BE
 “tram tracks”
 Signet ring sign
 Due to the enlarged bronchus which is
about 1.5 times bigger than the
adjacent vessel, parang may maliit tapos
malaki
 Tree in bud appearance
 synonymous to secretions which filled
up the bronchiectatic segment
 Cystic infiltrate
Approach
 Clinical history
 Approach is more of clinical history
 Get the history of recurrent infection –
skin or sinus infection especially if there
is immunoglobulin deficiency
 History of chronic productive cough
with copious amount of sputum
production  because during
exacerbation of chronic BE, wherein
they have infection, there is increase
volume of secretion with increase
purulence
 Chest imaging
 CXR is very important
 One clue that there is BE in CXR 
persistence of pulmonic infiltrates even
after treatment
 Pneumonia is resolved with treatment after
3 weeks, so if CXR is repeated and there is
still presence of pneumonia in the same
place, then after 2 or 3 months if CXR is
repeated still present  Possible BE
 Differentiated from obstructive pneumonia
 pneumonia will present even with
treatment
 Work up for etiology including diffuse bronchiectasis
 Diffuse BE – more of systemic disease
involved, so a lot of examinations is needed
 Bronchoscopy to rule out obstruction
 Obstruction – may be a tumor or foreign
body
 Example: story about a patient, young male
who present with history of recurrent
 MAYI 
BRONCHIECTASIS & LUNG ABSCESS
Dr. constantino
cough, bronchoscopy was done  earring
of his girlfriend was found (pano nangyari
yun? Di ko maimagine. Hehe. Medyo
hardcore  ) After removal, condition
resolves but has some degree of permanent
damage because of the chronic infection
 PFT for functional assessment
 Because BE is an obstructive lung disease 
bronchial obstruction  reversible with
bronchodilator
IX.
VIII. Algorithm
 Evaluation of GERD/aspiration – because
these are some of the common cause of
chronic cough
 If CT scan is abnormal, in focal BE – consider
bronchoscopy because obstruction may be
due to a tumor or a foreign body. And do
induced sputum for acid fast bacilli –
because one cause of obstruction is
endotracheal tuberculosis
 If diffuse BE:
 Quantitative immunoglobulin analysis
– to determine if it’s due to
immunodeficiency
 Sputum examination for tuberculosis
– because disseminated TB can lead
to BE
 Studies of ciliary morphology and
function – by doing biopsies of the
nasal and bronchial cilia
 Semen analysis – because it is
involved in primary ciliary dyskinesia
 α-1 antitypsin level – especially if
pateients are young, remember, BE
affects older individuals but in patient
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Pulmonology
with α-1 antitypsin deficiency, if they
do have BE, most of the time they
develop emphysema
 Aspergillus serum testing – especially
if the patient has symptoms of
asthma
 Rheumatic disease serology –
because the rheumatoid arthritis is
related to BE also
 HIV screening
Treatment
 Control of active infection
 They often have repeated bouts of bacterial
infection  increased sputum production,
increased purulence of sputum, may or may
not have fever so treat the infection with
antibiotics
 Improvement in secretion, clearance and bronchial
hygiene
 Done by doing Chest physiotherapy and
mucolytics to improve secretions
 Chest physiotherapy would consists of chest
tapping or percussion and postural drainage
 Decrease microbial load and minimize recurrent
infection
 By giving cyclic antibiotics for severe cases
A. Antibiotic treatment
 For causative and presumptive pathogen
 Antibiotic course would depend on the type
of BE
 One antibiotic to be used should cover
Pseudomonas  common pathogen in BE
 7-10 days
 Consider treating NTB (MAC)
 Can cause primary or secondary
infection in cases of BE
B. Bronchial hygiene
 Hydration
 Mucolytics
 Bronchodilator aerosolzation
 Not only improve airway
obstruction but also improves
mucociliary clearance
 Chest physiotherapy (postural
drainage/pneumonia)
 Proteolytic damage (Dnase) – CF related BE
C. Anti-inflammatory treatment
 The control of inflammation in BE may be
beneficial
 Inhaled GC: decreased dyspnea, dec. β
agonist, dec. sputum production
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BRONCHIECTASIS & LUNG ABSCESS
Dr. constantino
 Ex: Bumesonide, meticazone ?
(sound like)
 No significant difference in lung function on
exacerbation whether GC is use or not
 Risk of immunosuprresive adrenal
suppression
 Oral/systemic GC may be important in
ABPA, AI
 Autoimmune disease like
Sjogren’s syndrome or
rheumatoid arthritis
D. Refractory cases/complication
 Surgery of focal disease
 Surgery may be done for focal
disease especially if you have
bothersome symptoms like
chronic productive cough that
may interfere In the work (e.g.
patient is a “GRO” nakakandong
sa client ubo ubo  Kat GRO
ngaaa  )
 Surgery will just involved the
affected lobe
 Transplant for advanced cases
 For very severe advanced cases of BE, lung
transplant is an option
 Criteria for lung transplant donors is very
strict – no systemic diseases, no lung
disease
 Complication:
 Repeated antibiotic  resistance
 Go back to the more primitive
antibiotics
rd
 Instead of using 3 generation
cephalosporins or new generation
quinolone  COTRIMOXAZOLE,
FLUOROQUINOLONES (?) earlier
antibiotics because they have not been
use for a long time there is no
resistance from these drugs
 Toxicity from antibiotic combination
 Because of the multiple antibiotics
used  renal or hepatotoxicity
 Hemoptysis may require bronchial arterial
embolization or surgery
 Usually managed by providing an
adequate airway
 Bronchoscopy is done to know the
source of the bleeding
 Balloon catheter is used to stop the
bleeding
 But in focal BE wherein the bleeding is
massive  surgery (lobectomy)
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Pulmonology
 But in diffused BE, better option would
be bronchial artery embolization
 Prognosis:
 Vary with underlying etiology, frequency of
exacerbation and --- pathology
 If etiology is more serious, more
chronic or untreatable  POOR
PROGNOSIS because BE will progress
as time goes on and since it is
progressive, lung function is
compromised which is also
progressive, patient may become
dependent to oxygen and then
develop  COR PULMONALE  death
from respiratory failure
 If etiology is treatable like
immunoglobulin defiency,
immunoglobulin is given  GOOD
PROGNOSIS
 Prevention:
 Dec. risk of recurrent infection
 Reversal immunodeficient state
 Risk of infection can be decreased by vaccination
 Smoking cessation
 smoking contributes to the decrease
mucociliary clearance  Infection
E. Suppresive antibiotics
 Oral antibiotics given for 1-2 months
 Antibiotics should be rotated – give
different antibiotics not the same
antibiotics for several months to minimize
antibiotic resistance
 Marcolides may be added for 3 times a
week for acute inflammation
 Aerosolized antibiotics to reduce side effect
 Reduces S/E since these are not absorbed
clinically
 Intermittent IV antibiotics for severe infection or
resistance pathogens
LUNG ABSCESS
Microbial lung infection that result in
parenchymal necrosis
 Usually 3 diameter or 2 cm
 Multiple abscesses <2cm  NECROTIZING
PNEUMONIA
Classifications:
 Acute
 Chronic  4-6 weeks
 Cut off point for chronicity: 4 weeks
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BRONCHIECTASIS & LUNG ABSCESS 2014 -2015

Dr. constantino
Pulmonology
Presence of underlying lesions:  Problem is the presence of anaerobic
a. Primary – no underlying lesion bacteria and the possibility of rupturing
b. Secondary the abscess
 There is an underlying lesion like
tumor obstructing the bronchus or IV. Treatment
systemic condition that could lead to  Depends on pressumed or established etiologies
necrotizing pneumonia  Before, Pen G was the DOC for Lung
 Non-specific lung abscess  abscess but because of the freuquency of
unrecovered pathogen bacteria which produce beta-lactamase,
 Usually secondary to anaerobic Pen G was not used anymore
organism
 Putrid lung abscess  anaerobic  Clindamycin 600 mg IV QID  300 PO QID (once
bacteria symptoms subside, become afebrile )
 Putrid lung abscess have foul smelling  Duration depends on the condition of the
sputum patient, sometimes it is given for 4-6
I. Etiology weeks
 Anaerobes – most non-specific lung abscess  β-lactam/ β-lactamase inhibitors
 Major contributor to lung abscesses  Beta-lactam combination like amoxicillin +
 Pathogens are not recovered because clavilanate (?)  commonly known as CO-
of the use of anaerobic culture AMOXICLAV
 Mycobacteria  Carbapenem
 Important cause of lung abscess, especially  Used because of the anti-pseudomonal
in the Phils. Where TB is a common activity but the problem is the anaerobic
problem activity may not be so good
 Staph aureus – acute LA, post influenza  Metronidazole
 Highly necrotizing  Good drug for anaerobic bacteria but it
 Implicated in acute LA especially after a has no effect on aerobic bacteria which is
bout of influenza a common organism in lung abscess so it is
 Fungi/parasites not a DOC
 Vancomycin
Table 258-2 Microbial Patthogens causing cavitary lung  Used if S. aureus is considered as the
infection cause of Lung abscess
 Aspiration-prone host – those who have an  S. aureus abscess  multiple lung
impaired cough reflex abscesses due to the spread of s. aureus
due to bacteremic effect that’s why it is
II. Clinical features multiple abscesses
 Indolent infection, chronic infection which may have
a duration from days to weeks in a host predisposed V. Failure of treatment
to aspiration  Fever – 5-7 days after treatment
 Fatigue, cough, sputum production and fever  Progression of infiltrate
 Weight loss, anemia and leukocytosis  Consider obstruction, complications like empyema, and
possibility of drug resistance
III. Diagnosis  Surgery – for treatment failure, especially if due to
 CXR neoplasm or hemorrhage
 Very important diagnostic tool  Percutaneous drainage
 Air-fluid level  By doing CT scan guided
 Very large abscess  Lobectomy
 Microbiologic studies: gram stains, cultures including  For cases of neoplasm and hemorrhage
fungi and mycobacteria
 To identify pathogen for appropriate treatment
 Fungi and bacteria study especially for patient who
have immunodeficient state
 Pleural fluid
 If pleural effusions is present
 BAL (bronchoalveolar lavage)

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