BRONCHIECTASIS

Ectasia- dilatation
Bronkos- airways
Irreversible dilation that involves the lung in
either focal or diffuse manner.
Can arise from infectious and non-infectious
causes.
Classification:
o Radiographic patterns and distribution
may provide clues to diagnosis,
management and prognosis.
Cylindrical bronchiectasis
- Failure of the involved o Upper lung fields: cystic fibrosis, post
airways to taper radiation fibrosis
progressively in their o Middle lung fields: nontuberculous
distal course. mycobacteria congenital
- Bronchial walls are (dyskinetic/immotile cilia syndrome)
smooth or regular. o Lower lung fields: chronic recurrent
Varicoid bronchiectasis aspiration (esophageal motility
- Irregular dilatation, disorder, end stage fibrotic disease,
narrowing and pulmonary fibrosis)
outpouching of the o Central airway: allergic
airways. bronchopulmonary aspergillosis,
Cystic/Saccular bronchiectasis cartilage deficiency (mounier- Kuhn
- Focal or cystic syndrome), William Campbells
distortion of the distal syndrome.
airways o As a sequalae of granulomatous
- Isolated infection in increased tuberculosis
- Confluent (honeycomb burden:
pattern) Focal:
Etiology a. Extrinsic compression of
enlarged granulomatous
lymph node.
b. Intrinsic obstruction of
broncholith.
Diffuse
a. Parenchymal destruction
from infection
Epidemiology
o Varies with etiology
o CF-late adolescence or early adulthood.
o MAC infection nonsmoking women
more than 50 y/o
o Incidence increases with age
o More common among women.
Vicious Cycle Hypothesis
o Susceptibility to infection and poor
mucocillary clearance result in microbial
colonization of the bronchial tree.
o Presence of microbes incites continuous
chronic inflammation ->damage to
airway wall -> impairment of secretion
and microbial clearance ->ongoing
 propagation of infectious/inflammatory o More specific findings:
cycle. a. Airway dilation TRAM- TACKS or
Pathophysiology SIGNET RING SIGN
b. Lack of bronchial tapering
c. Bronchial wall thickening in dilated
airways
d. Inspissated secretions TREE IN
BUD pattern
e. Cysts emanating from the bronchial
wall.
Work-up
o Bronchoscopy to exclude airway
obstruction by an underlying mass or
foreign body.
o Analysis for major etiologies
o Pulmonary function tests for functional
assessment.
Management
o Directed at control of active infection
and improvement of airway clearance.
o Antimicrobial therapy
o 2 prerequisites: - Target causative agent
a. Infectious insult or presumptive
b. Impairment of drainage, airway pathogen in acute
obstruction and or a defect in host exacerbation for 7-10
defense. days.
o Release of proteases, reactive oxygen - NTM infection-
species, and proinflammatory cytokines macrolide combined
from small airways. with rifampin and
o Alpha 1 antitrypsin deficiency: loss of ethambutol.
proteases vs. neutrophil elastase and - NTM diagnostic
bacteria. criteria:
o Small-airway inflammation and larger a. At least 2 sputum
airway destruction. samples positive on
o Dilation, loss of elastin, smooth muscle culture
and cartilage. b. At least 1 BAL fluid
Clinical Manifestations positive on CS
o Recurrent LRI c. Biopsy sample with
o Cough histopathologic
o Sputum features of NTM
Copious (.200ml) and 1 positive
Purulent sputum CS
Foul smelling d. Pleural fluid
Hemoptysis positive on CS
o Auscultation o Airway hygiene
Wheezes - Mucous mobilizing
Crackles methods
o If widespread: dyspnea a. Inhaled B agonists
o Clubbing of fingers and or
o Increase pulmonary blood pressure -> anticholinergic
Cor pulmonale bronchodilators
High Resolution Ct-Scan b. Hypertonic saline or
o Gold standard for testing mannitol inhalation
 c. DNAse (in CF- o Vaccination of patients with chronic
related Bxtsis) respiratory conditions
d. N Acetylcysteine o Smoking cessation
- Tracheobronchial o Suggestive treatment with antibiotics:
clearing techniques - Daily oral antibiotic
a. Mechanical valve treatment (e.g.
devices Ciprofloxacin) for 1-2
b. Postural drainage weeks/month.
c. Chest - Rotating antibiotics
physiotherapy - Daily or three times
d. Therapeutic vest weekly use of
o Anti-inflammatory Airway macrolide antibiotics
Management - Aeorsolization of an
- Alleviated dyspnea, antibiotic (tobramycin)
deceased need for - Intermittent
bronchodilators, intravenous antibiotics
reduced sputum
production
- Systemic steroids (esp.
ABPA, autoimmune) LUNG ABSCESS
- Inhaled steroids Microbial infection of the lung resulting to
- Macrolide antibiotics necrosis of pulmonary parenchyma
- NSAIDs Necrotizing pneumonia/lung gangrene: multiple
o Surgery small pulmonary abscesses, usually from a more
- Resection of focal area virulent infection.
of suppuration in some Classification:
refractory cases o Based on clinical and pathologic
- Lung transplantation in features (duration of underlying lesion,
advanced cases. responsible microbe)
Complications o Acute: <4-6 weeks; Chronic: >4-6 weeks
o Microbial resistance to antibiotics ins o Secondary: with underlying pulmonary
severe cases lesion, tumor or systemic condition.
o Recurrent infection may lead to injury o Nonspecific: no likely pathogen isolated
of superficial mucosal vessels - from sputum
>bleeding/hemoptysis o Putrid: anaerobic bacterial lung abscess
o Massive hemoptysis may require Etiology:
intubation, bronchial artery o Aspiration-Prone Host
emobilization and surgery in severe - Anaerobic bacteria plus
cases. microaerophilic and or
Prognosis anaerobic streptococci,
o Outcomes vary widely with underlying Gemella spp.
etiology and presence of exacerbations. - Embolic (endovascular)
o Decline in lung function in non-CF lesions: Staphylococcus
bronchiectasis similar to COPD patients, aureus, Pseudomonas
with FEV1 declining by 50-55ml per year aeruginosa,
as opposed to 20-30ml for healthy Fusobacterium
controls. necrophorum
Prevention - Endemic fungi:
o Reversal of underlying immunodeficient Histoplasma,
state (e.g. gamma-globulin Blastomyces,
administration or immunoglobulin Coccidioides spp.
deficient patients)
 - Mycobacteria: o Transthoracic needle aspiration
M.tuberculosis, Treatment
M.kansaii, M. avium o Depends on presumed or established
o Immunocompromised Host pathology
- M. tuberculosis, a. Anaerobic infection:
Nocardia asteroids, Clindamycin, B
Rhodococcus equi, lactam/Blactamase
Legionella spp, P inhibitor, carbaenems
aeruginosa, b. Staphylococcus aureus:
Enterobacteriacease Vancomycin, linezolid
(klebsiella pneumoniae, c. Aerobic gram-negative:
Aspergillus spp, Carbapenems or B lactams
Cryptococcus spp. combined with
o Previously healthy Host aminoglycosides,
- Bacteria: S.aureus, Fluoroquinolones.
S.milleri, o Bronchoscopy or chest CT- for atypical
K.pneumoniae, Group A presentation unresponsive to treatment
streptococcus, Gemella, o Quantitative bacteriologic studies/BAL
Legionella, Actinomyce o Surgery
spp. - Reserved for 10-12%
- Parasites: Entamoeba - Failure to respond to
histolytica, medical treatment
Paragonimus - Suspected
westermani, neoplasm/obstruction
Stringyloides stercoralis - Hemorrhage
Clinical Features: - Lobectomy
o Indolent infection evolving over several - Percutaneous drainage
weeks in a host hos has predisposition Response to therapy
to aspiration. o Causes of failure of medical
o Periodontal infection with pyorrhea or management
gingivitis. - Failure to drain pleural
o Anaerobes and aerobic microaerophilic collection
streptococci that colonize the upper - Inappropriate
airways. antimicrobial therapy
Clinical Manifestations - Obstructed bronchus
o Cough - GIANT abscess>6cm
o Fatigue - Resistant pathogen
o Sputum production - Immunocompromised
o Fever host
o Chills-uncommon
o Weight loss
o Anemia
o Putrid smelling sputum
o Pleurisy
Diagnosis
o Imaging: CXR or chest CT
- Lymphadenopathy:
suggests alternative
diagnosis
o Microbiologic studies (GS/CS)
o Pleural fluid
o Quantitative bronchoalveolar lavage
o Transtracheal aspiration