Bronchiectasis Lecture 11

Irreversible increase in size of medium bronchi (subsegmentar) with structural alterations of the wall and
obstruction of distal ramifications.

•Not included:
-Reversible airway distension (transient) from pneumonia and atelectasis

-Preterminal cylindrical distension without distal obstruction from bronchitis

-Bronchiolectasias from diffuse pulmonary fibrosis ("Honeycomb")

Epidemiology:
Prevalence:
-Accurate estimates are rare
-Was high in preantibiotics period (100 -1ooo0/0000), with high proportion in children (0-10 years)
-severe forms have a high mortality
-Declining in recent decades, Significant decrease in children (5 times lower)
oDue to extension antibiotic and prophylactic vaccines (measles vaccinations, pertussis, tuberculosis)

-Geographic variations:
-Economic and social status
-Ethnic groups (genetic?) (Ex.polinezienii Samoa, Alaska Indians, maorii New Zealand)

MORPHO PATHOLOGY:(the common picture of infected bronchiectasis)

A) Form (classification):
-cylindrical (tubular)
-moniliform (varicose)
-saccular (ampullary)
-cystic

Macroscopic
-Atelectatic area, retracted -Bronchus enlarged, deformed, thick wall and secretions in the lumen -Continuity
with the bronchus, obstructed by secretions and / or fibrous inflammation -Mucosal surface swollen, inflamed,
ulcerated, polypoid

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 Etiopathogenesis
Major pathogen factors:
Bronchial wall with compromised resistance to deformation by alterations of support system
Cause:
-inflammation / necrosis

-Congenital disorders

•Increased centrifugal traction, applied to bronchial wall

Cause:
–atelectasis
–pneumonia
–fibrosis

PATHOGENIC CLASSIFICATION
•SECONDARY(known causes)

-Lung infection

-Inhalation of irritants

-Bronchial obstruction

-Congenital anatomical defects

-Immunodeficiency states

–hereditary diseases with abnormal:

 ciliary function
 bronchial mucus viscosity
 antiproteases

•PRIMARY, IDIOPATHIC (unknown cause)

Posttuberculous Bronchiectatic Syndrome

•Frequency: 15–20% (1/4 from postTB syndromes) (50% from bronchiectasis are due from TB)

Mechanism : Tuberculosis bronchitis, bronchial stenosis (by lymphadenopathy-Sdr. Brocq) fibroretractile

parenchymal lesions, lesions of the bronchial circulation, pleural lesions, ganglio-bronchic fistulas, microbial
infection

Clinical presentation: Abundant purulent sputum (periodic exacerbations), sputum stratified, with streaks of
blood, hemoptysis (dry form) or clinical latency.
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Bronchografia: ectasies mainly in the upper lobes, cylindrical dilatation, moniliform, ampullary, pseudocyst,
etc.
Spirometry: restriction, obstruction

Scintigraphy : "cold" areas in the bronchiectatic territories

Common pathogenic mechanism

Infections generating bronchiectasis

•Measles (measles pneumonia or pulmonary measles post: adenovirus, herpes virus, S. aureus, Klebsiella,
Pseudomonas)

•Whooping cough/ pertussis (necrotic bronchitis, secondary pneumonia)

•Bacterial pneumonia with necrosis: St. aureus, K. pneumoniae, Ps. aeruginosa, anaerobic bacteria, Myc.
tuberculosis

Similar mechanism: inhalation of irritants (NH3, SO2, NO2, talc, silicates), recurrent aspiration pneumonia,
Mc.Leod / Swyer–James syndrome (after acute bronchiolitis in infancy)

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Pathogenic mechanism obstructive

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 Congenital anatomical defects

•Tracheo-bronchomegalia(Mounjer–Kuhnsyndrome)

Affects the trachea and central airways

-Primary atrophy of musculo-elastic tissue
-Found, usually in adults
-Symmetrical saccular bronchiectasis (common)
-Mechanism: collapse exhale / cough / secretory stasis / infection

•Deficiency of bronchial cartilage (Wiliams –Campbell syndrome)

-Priority affects the subsegmentar airways

-Cartilage absent, few or small

-Usually in children (0-3 years)

-Symmetrical anomaly

-Mechanism: expansion in inhale and exhale collapse cough / infection

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 Hereditary diseases
•Ciliary dyskinesia syndrome

(mechanism: muco-ciliary transport deficient, secretory stasis, infection)

-Cilia and flagella immobile or hipomobili by ultrastructural defects or functional
Prototype: Kartagener syndrome (KS): Autosomal recessive, variable penetrance Situs inversus +
bronchiectasis + chronic sinusitis -SK incomplete: sinusitis + bronchiectasis

•Cysticfibrosis(CF)

Hyperviscosity of exocrine secretions Genetic (autosomal recessive) Bronchiectasis 64 -90% of adults

Mechanism: bronchial obstruction, secretion stasis, recurrent infections

•Α1-antitrypsin deficiency (antiprotease)

SYSTEMIC DISEASES ASSOCIATED WITH BRONCHIECTASIS

•Collagen disease: rheumatoid arthritis,

•Sdr. Sjogren, Ankylosing spondylitis, SLE, Sdr. Marfan

•Inflammatory Bowel Disease: Crohn's disease, ulcerative colitis, celiac Disease

•Yellow nail syndrome

•endometriosis bronchial

•amyloidosis

Clinical presentation:
-Clinical latency

-bronchial suppuration

-hemoptysis

-pneumonia

A) chronic suppuration -debut -onset-in childhood (<10 years) -Teenagers or adults: or insidious (recurrent) or
by acute respiratory infection

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B) Evolution in bursts alternating with remissions

-abundant purulent sputum production (50-200 ml / day)

-Mucopurulent sputum or sputum stratified, sometimes fetid

-Outbreaks of medium moist localized rales sometimes ronchus and diffuse wheezing

•Hemoptysis
-Often recurring
-Sputum with streaks of blood (the exacerbation)
-Micro hemoptysis isolated or repeated-Red blood hemoptysis patents
-Occasionally without suppuration (dry form)

•Pneumonia
-condensation –abscess

Chest X-ray:
-No obvious abnormalities

-Drawing peribronchovascular strengthened

-Clear tube ("tram")

-Aspect of "bronchitis full" (mucoid impact) or "finger glove"

-Clear ring with or without line level

-Dense retractile systematized opacities (medium lobe or lingula) or "the square" (paracardiac)

HRCT is the radiological investigation of choice to establish the diagnosis of bronchiectasis.

•►Bronchial wall dilation (internal lumen diameter greater than accompanying pulmonary artery or lack of
tapering) is the characteristic feature of bronchiectasis.

•►Bronchial wall thickening is often also present although harder to define.

•►HRCT features may be suggestive of certain underlying conditions but require correlation with clinical and
laboratory assessments.
•►HRCT images should be examined for features suggesting ABPA, CF, immobile cilia, opportunist
mycobacteria and tracheobronchomegaly

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 Cylindrical bronchiectasis

tubular dilatation linear contour 2 -3 cm

Moliniform bronchiectasis

irregular expansion “String of beads" affects peripheral bronchus

Cystic bronchiectasis Very strong expansion aspect cystic,

diffuse damage, advanced stage
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 Saccular bronchiectasis

•Ampullary aspect

Lung function tests

•Patients with bronchiectasis should have measures of FEV1, FVCand PEF.

•Repeat assessment of FEV1, FVC and PEF should be made at least annually in those patients attending
secondary care.

•Measurement of lung volumes and gas transfer coefficient may help in the identification of other causes of
airflow obstruction such as COPD/emphysema.

•Reversibility testing may identify improvement in lung function after bronchodilators and should always be
considered if airflow obstructionis identified, especially in young people.

Sputum microbiology

•Patients with bronchiectasis should have an assessmentof lower respiratory tract microbiology.

•Persistent isolation of S aureus (and/or P aeruginosa in children)should lead to consideration of underlying

ABPA or cystic fibrosis.
•Recurrent or chronic infections (repeated antibiotic treatments)-search: Staph.aureus, Klebsiella
Pneumoniae, Pseudomonas aeruginosa, Anaerobe

•Investigations should be performed to establish cause and severityof disease.

•BLOOD TESTS

•should be measured in all patients:

•►serum immunoglobulins (IgG, IgA, IgM) and serum electrophoresis; [A]

•►serum IgE, skin prick testing or serum IgE testing to Aspergillus fumigatus and Aspergillus precipitins.

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 Tests of ciliary function

•Ciliary investigations should be considered in children with bronchiectasis when there is:

–no other cause for bronchiectasis identified;

–a history of continuous rhinitis since the neonatal period;
–a history of neonatal respiratory distress;
–dextrocardia.

•Ciliary investigations should be considered in adults only if there is a history of chronic upper respiratory tract
problems or otitis media. Factorsfavouring investigation include:

–problems since childhood;

–childhood chronic otitis media;
–predominantly middle lobe bronchiectasis;
–infertility or dextrocardia.

Bronchoscopy

•In children, bronchoscopy is indicated when bronchiectasis affects asingle lobe to exclude a foreign body.

•In adults with localised disease, bronchoscopy may be indicated toexclude proximal obstruction.

•For patients in whom serial testing of sputum does not yield microbiologicalinformation and who are not
responding well to treatment,bronchoscopic sampling of lower respiratory tract secretions may beindicated.

•Bronchoscopy is indicated if HRCT suggests atypical mycobacterialinfection and sputum culture is negative.

•Cytological examination of bronchoscopic specimens can provide evidence supporting gastric aspiration.

Diagnostic
•Positive diagnosis

a) Presumptive:
-Recurring or chronic bronchial suppuration -Repeated hemoptysis -Repeated pneumonia (same location)
+
-Radiographic image evocative

b) Confirmation:
-Computed tomography (non-invasive) –bronchography

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 Evolution, complications, prognosis
•EVOLUTION

a)Aggravation

-Chronic purulent abundent sputum-Severe suppurative exacerbations, train -Transient effect of antibiotic -
Pulmonary failure, CPC

b) Good control of episodic infections, prolonged stationary evolution

c) Chronic latency

TREATAMENT
1.Objectives

-Control of symptoms -Prevention of exacerbations -Specific measures depending on the underlying

mechanism

2. Antibiotherapy
-episodic infections: as in chronic bronchitis (microscopy gram. Aminopenicillin, macrolides, quinolones) -
Failures, severe cases, chronic: culture + ABG, chemotherapy sensitivity depending on the identity and germs
(sometimes anaerobic -30% of cases)

3. Combat secretory stasis

-Drainage position
 mucolytics
 hydration
 bronchodilators

4. Treatment of respiratory failure

5. Surgical treatment
-young patients

-Localized bronchiectasis (even bilateral)

-No severe respiratory dysfunction

-With high or severe hemoptysis

-Interventions: lobar or segmental excision (unilateral or bilateral)

-Exceptional: bronchial arteriography + embolization (when excision is not possible)

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 PREVENTION
Immunizations
-measles
-pertussis
-BCG
-influenza
-pneumococcus

Antibiotics: on the first signs of respiratory infection

Lung abscess
Definition: heterogeneous group of lung disorders, non tuberculous characterized by:

•Infectiousetiology (Bacterial, fungal, parasitic)

•Suppurativeinflammation of the lung parenchyma and / or bronchial wall

•Abundant purulent sputum (Diagnostic criteria)

Common features:
•Clinical suppurative syndrome

•Central role of chemotherapy in the treatment

•Tendency to chronicity and respiratory disability

Pulmonary suppurative syndrome (morbid entities)

Primary(with or without pleural empyema)

-lung abscess

-necrotizing pneumonia

-(synonyms: diffuse suppuration prenecrotic phase: Anaerobic pneumonia,rarely chronic)

•Secondary (circumscribed or diffuse)

-bronchial stenosis (cancer, foreign bodies, et al.) -cavities -Cyst -chest trauma -bronchiectasis et al

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Morbid entities

•Hematogenic (sepsis, septic emboli)

•Contiguity (transdiaphragmatic)

Anaerobic bacterial abscesses Source of infection

1-Local germs (mouth, pharynx, nose)

-Fusobacterium Peptostreptococcus
-Bacteroides Veionella

-Propionibacterium Eubacterium

-Peptococcus et al.

2-Preexisting anaerobic infections

-oral or dental foci present in 50-70%

-outbreaks sinus, ear, mastoid chronic

-peritonsillar abscess

-abdominal infections(colon, appendix, peritoneum)

-pelvic infections(women)

Normal germs in the nose and oropharyngeal (germs/ml)

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Anaerobic bacteria with etiological role in respiratory tract infections (In order of frequency)

•Fusobacterium group (f.necrophorum, f.nucleatum)

•Gram (-), pleomorphism (bacilli, filaments fusiform, spheres)

•Melanogenicus Bacteroides group (only group resistant to penicillin)

•Gram (-) cocobacillus, monomorphism, black pigmented colonies)

•Bacteroides fragilis group (f.necrophorum, f.nucleatum to)

•Gram (-) short bacillus, similar to E. coli, bipolar staining)

•Group cocci gram (+) (pepptococcus, Peptostreptococcus)

•Group cocci gram (-) (Veillonella) Propionibacterium group (gram (+), similar morphologically c.diphteriae)

Note: usually polymicrobial flora (2-3 species or more) unsporulated bacteria (rarely sporulated,
ex.clostridium perfringens)

Favorable conditions of the anaerobic bacterial lung abscesses

1.Aspiration of oropharyngeal contents

-unconsciousness (narcosis, coma, epilepsy, intoxication)
-dysphagia (esophageal cancer)
-bowel obstruction (vomiting)
-ENT
-surgery (laryngectomy, tonsillectomy)
-dental surgery

2. Preexisting infection with anaerobic bacteria (see sources of infection)

3. Thoracotomy or chest wound

4.Local conditions
-latent pulmonary infarction ischemia
-bronchial cancer hypoxia
-bronchiectasis
-endobronchial foreign bodies necrosis

5. Systemic conditions
-diabetes
-extrapulmonary cancer
-corticosteroid
-chemotherapy or immunosuppressive
-antibiotic chemotherapy
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 Clinical suppurative syndrome
1-productive cough
2 -abundant purulent sputum
3 -Signs of infection fever, elevated VSH, leukocytosis
Primary diagnosis criteria: -abundant purulent sputum

Mechanism
•Aspiration of oropharyngeal contents (suppurations bronchogenic)

•and/orgastric contents: opportunistic bacteria

•Hematogenous dissemination of other infections (ex. septicmiscarriage)

•Contiguous propagation of othetinfections(ex. amoebianlungabcessfrom liver abscess)

Frequency of isolation of anaerobic bacteria in some infections

•Peritonitis ………………………….90%

•Appendiceal abscess ……………….95%

•Septicmiscarriage ………………………..81%

•Lung abscess ……………………85%

•Aspiration pneumonia ……………..90%

•Brain abscess ……………………85% •Bronchiectasis …………………………50%

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Mode of action of antibiotics active in anaerobic infections
•Bactericidal
-ß-lactams
-penicillins
-cephalosporins
-Metronidazole
-Rifampicin
-quinolone

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•bacteriostatic
-Chloramphenicol
-Lincomycin, clindamycin (lincosamides)
-Erythromycin (macrolide)
-tetracycline

Anaerobic producers of B.lactamasis *

•Group Bacteroides Fragilis**
•Group Bacteroides Melaninogenicus**
•Group B.Oralis**
B.Disiens
B.Oris -Buccae **
B.Splanchnicus
Megamonas Hypermegas
Mitsuokella Multiacidus
F.Nucleatum**
Clostridium Ramosum
C.Clostridiforme
C.Butyricum

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