Bronchiectasis

Chen Ring, MD
Department Of Respiratory
Medicine,
The first Affiliated Hospital,
University of Zhengzhou
 DEFINITION
- Bronchiectasis is an abnormal and permanent

dilatation of bronchi.

- It may be either focal, involving airways supplying a

limited region of pulmonary parenchyma, or diffuse,

involving airways in a more widespread distribution.

 Etiology and Pathogenesis
- Congenital bronchiectasis
a rare condition in which the lung periphery
fails to develop, resulting in cystic dilation of
developed bronchi.
- Acquired bronchiectasis
 Etiology and Pathogenesis
acquired bronchiectasis results from

① direct bronchial wall destruction ， due to

- infection
- inhalation of noxious chemicals
- immunologic reactions
- vascular abnormalities that interfere with
bronchial nutrition
Bacterial endotoxins and proteases;
proteases derived from circulating or
pulmonary inflammatory cells; superoxide
radicals; and antigen-antibody
complexes may mediate bronchial wall
damage.
 Acquired bronchiectasis
② mechanical alterations , due to
- atelectasis or loss of parenchymal volume
with increased traction on the walls of
airways, leading to bronchial dilation and
secondary infection.
 Conditions commonly leading to
bronchiectasis
① severe pneumonia
- especially when complicating measles,
pertussis, or certain adenovirus infections in
children
- necrotizing pulmonary infections due to
Klebsiella sp, staphylococci, influenza virus,
fungi, mycobacteria
 Conditions commonly leading to
bronchiectasis

② bronchial obstruction from any cause--

foreign body, enlarged lymph nodes,
mucus inspissation, lung cancer
 Noninfectious Causes
- exposure to a toxic substance that incites a
severe inflammatory response.
- Examples include inhalation of a toxic gas
such as ammonia or aspiration of acidic
gastric contents.
 ETIOLOGY AND PATHOGENESIS

primary ciliary dyskinesia

- responsible for 5 to 10% of bronchiectasis
- the primary disorders associated with ciliary
dysfunction
- the clinical effects include:
recurrent upper and lower respiratory tract
infections, such as sinusitis, otitis media,
and bronchiectasis.
- ½ of patients fall into the subgroup of primary
ciliary dyskinesia (PCD) syndromes----
Kartagener's syndrome ,in which situs
inversus accompanies bronchiectasis and
sinusitis.
 PATHOLOGY
- may be unilateral or bilateral
- most common in the lower lobes,
although the right middle lobe and
lingular portion of the left upper lobe are
often affected.
 PATHOLOGY
The bronchial dilatation of bronchiectasis
is associated with destructive and
inflammatory changes in the walls of
medium-sized airways, often at the level
of segmental or subsegmental bronchi.
 PATHOLOGY
- The normal structural components of the wall, may be
replaced by fibrous tissue
- The dilated airways frequently contain pools of thick,
purulent material
- more peripheral airways are often occluded by
secretions or obliterated and replaced by fibrous
tissue
 PATHOLOGY
Additional microscopic features include ：
- bronchial and peribronchial inflammation
and fibrosis
- ulceration of the bronchial wall
- squamous metaplasia
- mucous gland hyperplasia.
adjacent interstitial and alveolar areas are
destroyed, tissue reorganization and
fibrosis result in loss of volume.
Bronchiectasis is generally associated
with chronic bronchitis and/or emphysema
and some fibrosis.
 PATHOLOGY
As a result of the inflammation
- vascularity of the bronchial wall increases,
with associated enlargement of the bronchial
arteries
- anastomoses between the bronchial and
pulmonary arterial circulations.
Extensive anastomoses between the
bronchial and pulmonary arteries
increased blood flow, right-to-left shunts,
and hypoxemia lead to pulmonary
hypertension and cor pulmonale late in the
disease.
 PATHOLOGY
Three different patterns of bronchiectasis

 In cylindrical bronchiectasis
 In varicose bronchiectasis
 In saccular (cystic) bronchiectasis.
 PATHOLOGY

In cylindrical bronchiectasis
- the bronchi appear as uniformly dilated

tubes that end abruptly at the point that

smaller airways are obstructed by
secretions
In varicose bronchiectasis
- the affected bronchi have an irregular
or beaded pattern of dilatation
resembling varicose veins
In saccular (cystic) bronchiectasis
- the bronchi have a ballooned appearance
at the periphery, ending in blind sacs
without recognizable bronchial structures
distal to the sacs.
However, these distinctions have little
clinical value, and current pathologic
correlations with high-resolution and
helical CT characteristics are making this
classification obsolete.
 CLINICAL MANIFESTATIONS
  cough
 persistent or recurrent

 purulent sputum production.

(may separate into three layers: frothy at the top,
greenish and turbid in the middle, and thick with
pus at the bottom.)
 Hemoptysis.
 Dyspnea or wheezing
CLINICAL MANIFESTATIONS

crackles, rhonchi, and wheezes

hypoxemia, may have associated
cor pulmonale and right ventricular
failure.
 Physical signs
 Physical findings are nonspecific
 but persistent crackles over any part of the
lungs suggest bronchiectasis.
 Signs of airflow obstruction tend to be more
pronounced in smokers than in nonsmokers.
 Finger clubbing sometimes occurs with
extensive disease and persistent chronic
infection
 RADIOGRAPHIC AND LABORATORY
FINDINGS

 the chest radiograph is important ,but

often nonspecific:
- dilated airways are often crowded
together in parallel appearing as "tram
tracks“
- when seen in cross-section, they
produce "ring shadows."
High-resolution CT (HRCT)
- HRCT (1- to 2-mm cuts) has largely
replaced bronchography.
- provides an excellent view of dilated
airways as seen in cross-sectional images.
- the better resolution of HRCT provides
results comparable or preferable to
bronchography.
 Characteristic CT findings
- dilated airways indicated
by tram lines
by a signet ring appearance
or by grapelike clusters in more severely affected areas.
- thickening of the bronchial walls, obstruction
of airways and, sometimes, consolidation
seen
a signet ring appearance with a luminal
diameter > 1.5 times that of the adjacent
vessel in cross section,
 Pulmonary function tests
may demonstrate airflow obstruction as a
consequence of diffuse bronchiectasis or
associated chronic obstructive lung
disease.
 Examination of sputum
 often reveals an abundance of neutrophils and
colonization or infection with a variety of possible
organisms.
 Appropriate staining and culturing of sputum often
provide a guide to antibiotic therapy.
 TREATMENT
 
four major goals
-elimination of an identifiable underlying problem
- improved clearance of tracheobronchial secretions

- control of infection

- reversal of airflow obstruction

 TREATMENT
Antibiotics treatment
 empiric coverage (e.g., with ampicillin,
amoxicillin, or cefaclor) is often given initially.
 quinolone or parenteral therapy with an
aminoglycoside or third-generation
cephalosporin
 TREATMENT

 Bronchodilators
- to improve obstruction

- and aid clearance of secretions

- are particularly useful in patients with airway

hyperreactivity and reversible airflow obstruction.

 TREATMENT

 resection or bronchial arterial embolization

 long-term supplemental oxygen.
 lung transplantation

Lung Abscess
 Definination
 defined as necrosis of the pulmonary
tissue and formation of cavities
containing necrotic debris or fluid
caused by microbial infection.
 classified based on the duration
- acute abscesses :< 4-6 weeks
- chronic abscesses: being of longer duration
 classified based on the likely etiology
- primary abscess
- secondary abscess
 Pathophysiology
 Most frequently, the lung abscess arises
as a complication of aspiration
pneumonia caused by mouth anaerobes.
 Other mechanisms for lung abscess
formation include bacteremia or tricuspid
valve endocarditis, caused by septic
emboli to the lung.
 micobiology
 anaerobes up to 90%
Peptostreptococcus, Bacteroides,
Fusobacterium species, and
microaerophilic streptococcus.
 other organisms 10%
Staphylococcus aureus,
Streptococcus pyogenes
Streptococcus pneumoniae (rarely),
Klebsiella pneumoniae,
and gram-negative bacilli.
 History
 Symptoms depend on whether the
abscess is caused by anaerobic
or other bacterial infection.
 anaerobic infection.
 Patients often present with indolent
symptoms that evolve over a period of weeks
to months.
 The usual symptoms are fever, cough with
sputum production, night sweats, anorexia,
and weight loss.
 The expectorated sputum characteristically is
foul smelling and bad tasting.
 Patients may develop hemoptysis or pleurisy.
 bacterial infection
 These patients generally present with
conditions that are more emergent in nature
and are usually treated while they have
bacterial pneumonia.
 Cavitation occurs subsequently as
parenchymal necrosis ensues.
 Abscesses from fungi, Nocardia, and
mycobacteria tend to have an indolent course
and gradually progressive symptoms.
 physical

 low-grade fever in anaerobic infections

 temperatures higher than 38.5°C in other infections.
 generally, evidence of gingival disease is present
 consolidation may be present
 evidence of pleural friction rub , pleural effusion,
empyema, and pyopneumothorax may be present.
 Digital clubbing may develop rapidly.
 Lab Studies
 white blood cell count may reveal leukocytosis
and a left shift.
 Obtain sputum for Gram stain, culture, and
sensitivity.
 If tuberculosis is suspected, AFB&culture is
requested.
 Blood culture may be helpful in establishing the
etiology.
 Chest radiograph
 A typical appearance
-an irregularly shaped cavity with an air-fluid level inside.
 aspiration Lung abscesses

-frequently occur in the posterior segments of the upper

lobes or the superior segments of the lower lobes.
 the cavity wall
-being smooth or ragged but less commonly nodular,
which raises the possibility of cavitating carcinoma.
lung necrosis and abscess formation
A lateral chest radiograph shows air-fluid
level characteristic of lung abscess
 CT scan
 very useful in identification of concomitant
empyema or lung infarction.
 often showning a rounded radiolucent
lesion with a thick wall and ill-defined
irregular margins.
CT scan shows a thin-walled cavity with
surrounding consolidation.
 Medical Care.
 Antibiotic therapy
-standard treatment of an anaerobic lung infection is
clindamycin (600 mg IV q8h followed by 150-300 mg
PO qid).
-shown to be superior over parenteral penicillin in
published trials. Several anaerobes may produce
beta-lactamase (eg, various species of Bacteroides
and Fusobacterium) and therefore develop
resistance to penicillin.
 Antibiotic therapy
 Although metronidazole is an effective drug
against anaerobic bacteria, the experience with
metronidazole in treating lung abscess has been
rather disappointing because these infections
are generally polymicrobial. A failure rate of 50%
has been reported
 Antibiotic therapy
 In hospitalized patients who have aspirated and
developed a lung abscess, antibiotic therapy
should include coverage against S aureus and
Enterobacter and Pseudomonas species.
 Duration of therapy
 generally for 4-6 weeks.
 current recommendations
- should continued until the chest radiograph has shown
either the resolution of lung abscess or the presence
of a small stable lesion.
 the rationale for extended treat
- risk of relapse exists with a shorter antibiotic regimen.
 Response to therapy
 Usually show clinical improvement, with
improvement of fever, within 3-4 days after
initiating the antibiotic therapy.
 Defervescence is expected in 7-10 days.
 Persistent fever beyond this time indicates
therapeutic failure, and these patients should
undergo further diagnostic studies to determine
the cause of failure.
 Response to therapy
 Large cavity size (ie, >6 cm in diameter) usually
requires prolonged therapy.
 Surgical Care
 Surgery is very rarely required for patients with
uncomplicated lung abscesses.
 The usual indications for surgery are failure to
respond to medical management, suspected
neoplasm, or congenital lung malformation. The
surgical procedure performed is either
lobectomy or pneumonectomy.