Treatment of Bronchiectactasis by DR Bashir Ahmed Dar Associate Professor Medicine Sopore Kashmir

BRONCHIECTASIS
BY
DR.BASHIR AHMED DAR
ASSOCIATE PROFESSOR MEDICINE
CHINKIPORA SOPORE KASHMIR
EMAIL- drbashir123@gmail.com
BRONCHIECTASIS
 Bronchiectasis is
defined as the
irreversible dilatation
of the cartilage-
containing airways
bronchi or
bronchioles.
BRONCHIECTASIS
 Bronchiectasis is
defined as the
irreversible dilatation
of the cartilage-
containing airways
bronchi or
bronchioles.
BRONCHIECTASIS
 The airways are
dilated up to 4 times
the normal size
 Bronchi and
bronchioles are so
dilated they can be
followed out to the
pleural surfaces•
Respiratory tract
 The trachea is approximately 22 cm
long, with a cross-sectional area of 2
cm.
 At the tracheal carina it divides into two
major bronchi.
 Conductive structures of a size down to
2 mm are termed bronchi. Smaller ones
are called bronchioles .
Histology Respiratory tract
 The epithelium lining the
trachea is ciliated
pseudostratified columnar
which contains numerous
goblet cells. This epithelium
has an unusually thick
basement membrane, .
This epithelium plus its
underlying layer of loose
connective tissue (the
lamina propria) make up
the tracheal mucosa.
 The layer under the
mucosa is the
submucosa wherein
you'll find numerous
seromucous glands.
The mucosa is
separated from the
submucosa by a
layer of longitudinal
elastic fibers.
 The layer under the
mucosa is the
submucosa wherein
you'll find numerous
seromucous glands.
The mucosa is
separated from the
submucosa by a
layer of longitudinal
elastic fibers.
 Outside the
connective tissue
layers, observe the
C-shaped rings of
hyaline cartilage
which help to keep
the lumen of the
trachea from
collapsing.
 Mucous Membrane.
—The mucous
membrane is
continuous above
with that of the
larynx, and below
with that of the
bronchi
 Mucus membrane
consists of areolar and
lymphoid tissue, and
presents a well-marked
basement membrane,
supporting a stratified
epithelium, the surface
layer of which is
columnar and ciliated,
while the deeper layers
are composed of oval or
rounded cells.
 Beneath the
basement
membrane there is a
distinct layer of
longitudinal elastic
fibers with a small
amount of
intervening areolar
tissue.
 The submucous layer is
composed of a loose
mesh-work of
connective tissue,
containing large blood
vessels, nerves, and
mucous glands; the
ducts of the latter pierce
the overlying layers and
open on the surface
A. Bronchi
 The bronchial tree is
aptly named for its
resemblance to the
branches of a tree,
as larger tubes
perpetually concede
to smaller tube in an
intricate framework
of branches.
Bronchi
 The trachea bifurcates into two primary
bronchi, which enter the lung and then
branch several times to give rise to
smaller secondary and tertiary bronchi.
Bronchi differ from the trachea in
having plates rather than rings of
cartilage, and in having a layer of
smooth muscle between the lamina
propria and submucosa.
Bronchi
 The Right Bronchus (bronchus dexter),
wider, shorter, and more vertical in
direction than the left, is about 2.5 cm.
long, and enters the right lung nearly
opposite the fifth thoracic vertebra.
Bronchi
 Bronchioles are 
smaller branches of
the bronchi, and are
distinguished from
them by the
absence of cartilage
and glands
Bronchi
 In larger bronchioles,
the epithelium is still
ciliated, but is now
usually simple columnar,
whereas in the smallest
bronchioles, the
epithelium will be simple
cuboidal (mostly
containing Clara cells)
and lack cilia altogether.
Bronchi
 The smooth muscle
layer is generally
quite prominent in
these structures
circularly arranged
bundles of smooth
muscle in the
bronchiolar wall.
Bronchi
 As mentioned above,
the smallest conducting
bronchioles consist of a
simple cuboidal (or
perhaps "low columnar")
epithelium of mostly
Clara cells, a few ciliated
cells, and no goblet
cells, and are called
terminal bronchioles .
Bronchi
 In smaller branches, the amount of
cartilage decreases, whereas the
amount of smooth muscle increases.
Also, the number of glands and goblet
cells decreases or absent.
B. Bronchioles
 Bronchioles are smaller branches of the

bronchi, and are distinguished from
them by the absence of cartilage and
glands. In larger bronchioles, the
epithelium is still ciliated, but is now
usually simple columnar, whereas in the
smallest bronchioles, the epithelium will
be simple cuboidal (mostly Clara cells)
and lack cilia altogether.
Bronchioles
 Nearly 50 distinct types of cells have
been identified in the lungs, of which at
least 12 can be found in the airways.
Mucus is secreted onto the bronchial
surfaces by submucous glands and by
"goblet cells" that are present in
abundance on the bronchial epithelial
surface.
Bronchioles
 The coordinated
movement of the
cilia aid in the
transport of mucus
covering the airways
toward the mouth,
where approximately
500 mL of airway
fluid is swallowed
each day.
Bronchioles
 It is this "mucociliary
elevator" which is
largely responsible
for removing foreign
material, including
organisms that land
on the bronchial
surfaces.
Bronchioles
 Injury to these ciliated cells is characteristic in
smokers, who are likely to develop chronic
bronchitis, with colonization of the trachea
and bronchi by oral organisms and production
of excessive amounts of mucus. Patients with
congenital abnormalities of ciliary function
(Kartagener's syndrome) must raise mucus
from the airways by coughing.They are prone
to develop respiratory infections and dilation
of the bronchi, referred to as bronchiectasis.
Bronchioles
 Excess bronchoconstriction of small
bronchi between 2 and 5 mm in
diameter appears to be responsible for
increased airway resistance in most
patients with asthma.
Bronchioles
 The bronchioles contain very little cartilage,
and are controlled via thicker, smoother
muscles. The muscle controls whether or not
these smaller airways contract or expand. As
it refers to air flow resistance, bronchioles
provide the most resistance of the air flow
passages, similar to the functions associates
with the arterioles in the circulatory system.
Mechanisms of development
of Bronchiectasis
 Bronchiectasis may
result from one of three
main mechanisms:
 A.Bronchial wall injury

 Desquamation of the
epithelium and
necrotising ulceration•
of Bronchiectasis
 Chronic inflammation of bronchial wall:
 .lymphocytes predominate
 .Unusually squamous metaplasia
 More Advanced Stage
 •Granulation tissue in lamina propria
 •Cartilage fragmented or destroyed
 •Muscle erased or focal hyperplastic changes
of Bronchiectasis
 •Mucous glands persist longer than
other structures.
 •Bronchial arteries: often ¦greatly
enlarged
 ¦tortuous
 •Adjacent lung parenchyma Shows
varying changes from none to advanced
organizing pneumonia
of Bronchiectasis
 B.Bronchial lumen
obstruction
 Focal Congenital
bronchial atresia
 Foreign body
 Broncholithiasis
 Endobronchial
neoplasm
 Rt mid lobe synd
of Bronchiectasis
 C.And traction from

adjacent fibrosis
of Bronchiectasis
 Many conditions may lead to bronchial wall
injury.These include infections like
 Recurrent infections
 Impaired host defense leading to infection
 Exaggerated immune response
 Congenital structural defects of the bronchial
wall
 And extrinsic insults damaging the airway wall
of Bronchiectasis
 These conditions share the common denominator
of mucus plugging and superimposed bacterial
colonization. The mucus plugging is either a
result of abnormal mucus constituency or
abnormal mucus clearance. The toxins released
by the bacteria and the cytokines and enzymes
released by the surrounding inflammatory cells
create a vicious cycle of progressive wall damage,
mucus plugging, and increased bacterial
proliferation.Once bronchiectasis begins,
therefore, it is sure to progress.
of Bronchiectasis
 Airway obstruction is most commonly
caused by an intraluminal lesion such as
 Carcinoid tumor,
 Inflammatory myofibroblastic tumor,
 Or a fibrous stricture usually from prior
granulomatous infection such as
histoplasmosis or tuberculosis.
of Bronchiectasis
 When bronchiectasis is from bronchial
wall damage or bronchial obstruction,
the bronchial wall becomes thickened
because of infiltration by mononuclear
cells and fibrosis.
of Bronchiectasis
 Traction bronchiectasis, as its name implies,
is caused by retraction of mature fibrosis of
the parenchyma around the bronchi. Such
bronchiectasis follows the distribution of the
underlying fibrosis. The traction
bronchiectasis has an upper lobe distribution
in cases of radiation fibrosis, sarcoidosis, and
sequela of tuberculosis .
of Bronchiectasis
 In cases of usual interstitial pneumonitis
(UIP) (idiopathic pulmonary fibrosis)
and fibrosing nonspecific interstitial
pneumonitis (NSIP), the traction
bronchiectasis tends to be mostly in the
periphery and the lung bases.
of Bronchiectasis
 Congenital defects of the cartilage,
collagen, or other components of the
bronchial wall lead to abnormal
physiologic clearing of mucoid
excretions, predisposing the bronchial
epithelium to repeated infections and a
vicious cycle of progressive bronchial
dilatation.
of Bronchiectasis
 Structural wall defect is the common
feature of Mounier-Kuhn disease or
tracheobronchomegaly, William-
Campbell syndrome, and congenital
bronchial atresia.
of Bronchiectasis
 Tracheobronchomegaly (Mounier-Kuhn
disease)
 Tracheobronchomegaly is an uncommon
disease that presents mostly in men, in the
fourth and fifth decades. Although believed to
be congenital, it may be associated with
Ehlers-Danlos syndrome, Marfan syndrome,
and generalized elastosis (cutis laxa).
Tracheobronchomegaly
(Mounier-Kuhn disease)
 Pathological thinning of the muscle, cartilage,
and elastic tissue of the airway walls is seen.
 This results in uniform dilatation of the
tracheal and bronchial lumina and increased
distensibility of the tracheal and bronchial
walls. This tracheobronchomalacia leads to
recurrent infections in the dependent lungs.
of Bronchiectasis
 Congenital bronchial atresia or mucocele
 This condition is characterized by congenital
focal obliteration of the lumen of a segmental
bronchus, resulting in focal bronchiectasis
and air trapping more distally. The dilated
airway is commonly filled by inspissated
mucus, which may occasionally calcify and
looks like nodule .
of Bronchiectasis
 Conversely, acquired mucocele is caused by
focal scarring of a segmental bronchus
because of prior granulomatous infection or
from an endobronchial lesion. It should be
differentiated from congenital bronchial
atresia by the absence of air trapping of the
distal lung parenchyma.The presence of an
acquired mucocele should prompt further
interrogation to exclude the possibility of an
endobronchial neoplasm.
Mucociliary Clearance
Abnormalities
 Abnormalities of the structure and

function of the cilia of the airway
epithelium, as seen in primary ciliary
dyskinesia or immotile ciliary syndrome,
leads to ineffective mucus clearance
and secondary colonization of the
airway lumina by bacteria. This chronic
infection and repeated bouts of
pneumonia lead to bronchiectasis.
Mucociliary Clearance
Abnormalities
 Kartagener's syndrome or triad is
present in half of the PCD patients. This
triad consists of situs inversus,
bronchiectasis, and sinusitis.
Cystic fibrosis as cause of
Bronchiectasis
 Cystic fibrosis--- CF is an autosomal recessive
trait and occurs in approximately 1 in 3000
live births in the United States and Europe.
 Failed secretion of chloride leading to
dehydration of the endobronchial secretions.
 This thickened mucus cannot be efficiently
cleared by the mucociliary system, leading to
obstructed airways and bacterial
infection.Colonization and recurrent infection
Hyper-Immune Response as a
cause for Bronchiectasis
 Inflammatory bowel disease, rheumatoid
arthritis, Sjogren disease, antineutrophilic
cytoplasmic antibody (c-ANCA)–positive
vasculitis (Wegener disease), and allergic
bronchopulmonary aspergillosis all can lead to
bronchiectasis, possibly because of
inflammation of the airway wall in the setting of
a hyperimmune response to internal or external
antigens. The chronic inflammation damages
the bronchial walls, leading to bronchiectasis.
Hyper-Immune Response as a
cause for Bronchiectasis
 Granulomata in the bronchi and
bronchioles, associated with mucus
impaction.
 It is most commonly seen in patients
with atopic rhinitis, asthma, or CF
of Bronchiectasis
 It should be noted that bronchioles are
also line by surfactant and that
displacement of surfactant by
inflammatory exudates leads to the
bronchiolar instability and thus impairs
their function.
of Bronchiectasis
 Vaccines and antibiotics have
dramatically reduced the frequency and
the importance of bronchiectasis.
 At present, the most common cause of
bronchiectasis is adenovirus infection.
 Post-infectious conditions
 ¦e.g. necrotising bacterial, viral or
fungal pneumonia
of Bronchiectasis
 Rubella,whooping cough
(B.pertusis),measles in childhood
Post infective
Bronchiectasis
 Measles and Pertusis
 Adeno & Influenza virus
 Bacterial infection with
virulent organisms:
S.aureus, Klebsiella
Anaerobes
 Atypical mycobacteria
 Mycoplasma
 HIV
 TB
 Fungi
Types of Bronchiectasis
 1. Cylindrical or tubular bronchiectasis

 2. Varicose bronchiectasis
 3. Saccular or cystic bronchiectasis
1.Cylindrical or tubular or
fusiform bronchiectasis
1.Cylindrical/tubular
bronchiectasis
The luminal dilatation is
uniform and the wall
thickening is smooth and
there is failure of normal
tapering of the bronchi.
2.Varicose
bronchiectasis
 The bronchi resemble like varicose veins and also

like serpentine.The luminal dilatation is
characterized by alternating areas of luminal
dilatation and constriction, creating a beaded
appearance, and the wall thickening is
irregular.This varicose bronchiectasis serves as an
intermediate step before the development of
grossly dilated, cystic airways.
3.Saccular or cystic
bronchiectasis
 Most severe form of
bronchiectasis.The
bronchi are severely
dilated and the bronchi
end blindly in a dilated
thick-walled cyst
Clinical Manifestation of
Bronchiectasis
 Chronic Cough (90 %)
 Dyspnea (72%)
 Hemoptysis (56%)
 Chest pain
 Malnutrition/wasting
 Anemia
Bronchiectasis
 Use of accessory muscles
 Pursed lip breathing
 Cyanosis
 Signs of Cor pulmonale
 Increased respiratory rate
 Increased heart rate
Bronchiectasis
 Copious postural foul smelling

mucopurlant sputum
 Sputum production
 Mild <15 cc/d
 Moderate 15-150 cc/d
 Severe >150 cc/d
Bronchiectasis
 Clubbing of fingers
 Wheez
 Rhonchi
Symptoms of acute
exacerbation of Bronchiectasis
 Change in sputum production
 Increased dyspnea
 Increased cough
 Fever
 Increased wheezing
 Malaise,fatigue,lethargy or decreased tolerance
 Reduced pulmonary function
 Changes in chest sounds
 New radiographic changes
Bronchiectasis Complications
 Pneumonia
 Lung abscess
 Empyema
 Septicaemia
 Cor pulmonale
 Metastatic cerebral abscesses
 Secondary Amyloidosis with nephrotic
syndrome
 Recurrent pleurisy
Bronchiectasis Complications
 Broncho pleural fistula
 Purulent pericarditis
 Respiratory failure
 Metastic abcesses in bones etc
Investigations Bronchiectasis
 CRP
 Increased Sed’ rate
 Anaemia
Radiological features of
Bronchiectasis
 Bronchi, bronchioles
are dilated the
bronchial walls are
thickened and
shown as ring
shadows on plain x
ray.
Bronchiectasis
 Dilated and
thickened airways
that appear as ring-
like shadows (of
airways that are
seen on end) or
tram lines (in the
case of airways that
are perpendicular to
the x-ray beam)
Bronchiectasis
 Dilated and
thickened airways
that appear as ring-
like shadows (of
airways that are
seen on end) or
tram lines (in the
case of airways that
are perpendicular to
the x-ray beam)
Bronchiectasis
 In mild cases x ray may be normal.

RADIOLOGY - CXR
Bronchiectasis
- vessel ‘crowding’
- loss of vessel markings
- tramline/ring shadows
- cystic lesions/ air-fluid levels
- evidence of TB
Poor:

diagnostic sensitivity

monitoring of progression
Bronchiectasis
 The definitive
diagnosis is made
bronchographically
(by instillation of
radiographic
contrast medium
into the lung).
CT Scan of Bronchiectasis
 Shows peribronchial
thickening, dilated
bronchioles.
 Shows peribronchial
thickening, dilated
bronchioles
 CT scan also may show
Internal bronchial
diameter greater than
that of the adjacent
pulmonary artery Lack
of bronchial tapering,
Presence of bronchi
within 1 cm of the costal
pleura, Presence of
bronchi abutting the
mediastinal pleura,
Bronchial wall thickening
 Marked airway
dilatation both upper
lobes.
- Bronchial dilatation
- Bronchial wall
thickening
Further investigations of
Bronchiectasis
 IgE , IgM, IgG levels.
 Aspergillus precipitin .
 Sputum culture: fungi / Pseudomonas
aeuruginosa, H.influenzae.etc
 EKG.
 Film PNS
Bronchiectasis
 Diffuse bronchiectasis Yellow nail
syndrome Pleural fluid TG/Chol
lymphedema.
 Diffuse panbronchiolitis HRCT(bizzare
nodules) transbronchial biopsy.
Bronchiectasis
 Lung function:
 Airflow obstruction – FEV1 decreased.
 Air trapping - RV increased
Bronchiectasis
 Sweat test - Increased sodium and
chloride in cystic fibrosis
 Bronchoscopy: Obstruction – foreign
body, tumor.
 Immunoglobulin levels
 Cilia function and structure –
Kartagener's syndrome
 Alpha-1 antrip level.
Treatment of Bronchiectasis
 Treatment Goals:
 1.Eliminate cause
 2.Improve tracheo bronchial clearance
 3.Control infection
 4.Reverse airflow obstruction
 Proposed courses of treatment
 Short course
 Prolonged course
 Intermittent regular courses
 Inhalation
 Antibiotics and anti inflammatory
agents.
 Are used in these proposed courses

 To treat acute exacerbation,To prevent
infection or to reduce bacterial burden
 Drainage Procedures
 Postural drainage consists of adopting a
position in which the lobe to be drained
is uppermost.postural drainage should
be performed for a minimum of 5-10
minutes twice a day.
 Gentle percussion of the chest wall with
cupped hands aids dislodgement of sputum.
 Baroscopic removal of inspissated secretions

is rarely required.
 Role of mucolytic agents is controversial.

 Antibiotic theraphy.
 Choice of antibiotic sould primarily be based

on the results of culture and sensitivity.
 When no specific pathogen is identified and

the patient is not seriously ill,an oral agent
like
Amoxycillin
Ampicillin
Tetracycline
Cotrimoxazole
or a fixed combination of amoxycillin and
clavulanic acid should be used.more
seriously ill patients with pneumonitis
should be given parenteral antibiotics.
 Duration of theraphy is variable.
 A 5-10 days course is usually
sufficient.in some patients it may need
to be prolonged for several weeks.
 Brochiodilators
 Brochiodilators to improve obstruction
and aid clearance of secretions are
particularly usefull when some element
of reversible airway obstruction is
present.
 Other Measures
 Cigarette smoking should be stopped.
 A programme of graded exercise ,routine deep
breathing and maintance of nutrition form
essential part of general management.
 Episodes of sinusitis should be treated.
 Complicating allergic bronchopulmonary
aspergillosis should be treated with prednisolone.
.
 Primary Hypogammaglubolinemia
should be treated with human immune
serum albumin.
 Complicated cases may require nasal
oxygen on a chronic basis, to maintain
adequate oxygenation
 3 Strategies
 1. High oral dose for prolonged period
(at least 4 weeks) (macrolide
and FQ) Azithromycin 500mg plus
Levofloxacin 250mg 2/wk x 6Mn
(reduced exacerbation)
2. Aerosolized antibiotic (e.g during
alternate month) (Gentamicin 40mg bid
x 3 days.
 Tobramycin 300mg bid x 4wk,
 (Gatifloxacin) Fortum 1g + Tobramycin
100mg bid x 12mn.

 3. Regular pulsed course of iv antibiotic
(e.g.2-3 wk courses with 1 or 2
months in between).
 These episodic or suppressive
antibiotics
 Decrease inflammation
 Slow progression
 Eradication
 Anti-inflammatory agents :
 Inhaled Fluticasone 500ug bid decreased

density of leucocyte, concentration of
-inflammatory mediator 1B, IL-8 and LT-B4 in
sputum -improved sputum volume but no
change frequent of exacerbation, lung
function and purulence sputum.
 Anti-inflammatory agents :Systemic
corticosteroid May better at penetrating
the bronchial wall and therefore be
more effective but available data only
for CF-Bronchiectasis.inhibit neutrophil
mediated inflammation.
 NSAIDS inhibit neutrophil function and
release of elastase
(Indocid25mgtidx4wk but opened label
study, lung function, sputum vol/quality
did not change but high dose Ibuprofen
x 4 yr found significantly slowed
progression of lung disease in CF-
Bronchiectasis.
 Anti-inflammatory agents Macrolide
(Azithromycin) suppress inflammation.
 Azithromycin 500mg twice a week x

6mn Decrease daily sputum production
and exacerbation.
 3 Months of Clarithromycin decreased
total No. of leucocyte, proportion of
PMN and concentration of IL-8.
 Brochiodilators
 Anticholinergic or oral Methylxanthine in

patient with non-CF bronchiectasis.
Bronchopulmonary hygiene
physical therapy
 That aims to remove lung secretions in
pt with acute and chronic airway
disease. Many active and passive
technique are available Evidence is
variable and the literature is conflicting.
Physical therapy
 Rhythmic Chest clapping or cupping and
of back, while the patient assumes a
number of positions (head down,
primarily), may help the lungs to drain
more effectively. This is called chest
physical therapy, or percussion and
postural drainage.
Physical therapy
 Inflatable vests or mechanical
vibrators.Oral devices that apply
positive end-expiratory pressure
maintain the potency of the airway
during exhalation.
 Inspiratory muscle training X 8WKS.
Mucolytics
 Medications are available to help thin
the sputum, so that it can be more
effectively coughed up.
Mucolytics
 Maintain adequate systemic hydration
by normal saline,enhanced by
nebulization with saline.
 Acetylcysteine delivered by nebulizer
thins secretions.Aerosolized
recombinant human DNase (rhDNase)
in patients with cystic fibrosis.
 Alpha-1 antrip def Alpha-1 antritrip

replacement.
 Oxygen and diuretics

 Anti-inflammatory agents Macrolide
(Azithromycin) suppress inflammation.
 Azithromycin 500mg twice a week x

6mn Decrease daily sputum production
and exacerbation.
Surgical treatment of
Bronchiectasis
 Surgery :
 If the area of bronchiectasis is localized
and symptoms are debilitating or life
threatening.
Bronchiectasis
 When bleeding occurs from irritated
bronchial tubes and overgrown
bronchial blood vessels, surgery may be
required either to remove an area of
the bronchial tube, or to inject the
bleeding blood vessel with a material to
stop the bleeding.
Bronchiectasis
 In some patients, bronchiectasis eventually
leads to a constantly low level of blood
oxygen, despite other treatments. These
patients usually have an associated increase
in the size of the right side of their hearts,
along with a decrease in the heart's ability to
pump blood through the lungs. Some patients
with extremely severe symptoms and
disability have been treated with lung
transplantation.
Bronchiectasis
 Surgery
 Localized bronchiectasis
 Proximal obstructive lesion,Obstruction
may require the removal of a foreign
object or tumor or aspirated material
 Massive hemoptysis
 Recurrent infections
 Lung transplant
 Prevention of Bronchiectasis
 Adequate treatment and prophylaxis of

childhood whooping cough, measles,
and primary tuberculosis.
 Genetic counseling in cystic fibrosis.
PSEUDOBRONCHIECTASIS
 A true bronchiectasis is not
reversible.whereas the
pseudobronchiectasis is reversible.
PSEUDOBRONCHIECTASIS
 The bronchographic abnormalities displayed
by atelectasis and tracheo bronchitis
 with ulceration of bronchial mucosa simulate
cylindrical bronchiectasis.but re expansion of
collapsed lung in atelectasis and regeneration
of mucosa in trachiobroncitis result in
reversibility of bronchographic
appearance.this is known as
pseudobronchiectasis.
Bronchiectasis sicca
 ( dry bronchiectasis)

This is a condition where bronchiectasis

presents with repeated episodes of
hemoptysis without sputum
production.this usually occurs in upper
lobe bronchiectasis of post tuberculous
variety.
Middle lobe syndrome
 Or Brocks syndrome post obstructive.
bronchiectasis
THANK YOU SO MUCH
 Trust the Physician and the teacher , and drink his

remedy in silence and tranquility: For his hand,
though heavy and hard, is guided by the tender
hand of the unseen,And the cup he brings, though
it burn your lips, has been fashioned of the clay
which the Potter have moistened with His tears and
sacred feelings.

Treatment of Bronchiectactasis by DR Bashir Ahmed Dar Associate Professor Medicine Sopore Kashmir

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Treatment of Bronchiectactasis by DR Bashir Ahmed Dar Associate Professor Medicine Sopore Kashmir

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BRONCHIECTASIS

 Bronchioles are smaller branches of the

 A.Bronchial wall injury

 C.And traction from

 Abnormalities of the structure and

 1. Cylindrical or tubular bronchiectasis

 The bronchi resemble like varicose veins and also

 Copious postural foul smelling

 In mild cases x ray may be normal.

 Proposed courses of treatment

 Are used in these proposed courses

 Baroscopic removal of inspissated secretions

 Role of mucolytic agents is controversial.

 Choice of antibiotic sould primarily be based

 When no specific pathogen is identified and

100mg bid x 12mn.

 Inhaled Fluticasone 500ug bid decreased

 Azithromycin 500mg twice a week x

 Anticholinergic or oral Methylxanthine in

 Alpha-1 antrip def Alpha-1 antritrip

 Oxygen and diuretics

 Azithromycin 500mg twice a week x

 Adequate treatment and prophylaxis of

This is a condition where bronchiectasis

 Trust the Physician and the teacher , and drink his

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