Hemiplegia Part-1 By Prof Dr Bashir Ahmed Dar Sopore Kashmir
Treatment of Bronchiectactasis by Dr Bashir Ahmed Dar Associate Professor Medicine Sopore Kashmir
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Transcript of Treatment of Bronchiectactasis by Dr Bashir Ahmed Dar Associate Professor Medicine Sopore Kashmir
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BRONCHIECTASISBY
DR.BASHIR AHMED DAR
ASSOCIATE PROFESSOR MEDICINE
CHINKIPORA SOPORE KASHMIR
EMAIL- [email protected]
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BRONCHIECTASIS Bronchiectasis is
defined as the
irreversible dilatationof the cartilage-containing airwaysbronchi or
bronchioles.
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BRONCHIECTASIS Bronchiectasis is
defined as the
irreversible dilatationof the cartilage-containing airwaysbronchi or
bronchioles.
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BRONCHIECTASIS The airways are
dilated up to 4 times
the normal size Bronchi and
bronchioles are sodilated they can befollowed out to thepleural surfaces
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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 to2 mm are termed bronchi. Smaller onesare called bronchioles .
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Histology Respiratory tract The epithelium lining the
trachea is ciliatedpseudostratified columnarwhich contains numerousgoblet cells. Thisepithelium has anunusually thick basementmembrane, . This
epithelium plus itsunderlying layer of looseconnective tissue (thelamina propria) make upthe tracheal mucosa.
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Histology Respiratory tract The layer under the
mucosa is the
submucosa whereinyou'll find numerousseromucous glands.The mucosa isseparated from thesubmucosa by alayer of longitudinalelastic fibers.
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Histology Respiratory tract The layer under the
mucosa is the
submucosa whereinyou'll find numerousseromucous glands.The mucosa isseparated from thesubmucosa by alayer of longitudinalelastic fibers.
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Histology Respiratory tract Outside the
connective tissue
layers, observe theC-shaped rings ofhyaline cartilagewhich help to keep
the lumen of thetrachea fromcollapsing.
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Histology Respiratory tract Mucous
Membrane.The
mucous membraneis continuous abovewith that of thelarynx, and below
with that of thebronchi
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Histology Respiratory tract Mucus membrane
consists ofareolar andlymphoid tissue, and
presents a well-markedbasement membrane,supporting a stratifiedepithelium, the surfacelayer of which is
columnar and ciliated,while the deeper layersare composed of oval orrounded cells.
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Histology Respiratory tract Beneath the
basement
membrane there is adistinct layer oflongitudinal elasticfibers with a small
amount ofintervening areolartissue.
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Histology Respiratory tract The submucous layer is
composed of a loose
mesh-work ofconnective tissue,containing large bloodvessels, nerves, andmucous glands; the
ducts of the latterpierce the overlyinglayers and open on thesurface
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A. Bronchi The bronchial tree is
aptly named for its
resemblance to thebranches of a tree,as larger tubesperpetually concede
to smaller tube in anintricate frameworkof branches.
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Bronchi The trachea bifurcates into two primary
bronchi, which enter the lung and then
branch several times to give rise tosmaller secondary and tertiary bronchi.Bronchi differ from the trachea inhaving plates rather than rings of
cartilage, and in having a layer ofsmooth muscle between the laminapropria and submucosa.
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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 nearlyopposite the fifth thoracic vertebra.
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Bronchi Bronchioles are
smaller branches of
the bronchi, and aredistinguished fromthem by theabsence of cartilage
and glands
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Bronchi In larger bronchioles,
the epithelium is still
ciliated, but is nowusually simplecolumnar, whereas inthe smallestbronchioles, the
epithelium will besimple cuboidal (mostlycontaining Clara cells)and lack cilia altogether.
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Bronchi The smooth muscle
layer is generally
quite prominentinthese structurescircularly arrangedbundles of smooth
muscle in thebronchiolar wall.
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Bronchi As mentioned above,
the smallest conducting
bronchioles consist of asimple cuboidal (orperhaps "lowcolumnar") epitheliumof mostly Clara cells, a
few ciliated cells, andno goblet cells, and arecalled terminalbronchioles .
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Bronchi In smaller branches, the amount of
cartilage decreases, whereas the
amount of smooth muscle increases.Also, the number of glands and gobletcells decreases or absent.
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B. Bronchioles
Bronchioles are smaller branches of thebronchi, and are distinguished from
them by the absence of cartilage andglands. In larger bronchioles, theepithelium is still ciliated, but is nowusually simple columnar, whereas in the
smallest bronchioles, the epithelium willbe simple cuboidal (mostly Clara cells)and lack cilia altogether.
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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 bronchialsurfaces by submucous glands and by
"goblet cells" that are present inabundance on the bronchial epithelialsurface.
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Bronchioles It is this "mucociliary
elevator" which is
largely responsiblefor removing foreignmaterial, includingorganisms that land
on the bronchialsurfaces.
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Bronchioles Injury to these ciliated cells is characteristic in
smokers, who are likely to develop chronic
bronchitis, with colonization of the tracheaand bronchi by oral organisms and productionof excessive amounts of mucus. Patients withcongenital abnormalities of ciliary function(Kartagener's syndrome) must raise mucus
from the airways by coughing.They are proneto develop respiratory infections and dilationof the bronchi, referred to as bronchiectasis.
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Bronchioles Excess bronchoconstriction of small
bronchi between 2 and 5 mm in
diameter appears to be responsible forincreased airway resistance in mostpatients with asthma.
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Bronchioles The bronchioles contain very little cartilage,
and are controlled via thicker, smoother
muscles. The muscle controls whether or notthese smaller airways contract or expand.Asit refers to air flow resistance, bronchiolesprovide the most resistance of the air flow
passages, similar to the functions associateswith the arterioles in the circulatory system.
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Mechanisms of development
of Bronchiectasis Bronchiectasis may
result from one of threemain mechanisms:
A.Bronchial wall injury
Desquamation of theepithelium andnecrotising ulceration
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Mechanisms of development
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
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Mechanisms of development
of Bronchiectasis Mucous glands persist longer than
other structures.
Bronchial arteries: often greatlyenlarged
tortuous
Adjacent lung parenchyma Showsvarying changes from none to advancedorganizing pneumonia
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Mechanisms of development
of Bronchiectasis B.Bronchial lumen
obstruction
Focal Congenitalbronchial atresia
Foreign body
Broncholithiasis
Endobronchialneoplasm
Rt mid lobe synd
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Mechanisms of development
of Bronchiectasis
C.And traction fromadjacent fibrosis
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Mechanisms of development
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
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Mechanisms of development
of Bronchiectasis These conditions share the common
denominator ofmucus plugging and
superimposed bacterial colonization. Themucus plugging is either a result of abnormalmucus constituency or abnormal mucusclearance. The toxins released by the bacteriaand the cytokines and enzymes released by
the surrounding inflammatory cells create avicious cycle ofprogressive wall damage,mucus plugging, and increased bacterialproliferation.Once bronchiectasis begins,
therefore, it is sure to progress.
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Mechanisms of development
of BronchiectasisAirway obstruction is most commonly
caused by an intraluminal lesion such as
Carcinoid tumor,
Inflammatory myofibroblastic tumor,
Or a fibrous stricture usually from priorgranulomatous infection such ashistoplasmosis or tuberculosis.
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Mechanisms of development
of Bronchiectasis When bronchiectasis is from bronchial
wall damage or bronchial obstruction,
the bronchial wall becomes thickenedbecause of infiltration by mononuclearcells and fibrosis.
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Mechanisms of development
of Bronchiectasis Traction bronchiectasis, as its name implies,
is caused by retraction of mature fibrosis of
the parenchyma around the bronchi. Suchbronchiectasis follows the distribution of theunderlying fibrosis. The tractionbronchiectasis has an upper lobe distribution
in cases ofradiation fibrosis, sarcoidosis, andsequela oftuberculosis .
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Mechanisms of development
of Bronchiectasis In cases of usual interstitial pneumonitis
(UIP) (idiopathic pulmonary fibrosis)
and fibrosing nonspecific interstitialpneumonitis (NSIP), the tractionbronchiectasis tends to be mostly in the
periphery and the lung bases.
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Mechanisms of development
of Bronchiectasis Congenital defects of the cartilage,
collagen, or other components of the
bronchial wall lead to abnormalphysiologic clearing of mucoidexcretions, predisposing the bronchial
epithelium to repeated infections and avicious cycle of progressive bronchialdilatation.
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Mechanisms of development
of Bronchiectasis Structural wall defectis the common
feature ofMounier-Kuhn disease or
tracheobronchomegaly, William-Campbell syndrome, and congenitalbronchial atresia.
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Mechanisms of development
of Bronchiectasis Tracheobronchomegaly (Mounier-Kuhn
disease)
Tracheobronchomegaly is an uncommondisease that presents mostly in men, in thefourth and fifth decades. Although believed tobe congenital, it may be associated with
Ehlers-Danlos syndrome, Marfan syndrome,and generalized elastosis (cutis laxa).
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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 thetracheal and bronchial lumina and increaseddistensibility of the tracheal and bronchialwalls. This tracheobronchomalacia leads to
recurrent infections in the dependent lungs.
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Mechanisms of development
of Bronchiectasis Congenital bronchial atresia or mucocele
This condition is characterized by congenital
focal obliteration of the lumen of a segmentalbronchus, resulting in focal bronchiectasisand air trapping more distally. The dilatedairway is commonly filled by inspissated
mucus, which may occasionally calcify andlooks like nodule .
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Mechanisms of development
of Bronchiectasis Conversely, acquired mucocele is caused by
focal scarring of a segmental bronchus
because of prior granulomatous infection orfrom an endobronchial lesion. It should bedifferentiated from congenital bronchialatresia by the absence of air trapping of thedistal lung parenchyma.The presence of an
acquired mucocele should prompt furtherinterrogation to exclude the possibility of anendobronchial neoplasm.
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Abnormalities
Abnormalities of the structure andfunction of the cilia of the airway
epithelium, as seen in primary ciliarydyskinesia or immotile ciliary syndrome,leads to ineffective mucus clearanceand secondary colonization of the
airway lumina by bacteria. This chronicinfection and repeated bouts ofpneumonia lead to bronchiectasis.
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Mucociliary Clearance
Abnormalities Kartagener's syndrome or triad is
present in half of the PCD patients. This
triad consists ofsitus inversus,bronchiectasis, and sinusitis.
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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 toobstructed airways and bacterialinfection.Colonization and recurrent infection
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Hyper-Immune Response as a
cause for Bronchiectasis Inflammatory bowel disease, rheumatoid
arthritis, Sjogren disease, antineutrophilic
cytoplasmic antibody (c-ANCA)positivevasculitis (Wegener disease), and allergicbronchopulmonary aspergillosis all can lead tobronchiectasis, possibly because ofinflammation of the airway wall in the setting
of a hyperimmune response to internal orexternal antigens. The chronic inflammationdamages the bronchial walls, leading tobronchiectasis.
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Hyper-Immune Response as a
cause for Bronchiectasis Granulomata in the bronchi and
bronchioles, associated with mucus
impaction.
It is most commonly seen in patientswith atopic rhinitis, asthma, or CF
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Mechanisms of development
of Bronchiectasis It should be noted thatbronchioles are
also line by surfactantand that
displacement of surfactant byinflammatory exudates leads to thebronchiolar instability and thus impairs
their function.
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Mechanisms of development
of BronchiectasisVaccines 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 orfungal pneumonia
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Mechanisms of development
of Bronchiectasis Rubella,whooping cough
(B.pertusis),measles in childhood
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Post infective
Bronchiectasis Measles and Pertusis
Adeno & Influenza virus
Bacterial infection withvirulent organisms:S.aureus, Klebsiella
Anaerobes
Atypical mycobacteria
Mycoplasma HIV
TB
Fungi
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Types of Bronchiectasis
1. Cylindrical or tubular bronchiectasis
2. Varicose bronchiectasis
3. Saccular or cystic bronchiectasis
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1.Cylindrical or tubular or
fusiform bronchiectasis1.Cylindrical/tubular
bronchiectasis
The luminal dilatation isuniform and the wall
thickening is smooth and
there is failure of normal
tapering of the bronchi.
2 Varicose
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2.Varicosebronchiectasis
The bronchi resemble like varicose veins and also
like serpentine.The luminal dilatation ischaracterized by alternating areas of luminaldilatation and constriction, creating a beadedappearance, and the wall thickening is
irregular.This varicose bronchiectasis serves as anintermediate step before the development ofgrossly dilated, cystic airways.
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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
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Clinical Manifestation of
Bronchiectasis Chronic Cough (90 %)
Dyspnea (72%)
Hemoptysis (56%)
Chest pain
Malnutrition/wasting
Anemia
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Clinical Manifestation of
Bronchiectasis Use of accessory muscles
Pursed lip breathing
Cyanosis
Signs of Cor pulmonale
Increased respiratory rate
Increased heart rate
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Clinical Manifestation of
Bronchiectasis
Copious postural foul smellingmucopurlant sputum
Sputum production
Mild 150 cc/d
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Clinical Manifestation of
Bronchiectasis Clubbing of fingers
Wheez
Rhonchi
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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
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Bronchiectasis Complications Pneumonia
Lung abscess
Empyema Septicaemia
Cor pulmonale
Metastatic cerebral abscesses
Secondary Amyloidosis with nephroticsyndrome
Recurrent pleurisy
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Bronchiectasis Complications Broncho pleural fistula
Purulent pericarditis
Respiratory failure
Metastic abcesses in bones etc
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Investigations Bronchiectasis CRP
Increased Sed rate
Anaemia
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Radiological features of
Bronchiectasis Bronchi, bronchioles
are dilated the
bronchial walls arethickened andshown as ringshadows on plain x
ray.
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Radiological features of
Bronchiectasis Dilated and
thickened airwaysthat appear as ring-like shadows (ofairways that areseen on end) ortram lines (in the
case of airways thatare perpendicular tothe x-ray beam)
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Radiological features of
Bronchiectasis Dilated and
thickened airwaysthat appear as ring-like shadows (ofairways that areseen on end) ortram lines (in the
case of airways thatare perpendicular tothe x-ray beam)
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Radiological features of
Bronchiectasis
In mild cases x ray may be normal.
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RADIOLOGY - CXRBronchiectasis
- vessel crowding
- loss of vessel markings- tramline/ring shadows
- cystic lesions/ air-fluidlevels
- evidence of TB
Poor: diagnostic sensitivity
monitoring ofprogression
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CT Scan of Bronchiectasis
Shows peribronchial
thickening, dilatedbronchioles.
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CT Scan of Bronchiectasis
Shows peribronchial
thickening, dilatedbronchioles
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CT Scan of Bronchiectasis CT scan also may show
Internal bronchialdiameter greater than
that of the adjacentpulmonary artery Lackof bronchial tapering,Presence of bronchiwithin 1 cm of the
costal pleura, Presenceof bronchi abutting themediastinal pleura,Bronchial wallthickening
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CT Scan of Bronchiectasis
Marked airwaydilatation both upperlobes.
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CT Scan of Bronchiectasis
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CT Scan of Bronchiectasis
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CT Scan of Bronchiectasis- Bronchial dilatation
- Bronchial wallthickening
F th i ti ti f
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Further investigations of
Bronchiectasis IgE , IgM, IgG levels.
Aspergillus precipitin .
Sputum culture: fungi / Pseudomonasaeuruginosa, H.influenzae.etc
EKG.
Film PNS
F th i ti ti f
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Further investigations of
Bronchiectasis Diffuse bronchiectasis Yellow nail
syndrome Pleural fluid TG/Chol
lymphedema. Diffuse panbronchiolitis HRCT(bizzare
nodules) transbronchial biopsy.
F th i ti ti f
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Further investigations of
Bronchiectasis Lung function:
Airflow obstruction FEV1 decreased.
Air trapping - RV increased
F th i ti ti f
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Further investigations of
Bronchiectasis Sweat test - Increased sodium and
chloride in cystic fibrosis
Bronchoscopy: Obstruction foreignbody, tumor.
Immunoglobulin levels
Cilia function and structure Kartagener's syndrome
Alpha-1 antrip level.
T f B hi i
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Treatment of Bronchiectasis
Treatment Goals:
1.Eliminate cause
2.Improve tracheo bronchial clearance
3.Control infection
4.Reverse airflow obstruction
T t t f B hi t i
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Treatment of Bronchiectasis
Proposed courses of treatment
Short course
Prolonged course
Intermittent regular courses
Inhalation
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Treatment of BronchiectasisAntibiotics and anti inflammatory
agents.
Are used in these proposed courses
To treat acute exacerbation,To prevent
infection or to reduce bacterial burden
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Treatment of Bronchiectasis Drainage Procedures
Postural drainage consists of adopting a
position in which the lobe to be drainedis uppermost.postural drainage shouldbe performed for a minimum of 5-10
minutes twice a day.
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Treatment of Bronchiectasis Gentle percussion of the chest wall with
cupped hands aids dislodgement of sputum.
Baroscopic removal of inspissated secretionsis rarely required.
Role of mucolytic agents is controversial.
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Treatment of Bronchiectasis Antibiotic theraphy.
Choice of antibiotic sould primarily be basedon the results of culture and sensitivity.
When no specific pathogen is identified andthe patient is not seriously ill,an oral agentlike
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Treatment of BronchiectasisAmoxycillin
Ampicillin
TetracyclineCotrimoxazole
or a fixed combination of amoxycillin andclavulanic acid should be used.moreseriously ill patients with pneumonitisshould be given parenteral antibiotics.
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Treatment of Bronchiectasis Duration of theraphy is variable.
A 5-10 days course is usually
sufficient.in some patients it may needto be prolonged for several weeks.
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Treatment of Bronchiectasis Brochiodilators
Brochiodilators to improve obstruction
and aid clearance of secretions areparticularly usefull when some elementof reversible airway obstruction is
present.
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Treatment of Bronchiectasis Primary Hypogammaglubolinemia
should be treated with human immune
serum albumin. Complicated cases may require nasal
oxygen on a chronic basis, to maintain
adequate oxygenation
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Treatment of Bronchiectasis
3 Strategies
1. High oral dose for prolonged period(at least 4 weeks) (macrolideand FQ) Azithromycin 500mg plus
Levofloxacin 250mg 2/wk x 6Mn(reduced exacerbation)
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Treatment of Bronchiectasis2. 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.
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Treatment of Bronchiectasis 3. Regular pulsed course of iv antibiotic
(e.g.2-3 wk courses with 1 or 2
months in between).
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Treatment of Bronchiectasis These episodic or suppressive
antibiotics
Decrease inflammation
Slow progression
Eradication
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Treatment of Bronchiectasis Anti-inflammatory agents :
Inhaled Fluticasone 500ug bid decreaseddensity of leucocyte, concentration of -inflammatory mediator 1B, IL-8 and LT-B4 insputum -improved sputum volume but no
change frequent of exacerbation, lungfunction and purulence sputum.
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Treatment of BronchiectasisAnti-inflammatory agents :Systemic
corticosteroid May better at penetrating
the bronchial wall and therefore bemore effective but available data onlyfor CF-Bronchiectasis.inhibit neutrophilmediated inflammation.
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Treatment of Bronchiectasis NSAIDS inhibit neutrophil function and
release of elastase
(Indocid25mgtidx4wk but opened labelstudy, lung function, sputum vol/qualitydid not change but high dose Ibuprofenx 4 yr found significantly slowedprogression of lung disease in CF-Bronchiectasis.
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Treatment of Bronchiectasis 3 Months of Clarithromycin decreased
total No. of leucocyte, proportion of
PMN and concentration of IL-8.
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Treatment of Bronchiectasis Brochiodilators
Anticholinergic or oral Methylxanthine inpatient with non-CF bronchiectasis.
Bronchopulmonary hygiene
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Bronchopulmonary hygiene
physical therapy That aims to remove lung secretions in
pt with acute and chronic airway
disease. Many active and passivetechnique are available Evidence isvariable and the literature is conflicting.
Bronchopulmonary hygiene
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Bronchopulmonary hygiene
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 drainmore effectively. This is called chestphysical therapy, or percussion andpostural drainage.
Bronchopulmonary hygiene
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Bronchopulmonary hygiene
Physical therapy Inflatable vests or mechanical
vibrators.Oral devices that apply
positive end-expiratory pressuremaintain the potency of the airwayduring exhalation.
Inspiratory muscle training X 8WKS.
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Mucolytics Medications are available to help thin
the sputum, so that it can be more
effectively coughed up.
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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.
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Treatment of Bronchiectasis
Alpha-1 antrip def Alpha-1 antritrip
replacement.
Oxygen and diuretics
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Treatment of BronchiectasisAnti-inflammatory agents Macrolide
(Azithromycin) suppress inflammation.
Azithromycin 500mg twice a week x6mn Decrease daily sputum production
and exacerbation.
Surgical treatment of
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Surgical treatment of
Bronchiectasis Surgery :
If the area of bronchiectasis is localized
and symptoms are debilitating or lifethreatening.
Surgical treatment of
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Surgical treatment of
Bronchiectasis When bleeding occurs from irritated
bronchial tubes and overgrown
bronchial blood vessels, surgery may berequired either to remove an area ofthe bronchial tube, or to inject thebleeding blood vessel with a material tostop the bleeding.
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Surgical treatment of
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Surgical treatment of
Bronchiectasis Surgery
Localized bronchiectasis
Proximal obstructive lesion,Obstructionmay require the removal of a foreignobject or tumor or aspirated material
Massive hemoptysis
Recurrent infections
Lung transplant
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Treatment of Bronchiectasis Prevention of Bronchiectasis
Adequate treatment and prophylaxis ofchildhood whooping cough, measles,and primary tuberculosis.
Genetic counseling in cystic fibrosis.
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PSEUDOBRONCHIECTASISA true bronchiectasis is not
reversible.whereas the
pseudobronchiectasis is reversible.
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PSEUDOBRONCHIECTASIS The bronchographic abnormalities displayed
by atelectasis and tracheo bronchitis
with ulceration of bronchial mucosa simulatecylindrical bronchiectasis.but re expansion ofcollapsed lung in atelectasis and regenerationof mucosa in trachiobroncitis result in
reversibility of bronchographicappearance.this is known aspseudobronchiectasis.
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Bronchiectasis sicca ( dry bronchiectasis)
This is a condition where bronchiectasispresents with repeated episodes ofhemoptysis without sputum
production.this usually occurs in upperlobe bronchiectasis of post tuberculousvariety.
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Middle lobe syndrome Or Brocks syndrome post obstructive.
bronchiectasis
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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 tenderhand of the unseen,And the cup he brings, thoughit burn your lips, has been fashioned of the clay
which the Potter have moistened with His tears andsacred feelings.