PATHOGENESIS OF BRONCHIECTASIS BY DR BASHIR AHMED DAR ASSOCIATE PROFESSOR MEDICINE SOPORE KASHMIR

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Dr Bashir Ahmed Dar associate professor medicine chinkipora sopore kashmir presently working in malaysia speaks about bronchiectasis.Bronchiectasis which is defined as the irreversible dilatation of …

Dr Bashir Ahmed Dar associate professor medicine chinkipora sopore kashmir presently working in malaysia speaks about bronchiectasis.Bronchiectasis which is defined as the irreversible dilatation of the cartilage-containing airways bronchi or bronchioles.

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  • Very helpful in understanding bronchiectasis. Thank you!
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  • thank you sir for the slides.. was really helpful!
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  • thanks alot sir..definitely help shed light on this topic :)
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  • very good slides, sir...i learn a lot...
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  • 1. BRONCHIECTASIS
    • BY
    • DR.BASHIR AHMED DAR
    • ASSOCIATE PROFESSOR MEDICINE
    • CHINKIPORA SOPORE KASHMIR
    • EMAIL- drbashir123@gmail.com
  • 2.  
  • 3.  
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  • 5.  
  • 6.  
  • 7.  
  • 8.  
  • 9.  
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  • 11.  
  • 12. BRONCHIECTASIS
    • Bronchiectasis is defined as the irreversible dilatation of the cartilage-containing airways bronchi or bronchioles.
  • 13. BRONCHIECTASIS
    • Bronchiectasis is defined as the irreversible dilatation of the cartilage-containing airways bronchi or bronchioles.
  • 14. 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•
  • 15. 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 .
  • 16. 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.
  • 17. Histology Respiratory tract
    • 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.
  • 18. Histology Respiratory tract
    • 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.
  • 19. Histology Respiratory tract
    • Outside the connective tissue layers, observe the C-shaped rings of hyaline cartilage which help to keep the lumen of the trachea from collapsing.
  • 20. Histology Respiratory tract
    • Mucous Membrane.—The mucous membrane is continuous above with that of the larynx, and below with that of the bronchi
  • 21. Histology Respiratory tract
    • 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.
  • 22. Histology Respiratory tract
    • Beneath the basement membrane there is a distinct layer of longitudinal elastic fibers with a small amount of intervening areolar tissue.
  • 23. Histology Respiratory tract
    • 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
  • 24. 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.
  • 25. 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.
  • 26. 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.
  • 27. Bronchi
    • Bronchioles are smaller branches of the bronchi, and are distinguished from them by the absence of cartilage and glands
  • 28. 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.
  • 29. Bronchi
    • The smooth muscle layer is generally quite prominent in these structures circularly arranged bundles of smooth muscle in the bronchiolar wall.
  • 30. 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 .
  • 31. 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.
  • 32. 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.
  • 33. 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.
  • 34. 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.
  • 35. Bronchioles
    • It is this "mucociliary elevator" which is largely responsible for removing foreign material, including organisms that land on the bronchial surfaces.
  • 36. 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.
  • 37. 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.
  • 38. 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.
  • 39. 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•
  • 40. 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
  • 41. Mechanisms of development 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
  • 42. Mechanisms of development of Bronchiectasis
    • B.Bronchial lumen obstruction
    • Focal Congenital bronchial atresia
    • Foreign body
    • Broncholithiasis
    • Endobronchial neoplasm
    • Rt mid lobe synd
  • 43. Mechanisms of development of Bronchiectasis
    • C.And traction from adjacent fibrosis
  • 44. 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
  • 45. Mechanisms of development 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.
  • 46. Mechanisms of development 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.
  • 47. Mechanisms of development 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.
  • 48. Mechanisms of development 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 .
  • 49. Mechanisms of development 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 .
  • 50. Mechanisms of development 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.
  • 51. Mechanisms of development of Bronchiectasis
    • Structural wall defect is the common feature of Mounier-Kuhn disease or tracheobronchomegaly, William-Campbell syndrome , and congenital bronchial atresia.
  • 52. Mechanisms of development 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).
  • 53. 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.
  • 54. Mechanisms of development 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 .
  • 55. Mechanisms of development 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.
  • 56. 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.
  • 57. 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 .
  • 58. 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
  • 59. 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.
  • 60. 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
  • 61. Mechanisms of development 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.
  • 62. Mechanisms of development 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
  • 63. Mechanisms of development of Bronchiectasis
    • Rubella,whooping cough (B.pertusis),measles in childhood
  • 64. Post infective Bronchiectasis
    • Measles and Pertusis
    • Adeno & Influenza virus
    • Bacterial infection with virulent organisms: S.aureus, Klebsiella Anaerobes
    • Atypical mycobacteria
    • Mycoplasma
    • HIV
    • TB
    • Fungi
  • 65. Types of Bronchiectasis
    • 1. Cylindrical or tubular bronchiectasis
    • 2. Varicose bronchiectasis
    • 3. Saccular or cystic bronchiectasis
  • 66. 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.
  • 67. 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.
  • 68. 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
  • 69. Clinical Manifestation of Bronchiectasis
    • Chronic Cough (90 %)
    • Dyspnea (72%)
    • Hemoptysis (56%)
    • Chest pain
    • Malnutrition/wasting
    • Anemia
  • 70. Clinical Manifestation of Bronchiectasis
    • Use of accessory muscles
    • Pursed lip breathing
    • Cyanosis
    • Signs of Cor pulmonale
    • Increased respiratory rate
    • Increased heart rate
  • 71. Clinical Manifestation of Bronchiectasis
    • Copious postural foul smelling mucopurlant sputum
    • Sputum production
    • Mild <15 cc/d
    • Moderate 15-150 cc/d
    • Severe >150 cc/d
  • 72. Clinical Manifestation of Bronchiectasis
    • Clubbing of fingers
    • Wheez
    • Rhonchi
  • 73. 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
  • 74. Bronchiectasis Complications
    • Pneumonia
    • Lung abscess
    • Empyema
    • Septicaemia
    • Cor pulmonale
    • Metastatic cerebral abscesses
    • Secondary Amyloidosis with nephrotic syndrome
    • Recurrent pleurisy
  • 75. Bronchiectasis Complications
    • Broncho pleural fistula
    • Purulent pericarditis
    • Respiratory failure
    • Metastic abcesses in bones etc
  • 76. Investigations Bronchiectasis
    • CRP
    • Increased Sed’ rate
    • Anaemia
  • 77. Radiological features of Bronchiectasis
    • Bronchi, bronchioles are dilated the bronchial walls are thickened and shown as ring shadows on plain x ray.
  • 78. Radiological features of 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)
  • 79. Radiological features of 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)
  • 80. Radiological features of Bronchiectasis
    • In mild cases x ray may be normal.
  • 81. 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
  • 82.  
  • 83. Radiological features of Bronchiectasis
    • The definitive diagnosis is made bronchographically (by instillation of radiographic contrast medium into the lung).
  • 84. CT Scan of Bronchiectasis
    • Shows peribronchial thickening, dilated bronchioles.
  • 85. CT Scan of Bronchiectasis
    • Shows peribronchial thickening, dilated bronchioles
  • 86. CT Scan of Bronchiectasis
    • 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
  • 87. CT Scan of Bronchiectasis
    • Marked airway dilatation both upper lobes.
  • 88. CT Scan of Bronchiectasis
  • 89. CT Scan of Bronchiectasis
  • 90. CT Scan of Bronchiectasis
    • - Bronchial dilatation
    • - Bronchial wall thickening
  • 91. Further investigations of Bronchiectasis
    • IgE , IgM, IgG levels.
    • Aspergillus precipitin .
    • Sputum culture: fungi / Pseudomonas aeuruginosa, H.influenzae.etc
    • EKG.
    • Film PNS
  • 92. Further investigations of Bronchiectasis
    • Diffuse bronchiectasis Yellow nail syndrome Pleural fluid TG/Chol lymphedema.
    • Diffuse panbronchiolitis HRCT(bizzare nodules) transbronchial biopsy.
  • 93. Further investigations of Bronchiectasis
    • Lung function:
    • Airflow obstruction – FEV1 decreased.
    • Air trapping - RV increased
  • 94. Further investigations of 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.
  • 95. Treatment of Bronchiectasis
    • Treatment Goals:
    • 1.Eliminate cause
    • 2.Improve tracheo bronchial clearance
    • 3.Control infection
    • 4.Reverse airflow obstruction
  • 96. Treatment of Bronchiectasis
    • Proposed courses of treatment
    • Short course
    • Prolonged course
    • Intermittent regular courses
    • Inhalation
  • 97. Treatment of Bronchiectasis
    • Antibiotics and anti inflammatory agents.
    • Are used in these proposed courses
    • To treat acute exacerbation,To prevent infection or to reduce bacterial burden
  • 98. Treatment of Bronchiectasis
    • 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.
  • 99. Treatment of Bronchiectasis
    • 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.
  • 100. Treatment of Bronchiectasis
    • 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
  • 101. Treatment of Bronchiectasis
      • 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.
  • 102. Treatment of Bronchiectasis
    • 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.
  • 103. Treatment of Bronchiectasis
    • Brochiodilators
    • Brochiodilators to improve obstruction and aid clearance of secretions are particularly usefull when some element of reversible airway obstruction is present.
  • 104. Treatment of Bronchiectasis
    • 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.
    • .
  • 105. 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
  • 106. Treatment of Bronchiectasis
    • 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)
  • 107. Treatment of Bronchiectasis
    • 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.
  • 108. Treatment of Bronchiectasis
    • 3. Regular pulsed course of iv antibiotic (e.g.2-3 wk courses with 1 or 2 months in between).
  • 109. Treatment of Bronchiectasis
    • These episodic or suppressive antibiotics
    • Decrease inflammation
    • Slow progression
    • Eradication
  • 110. Treatment of Bronchiectasis
    • 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.
  • 111. Treatment of Bronchiectasis
    • 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.
  • 112. Treatment of Bronchiectasis
    • 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.
  • 113. Treatment of Bronchiectasis
    • Anti-inflammatory agents Macrolide (Azithromycin) suppress inflammation.
    • Azithromycin 500mg twice a week x 6mn Decrease daily sputum production and exacerbation.
  • 114. Treatment of Bronchiectasis
    • 3 Months of Clarithromycin decreased total No. of leucocyte, proportion of PMN and concentration of IL-8.
  • 115. Treatment of Bronchiectasis
    • Brochiodilators
    • Anticholinergic or oral Methylxanthine in patient with non-CF bronchiectasis.
  • 116. 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.
  • 117. 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 drain more effectively. This is called chest physical therapy, or percussion and postural drainage.
  • 118. Bronchopulmonary hygiene 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.
  • 119. Mucolytics
    • Medications are available to help thin the sputum, so that it can be more effectively coughed up.
  • 120. 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.
  • 121. Treatment of Bronchiectasis
    • Alpha-1 antrip def Alpha-1 antritrip replacement.
    • Oxygen and diuretics
  • 122. Treatment of Bronchiectasis
    • Anti-inflammatory agents Macrolide (Azithromycin) suppress inflammation.
    • Azithromycin 500mg twice a week x 6mn Decrease daily sputum production and exacerbation.
  • 123. Surgical treatment of Bronchiectasis
    • Surgery :
    • If the area of bronchiectasis is localized and symptoms are debilitating or life threatening.
  • 124. Surgical treatment of 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.
  • 125. Surgical treatment of 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.
  • 126. Surgical treatment of 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
  • 127. Treatment of Bronchiectasis
    • Prevention of Bronchiectasis
    • Adequate treatment and prophylaxis of childhood whooping cough, measles, and primary tuberculosis.
    • Genetic counseling in cystic fibrosis.
  • 128. PSEUDOBRONCHIECTASIS
    • A true bronchiectasis is not reversible.whereas the pseudobronchiectasis is reversible.
  • 129. 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.
  • 130. 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.
  • 131. Middle lobe syndrome
    • Or Brocks syndrome post obstructive.
    • bronchiectasis
  • 132. 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.