Bronchiectasis Hassan Ghobadi MD. Assistant professor of Internal Medicine Ardabil University of Medical sciences.

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1 Bronchiectasis Hassan Ghobadi MD. Assistant professor of Internal Medicine Ardabil University of Medical sciences

2 CONTENTS  Definition  Pathology  Etiology  Pathogenesis  Clinical manifestations  Diagnosis  Treatment

3 BRONCHIECTASIS Definition : Abnormal and permanent dilation of bronchi. It may be focal or diffuse distribution

4 Pathology  The bronchial dilatation of bronchiectasis is associated with destructive and inflammatory changes in the walls of airways.  The normal structural components of the wall, including cartilage, muscle, and elastic tissue, are destroyed and may be replaced by fibrous tissue.  The dilated airways frequently contain pools of thick, purulent material, while more peripheral airways are often occluded by secretions or obliterated and replaced by fibrous tissue.

5 Pathology  Three different patterns of bronchiectasis have been described.  1- Cylindrical bronchiectasis,  2- Varicose bronchiectasis,  3- Saccular (cystic) bronchiectasis,

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7 ETIOLOGY : IMPAIRED HOST DEFENCE  Local causes: Endobronchial obstruction  Generalized impairment: 1. Immunoglobulin deficiency 2. Primary ciliary disorders (PCD) 3. Cystic fibrosis

8 Etiology: A. Impaired host defense  Impaired host defense mechanisms are often involved in the predisposition to recurrent infections.  Generalized impairment of pulmonary defense mechanisms occurs with immunoglobulin deficiency, primary ciliary disorders, or cystic fibrosis (CF).  primary ciliary dyskinesia, are responsible for 5–10% of cases of bronchiectasis. Primary ciliary dyskinesia is inherited in an autosomal recessive fashion.  In CF impaired bacterial clearance, resulting in colonization and infection with particularly P. aeruginosa & S. aureus, H. influenzae, Escherichia coli, and Burkholderia cepacia.

9 Etiology: B. Infections Causes  Adeno & Influenza virus  Measles and Pertussis  Atypical mycobacteria  Bacterial infection with virulent organisms: S.aureus, Klebsiella Anaerobes Bordetella pertussis  Mycoplasma  HIV  Tuberculosis  Fungi  Mycobacterium avium complex

10 Etiology: C. Noninfectious Causes  Exposure to a toxic substance  An immune response in the airway (ABPA),  Inflammatory diseases: ulcerative colitis, rheumatoid arthritis, Sjögren syndrome.  Alpha 1- antitrypsin deficiency,  Yellow nail syndrome,

11 Bronchiectasis: Clinical Manifestation  Cough (90 %)  Daily sputum production (76%)  Dyspnea (72%)  Hemoptysis (56%)  Recurrent pleurisy

12 PHYSICAL EXAMINATION  Any combination of, rhonchi, crepitus or wheezes  Clubbing of digits,  Chronic hypoxemia  cor pulmonale  Rt. heart failure  Amiloidosis (rare)

13 Bronchiectasis: Radiographic Findings  CXR may be normal with mild disease.  Patients with saccular bronchiectasis may have prominent cystic spaces,  Other findings are due to dilated airways with thickened walls, which result from peribronchial inflammation as ("tram tracks“&"ring shadows“).  HRCT provides an excellent view of dilated airways (standard technique for detecting or confirming the diagnosis of bronchiectasis).

14 Bronchiectasis: Laboratory Findings  Pulmonary function tests may demonstrate airflow obstruction.  Upper lobe involvement may be suggestive of either tuberculosis or ABPA.  With more widespread disease, measurement of sweat chloride levels for CF,  Structural or functional assessment of nasal or bronchial cilia or sperm for primary ciliary dyskinesia.

15 Pathophysiology  Infection: Bacterial, mycobacterial, esp. ABPA  central airway bronchiectasis  Airway obstruction: Intra luminal tumor, foreign body, lymph nodes, COPD  Immunodeficiency: Ciliary dyskinesia, HIV, hypogammaglobulinemia, cystic fibrosis (obstruction and immunodeficiency.)

16 Compares primary bronchiectasis with COPD

17 Exacerbation: Etiology Colonization/infection:  Hemophilus  Pseudomonas  MAI  Aspergillus Very difficult to distinguish colonization from acute infection with these bacteria.

18 Cystic air spaces

19 Ring shadow

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22 DIAGNOSIS  Lung function: Airflow obstruction – FEV1 decreased. Air trapping - RV increased  Sweat test: Increased sodium and chloride in cystic fibrosis  Bronchoscopy: Obstruction – foreign body, tumor.  Immunoglobulin  Cilia function and structure: Kartagener syndrome.

23 TREATMENT four Goals: 1. Eliminate cause 2. Improve tracheo bronchial clearance 3. Control infection 4. Reverse airflow obstruction

24 TREATMENT - 2 1. Immunoglobulin 2. Antituberculous drugs 3. Corticosteroids (ABPA) 4. Remove aspirated material  Chest physical therapy  Mucolytics agents  Bronchodilators

25 TREATMENT - 3  Antibiotics : short course, prolonged course, intermittent regular courses, inhalation.  Initial empiric Rx: Ampicillin, Amoxicilin, Cefaclor, Septran Pseudomona aeruginosa = 3rd gen. Cephalosporin, Quinolone, Aminoglycoside, Pipracillin.  Surgery  Oxygen and diuretics  Lung transplant

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27 Lung Abscess  Definition: A pulmonary parenchymal necrosis and cavitation resulting from infection. Aspiration is the most common cause.  Risk Factors: E sophageal dysmotility, Seizure disorders, Neurologic conditions causing bulbar dysfunction. Periodontal disease and Alcoholism.

28 Microbiology  Anaerobic bacteria are the most common causative organisms for lung abscess.  Aerobic or facultative bacteria such as S. aureus, Klebsiella pneumoniae, Nocardia sp., and gram-negative organisms.  Nonbacterial pathogens like fungi and parasites, may also cause abscess formation.  In the immunocompromised host, aerobic bacteria and opportunistic pathogens may predominate.

29 Clinical Manifestations  The symptoms may include cough, purulent sputum production, pleuritic chest pain, fever, and hemoptysis.  In anaerobic infection, the clinical course may be chronic, and some patients may be asymptomatic. Physical examination : Rales or evidence of consolidation Fetid breath and poor dentition may be diagnostic clues. Clubbing or hypertrophic pulmonary osteoarthropathy may occur in chronic cases.

30 Clinical Manifestations  The CXR classically reveals one or two thick-walled cavities in dependent areas of the lung. An air-fluid level is often present.  Laboratory studies may reveal leukocytosis, anemia, and an elevated erythrocyte sedimentation rate.  CT of the chest is helpful in defining the size and location of the abscess, as well as to evaluate for additional cavities and the presence of pleural disease.  Cavitary lesions in nondependent regions like the right middle lobe or anterior segments of the upper lobes should raise the possibility of other etiologies, including malignancy.

31 Diagnosis  The diagnosis of lung abscess is based on clinical symptoms, identification of predisposing conditions, and chest radiographic findings.  Anaerobic bacteria are particularly difficult to isolate.  Blood, sputum cultures, pleural fluid cultures should be obtained from patients with lung abscess.  Bronchoscopy is perhaps most useful to rule out airway obstruction, mycobacterial infection, or malignancy.

32 CXR Finding

33 CT Finding

34 Differential diagnosis  Mycobacterial infection,  Pulmonary sequestration,  Malignancy,  Pulmonary infarction,  Infected bulla.

35 Lung Abscess: Treatment  Penicillin was the mainstay of empiric antibiotic therapy for lung abscess.  Due to the emergence of beta-lactamase producing organisms, clindamycin (150 mg–300 mg every 6 h) is now standard therapy.  Other agents, such as carbapenems and beta-lactam/ beta- lactamase inhibitor combinations, may be useful in selected cases.  The duration of treatment for lung abscess is controversial. Four to six weeks of antibiotic therapy is typically employed.  Treatment failure suggests the possibility of a noninfectious etiology.

36 Treatment : Surgery  Refractory hemoptysis,  Inadequate response to medical therapy,  The need for a tissue diagnosis when there is concern for a noninfectious etiology.

37 الهی عاقبت محمود گردان به حق صالحان و نیک مردان