Bronchiectasis

Kayima James

CONTENTS
Definition Aetiology Pathogenesis Clinical manifestations Diagnosis Treatment

BRONCHIECTASIS
Definition: Abnormal and permanent dilation of bronchi. Focal or diffuse distribution Clinical consequences chronic and recurrent infection and Pooling of secretions in dilated airways. Classification: 1. Cylindrical (fusiform) 2. Saccular 3. Varicose

AETIOLOGY : IMPAIRED HOST DEFENCE

Local causes: Endobronchial obstruction Generalised impairment: 1. Immunoglobulin deficiency 2. Primary ciliary disorders 3. Cystic fibrosis

Aetiology: A. InfectionsMicro-organisms
Measles and Pertussis Adeno & Influenza virus Bacterial infection with virulent organisms: S.aureus, Klebsiella Anaerobes Atypical mycobacteria Mycoplasma HIV Tuberculosis Fungi

AETIOLOGY : NONINFECTIOUS
Toxins or toxic substances NH3; gastric contents Immune responses, ABPA Inflammatory diseases: ulcerative colitis, rheumatoid arthritis, Sjgren syndrome. -1-Antitrypsin deficiency Yellow nail syndrome

Pathophysiology
2 Prerequisites: Infectious insult Impairment of drainage, airway obstruction, and/or a defect in host defense.

Pathophys Continued
Infection: Bacterial, mycobacterial, esp. ABPA central airway bronchiectasis Airway obstruction: intraluminal tumor, foreign body, lymph nodes, COPD Immunodeficiency: ciliary dyskinesia, HIV, hypogammaglobulinemia, cystic fibrosis (obstruction and immunodef.)

CLINICAL MANIFESTATIONS
Persistent or recurrent cough with purulent sputum. Haemoptysis Initiating episode: Severe pneumonia, or insidious onset of symptoms or asymptomatic or non-productive cough dry bronchiectasis in upper lobe, Dyspnoea, wheezing widespread bronchiectasis or underlying COPD. Exacerbation of infection: Sputum volume increase, purulence or blood.

Bronchiectasis: Clinical
Note: Bronchiectasis may happen 2/2 COPD or may be a separate process with very similar symptoms

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

PHYSICAL EXAMINATION
Any combination of rhonchi, creps or wheezes. Clubbing of digits. Chronic hypoxaemia cor pulmonale R heart failure Amiloidosis (rare)

DIAGNOSIS - 1
Clinical Radiology: Chest XR: May be non-specific mild disease normal XRC advanced disease cysts + fluid levels peribronchial thickening, tram tracks, ring shadows CT Scan: Peribronchial thickening, dilated bronchioles. Sputum culture: Pseudomonas aeuruginosa, H.influenzae.

Gross pathology

DIAGNOSIS - 2
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.

Exacerbation

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

TREATMENT - 2
1. Immunoglobulin

2. Antituberculous drugs 3. Corticosteroids (ABPA) 4. Remove aspirated material

Chest physical therapy Mucolytics Bronchodilators

TREATMENT - 3
Antibiotics short course, prolonged course, intermittent regular courses, inhalation. Initial empiric Rx: Ampi, Amox, Cefaclor, Septran Ps.aeruginosa Quinolone, aminoglycoside, 3rd generation cephalosporin, pipracillin. Surgery: Oxygen and diuretics Lung transplant

Lung Abscess

LUNG ABSCESS
Lung abscess is a cavity containing pus and necrotic debris. It is distinguished from empyema, which is a collection of pus within the pleural space rather than the lung parenchyma. Usually reflects infection with an unusual microbial burden (e.g., acute aspiration), an especially virulent organism (e.g., Staphylococcus aureus), and/or a failure in microbial clearance mechanisms (e.g., bronchial obstruction(

Any necrotizing pneumonia can also present with areas of abscess, which are commonly small and multiple .

Bronchial obstruction.
Immunocompromising conditions: diabetes, malignancy, and other.

 Most lung abscesses involve the indigenous flora of the oropharynx. Abscesses involving S. aureus or gram-negative bacilli are most often nosocomial. Nocardia and Rhodococcus are found almost exclusively in immunocompromised hosts. Septic pulmonary emboli are usually due to S. aureus, primarily in intravenous drug abusers with tricuspid valve endocarditis. Lung abscesses due to Paragonimus westermani and melioidosis are usually acquired in the Far East or Indonesia.

EPIDEMIOLOGY

PATHOGENESIS
Among the anaerobes, organisms more likely to cause infection as sole agents are Fusobacterium nucleatum, F. necrophorum, B. fragilis, and Clostridium perfringens. Organisms such as S. aureus and K. pneumoniae, which produce extracellular toxins or enzymes, often produce abscesses.

CLINICAL MANIFESTATIONS
Relatively insidious onset of infection. Involvement of dependent segments of lung, predisposition to aspiration, and, often, periodontal disease. After 1 to 2 weeks, tissue necrosis, with abscess formation or empyema, occurs. Putrid sputum is noted in 50% or more of patients+/hemoptysis Weeks to months of malaise and low-grade fever may be associated with cough, weight loss, and anemia. Occasionally acute fever, malaise, cough, and, pleurisy. Esp in S. aureus or gram-negative bacilli

Lung abcess

DIAGNOSIS
SPUTUM CULTURE? BLOOD CULTURE (not helpfull) CULTURE OF EMPYEMA TRANSTRACHEAL ASPIRATION PROTECTED BAL SPECIMEN

TREATMENT
Antimicrobial therapy and drainage are the keystones of treatment. Periods of 1 to 3 months or more may be required PCN+METRONIDAZOLE CLINDAMYCIN

TREATMENT
Postural drainage is important in therapy of lung abscess. Bronchoscopy may help in effecting good drainage, removal of foreign bodies, and diagnosis of tumor. Surgical resection of necrotic lung may occasionally be needed if the response to antibiotics is poor or if airway obstruction limits drainage. In patients who are poor surgical risks, percutaneous drainage via catheters may be useful.