SUPPURATIVE LUNG DISEASES

By Dr A.O. Odeyemi Department of Medicine,

College of Health Sciences, Bowen University Ogbomoso.

INTRODUCTION

• Suppuration means pus formation

• Components of suppurative lung diseases includes;

– Bronchiectasis

– Lung abscess

– Empyema

INTRODUCTION 2

• These are based on site of pus formation;

– Bronchi (= bronchiectasis)

– Lung parenchyma (= lung abscess).

– Pleura (= empyema).

BRONCHIECTASIS

• Bronchiectasis refers to an irreversible airway dilation

• It involves the lung in either a focal or a diffuse manner

• Focal bronchiectasis refers to bronchiectatic changes in a localized area of the lung

• Diffuse bronchiectasis is refers to widespread bronchiectatic changes throughout the lung

CLASSIFICATION

• Cylindrical or tubular

• Characterized by smooth dilation of the bronchi (the most common form)

• Varicose

• Characterized by dilated bronchi with multiple indentations

• Cystic

• Defined by dilated bronchi that terminate in blind ending

AETIOLOGY

• Focal bronchiectasis: Usually due to airway obstruction – either extrinsic; e.g., due to compression by

adjacent lymphadenopathy or parenchymal tumor mass;

– or intrinsic; e.g., due to an airway tumor or aspirated foreign body

• Diffuse bronchiectasis: Often due to underlying systemic or infectious disease process

Causes of diffuse bronchiectasis

• Infections such as TB, necrotizing pneumonias and measles

• Immunodeficiency such as hypogammaglobulinemia and HIV infection

• Genetic causes such as cystic fibrosis, Kartagener’s syndrome and α1 antitrypsin deficiency

• Immune mediated disease especially allergic bronchopulmonary aspergillosis

Causes of diffuse bronchiectasis 2

• Autoimmune or rheumatologic causes such as rheumatoid arthritis, Sjögren’s syndrome and inflammatory bowel disease

• Recurrent aspiration

• Miscellaneous causes such as traction bronchiectasis (from postradiation fibrosis or idiopathic pulmonary fibrosis) and yellow nail syndrome

• Idiopathic

PATHOGENESIS

• The most widely cited mechanism of infectious bronchiectasis is the “vicious cycle hypothesis,” in which susceptibility to infection and poor mucociliary clearance result in microbial colonization of the bronchial tree.

• The microbial infection incites chronic inflammation resulting in tissue damage and impaired mucociliary motility.

PATHOGENESIS 2

• In turn this led to more infection with a cycle of progressive inflammation causing lung damage.

• The current view is that the two factors required for the development of this condition are persistent infection and a defect in host defense.

PATHOGENESIS 2

• Proposed mechanisms for noninfectious bronchiectasis include immune-mediated reactions that damage the bronchial wall such as those associated with systemic autoimmune conditions

• Traction bronchiectasis refers to dilated airways arising from parenchymal distortion as a result of lung fibrosis e.g. idiopathic pulmonary fibrosis and post radiation fibrosis

CLINICAL FEATURES

• Persistent cough with mucopurulent sputum production

• Frequently worse in the morning (having accumulated during recumbency in sleep).

• Hemoptysis may be seen in 40 to 70 percent of patients and may vary from blood streaks to large clots.

CLINICAL FEATURES 2

• Physical findings often include crackles and rhonchi on lung auscultation

• Bronchial breath sounds may be heard in severe cases or patients with a complicating pneumonia.

• Finger clubbing may be seen in some patients.

CLINICAL FEATURES 3

• Acute exacerbations of bronchiectasis are usually characterized by changes in the nature of sputum production, with increased volume and purulence.

• However, typical signs symptoms and signs of lung infection, such as fever and new infiltrates, may not be present.

INVESTIGATIONS

• Chest radiograph which reveals “tram tracks” indicating dilated airways (low sensitivity)

• Chest computed tomography (CT) is the imaging modality of choice for confirming the diagnosis.

• CT findings include airway dilation (detected as parallel “tram tracks” or as the “signet-ring sign”—a cross-sectional area of the airway with a diameter at least 1.5 times that of the adjacent vessel),

INVESTIGATIONS 2

• lack of bronchial tapering (including the presence of tubular structures within 1 cm from the pleural surface),

• bronchial wall thickening in dilated airways,

• inspissated secretions (e.g., the “tree-in-bud” pattern),

• Cysts emanating from the bronchial wall (especially pronounced in cystic bronchiectasis)

CT Features of bronchiectasis

• Many severely dilated airways, seen both longitudinally (arrowhead) and in cross-section (arrow).

INVESTIGATIONS 3

• Bronchoscopy – to evaluate patients with focal bronchiectasis to exclude airway obstruction

• Other investigations may be necessary to diagnose any suspected underlying cause as earlier listed

TREATMENT

• Use of antibiotics to treat active infection

• Bronchial hygiene so as to decrease the microbial load within the airways and minimize the risk of repeated infections

• Anti-inflammatory medications

• Surgery

Bronchial hygiene

• This helps to enhance secretion clearance. Various options are listed below

• Hydration and mucolytic administration e.g. dornase in cystic fibrosis

• Aerosolization of bronchodilators and hyperosmolar agents (e.g. hypertonic saline)

• Chest physiotherapy such as – postural drainage,

– chest percussion via hand clapping to the chest,

Bronchial hygiene 2

– use of devices such as an oscillatory positive expiratory pressure flutter valve

– high-frequency chest wall oscillation vest.

• Pulmonary rehabilitation may also assist with secretion clearance as well as with other aspects of bronchiectasis, including improved exercise capacity and quality of life.

Anti-inflammatory therapy

• Inhaled corticosteroids

• Oral or systemic glucocorticoids particularly in treatment of bronchiectasis due to certain aetiologies, such as allergic bronchopulmonary aspergillosis, or rheumatoid arthritis

Surgery

• This can be considered in select cases, in which case resection of a focal area of suppuration can be done.

• Lung transplantation can also be considered in advanced cases

COMPLICATIONS

• Pneumonia

• Pneumothorax

• Empyema

• Metastatic cerebral abscess

• Massive haemoptysis

• Microbial resistance to antibiotics

– This is due to recurrent infections and repeated courses of antibiotics.

PREVENTION

• Treating any underlying immunodeficient state

• Vaccination

• Patients who smoke should be counseled to quit smoking

LUNG ABSCESS

• Lung abscess represents necrosis and cavitation of the lung following microbial infection.

• Lung abscesses can be single or multiple but usually are marked by a single dominant cavity >2 cm in diameter.

• A similar process with multiple small cavities less than 2 cm in diameter is sometimes called necrotizing pneumonia.

CLASSIFICATION

• Based on duration – Acute - <4-6weeks

– Chronic - >6weeks

• Based on aetiology – Primary: caused by aspiration or pneumonia

– Secondary: caused by a preexisting condition (e.g. obstruction), spread from an extrapulmonary site, bronchiectasis and/or immunocompromised state.

• Based on responsible pathogen e.g. aspergillus lung abscess

PATHOGENESIS

• Lung abscesses most frequently arises as a complication of aspiration pneumonia caused by mouth anaerobes.

• Bacterial inoculum from the gingivial crevice reaches the lower airways and infection is initiated because the bacteria are not cleared by the patient’s host defence mechanism.

• Aspiration pneumonitis develops initially and progresses to tissue necrosis 7 – 14 days later, leading to the formation of lung abscess

PATHOGENESIS 2

• Other mechanisms for lung abscess formation include bacteremia or tricuspid valve endocarditis, caused by septic emboli to the lung

• Lemierre’s syndrome (a rare cause of lung abscess), in which an infection begins in the pharynx and then spreads to the neck and the carotid sheath (which contains the jugular vein) to cause septic thrombophlebitis.

PATHOGENESIS 3

• In primary lung abscesses, the dependent segments (posterior segments of the upper lobes and superior segments of the lower lobes) are the most common locations, given the predisposition of aspirated materials to be deposited in these areas.

• The right lung is generally more commonly affected than the left because the right main stem bronchus is less angulated.

PATHOGENESIS 4

• In secondary abscesses, the location of the abscess may vary with the underlying cause.

CAUSATIVE ORGANISMS

• The microbiology of primary lung abscesses is often polymicrobial, primarily including anaerobic organisms as well as microaerophilic streptococci

• The most common anaerobes are Peptostreptococcus, Bacteroides, Fusobacterium species and microaerophilic streptococcus.

CAUSATIVE ORGANISMS 2

• In contrast, the microbiology of secondary lung abscesses involves quite a broad bacterial spectrum, with infection by Pseudomonas aeruginosa and other gram-negative rods most common.

• Other organisms include S. aureus, Streptococcus pyogenes, S. pneumoniae (rarely), Klebsiella pneumoniae, Haemophilus influenzae; Actinomyces and Nocardia species

RISK FACTORS

• Poor dentition

• Seizure disorder

• Alcohol abuse

• Individuals with an inability to protect their airways because of an absent gag reflex, such as during coma, loss of consciousness, or general anesthetic and sedation.

CLINICAL FEATURES

• May initially be similar to those of pneumonia, with fevers, cough, sputum production, and chest pain

• A more chronic and indolent presentation that includes night sweats, fatigue, and anaemia is often observed with anaerobic lung abscesses.

• The sputum is characteristically discoloured, foul-tasting and foul-smelling.

CLINICAL FEATURES 2

• Lung abscesses due to non-anaerobic organisms, such as S. aureus, may present with a more fulminant course characterized by high fevers and rapid progression.

• Physical examination findings may include fevers, poor dentition, and/or gingival disease as well as amphoric and/or cavernous breath sounds on lung auscultation.

CLINICAL FEATURES 3

• Additional findings may include digital clubbing and the absence of a gag reflex.

• Clinical findings of concomitant consolidation such as decreased breath sounds, dullness to percussion, bronchial breath sounds and crackles may be present

• Evidence of pleural friction rub and signs of associated pleural effusion, empyema, and pyopneumothorax may be present.

INVESTIGATIONS

• The presence of a lung abscess is determined by chest imaging.

• Typical chest radiographic appearance is an irregularly shaped thick-walled cavity with an air-fluid level inside

• Computed tomography (CT) permits better definition and may provide earlier evidence of cavitation.

INVESTIGATIONS 2

• CT may also yield additional information regarding a possible underlying cause of lung abscess, such as malignancy.

• Blood tests including FBC & ESR, blood culture & sensitivity

• Sputum for gram & ZN stains, Culture & Sensitivity ( for aerobes, anaerobes & fungi)

• Other investigations based on suspected causes

INVESTIGATIONS 3

TREATMENT

• Antibiotics is the main stay of treatment

• Drug of choice is clindamycin

• Other antibiotics include – Metronidazole in combination with other

antibiotics

– Penicillin G

– Ciprofloxacin

– Moxifloxacin

– Vancomycin

• Duration of treatment is 4 – 6 weeks

TREATMENT 2

• Surgery (rarely required).

• Indications for surgery include; – failure to respond to medical management,

– large cavities (>6-8cm) or;

– suspected neoplasm.

• The surgical procedure performed is either lobectomy or pneumonectomy.

• Percutaneous drainage of the abscess, especially in poor surgical candidates, can also be performed

COMPLICATIONS

• Rupture into the pleural space causing empyema

• Pleural fibrosis

• Trapped lung

• Respiratory failure

• Bronchopleural fistula

PREVENTION

• Prevention of aspiration is important to minimize the risk of lung abscess.

• Early intubation and protection of airway in patients who do not have a gag reflex is essential.

• Positioning the supine patient at a 30° head up minimizes the risk of aspiration.

• Vomiting patients should be placed on their sides.

PREVENTION 2

• Improving oral hygiene and dental care in elderly and debilitated patients may decrease the risk of anaerobic lung abscess.

PROGNOSIS

• The prognosis for lung abscess following antibiotic treatment is generally favorable.

• Over 90% of lung abscesses are cured with medical management alone, unless caused by bronchial obstruction secondary to carcinoma.

EMPYEMA

• Defined by the presence of pus in the pleural space.

• It typically is a complication of pulmonary parenchymal infection (i.e. pneumonia or lung abscess)

• Other causes include penetrating chest trauma, oesophageal rupture or complication of a lung surgery

• Subdiaphragmatic abscess (abscess crosses the diaphragm and enter the pleural space)

EMPYEMA 2

• Physical findings is that of pleural effusion and underlying condition

• Diagnosis is confirmed by chest radiography

• Treatment is by pleural drainage and appropriate antibiotics

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