SUPPURATIVE LUNG

DISEASES
DR S CONTEH
 Introduction

• Suppurative lung diseases are a group of disorders which result in chronic

lung infection, with pus in the lungs

• Individuals with suppurative lung diseases present with chronic purulent

sputum and recurrent respiratory tract infections

• The aetiology of these conditions is variable and they include the following:
• Bronchiectasis
• Lung abscess
• Empyema
BRONCHIECTSIS
Outline

• Introduction
• Causes
• Pathophysiology
• Clinical features
• Investigations
• Treatment
 Introduction

• Bronchiectasis refers to abnormal and permanently dilated airways

• The bronchial walls become inflamed, thickened and irreversibly damaged

• The mucociliary transport mechanism is impaired and frequent bacterial

infections ensue

• Bronchiectasis shares many clinical features with COPD, including

inflamed and easily collapsible airways, obstruction to airflow, and
frequent clinic visits and hospitalizations
 Causes of Bronchiectasis
• Congenital • Granuloma
• Deficiency of bronchial wall elements • Tuberculosis
• Pulmonary sequestration • Sarcoidosis
• Mechanical bronchial obstruction • Diffuse diseases of the lung parenchyma
• Intrinsic: • Idiopathic pulmonary fibrosis
• Foreign body
• Immunological over-response
• Inspissated mucus
• Allergic bronchopulmonary aspergillosis
• Post-tuberculous stenosis
• Tumour
• Post-lung transplant
• Extrinsic: • Immune deficiency
• Lymph node • Primary:
• Tumour • Panhypogammaglobulinaemia
• Postinfective bronchial damage • Selective immunoglobulin deficiencies (IgA and IgG2)
• Bacterial and viral pneumonia, including • Secondary:
pertussis, measles • HIV
• Aspiration pneumonia • Malignancy
Causes of Bronchiectasis

• Mucociliary clearance defects

• Genetic:
• Primary ciliary dyskinesia (Kartagener’s syndrome with
dextrocardia and situs-inversus)
• Cystic fibrosis
• Acquired:
• Young’s syndrome – azoospermia, sinusitis
 Pathophysiology
• Bronchiectasis may result from congenital defect
affecting airway ion transport or ciliary function
(cystic fibrosis)
• It may be acquired; secondary to damage to the
airways by a destructive infection, inhaled toxin
or foreign body
• The result is chronic inflammation and infection
in airways, then dilatation
• Localised bronchiectasis may occur due to
accumulation of pus beyond an obstructing
bronchial lesion; eg. enlarged tuberculous hilar
lymph nodes, bronchial tumour or inhaled
foreign body (eg aspirated peanut)
 Pathophysiology
• The bronchiectatic cavities may be lined by granulation tissue, squamous
epithelium or normal ciliated epithelium

• There may also be inflammatory changes in the deeper layers of the bronchial
wall and hypertrophy of the bronchial arteries

• Chronic inflammatory and fibrotic changes are usually found in the

surrounding lung tissue, resulting in progressive destruction of the normal
lung architecture in advanced cases
Clinical features

• Cough with production of large amounts of sputum

• With mild bronchiectasis sputum only becomes yellow or green sputum

after an infection

• Localized areas of the lung may be particularly affected, and sputum

production will depend on position

• As condition worsens, patient suffers from persistent halitosis, recurrent

febrile episodes, malaise and pneumonia
Clinical features

• Clubbing occurs, and coarse crackles can be heard over the infected
areas, usually the lung bases

• In severe cases there is continuous production of foul-smelling, thick,

khaki-coloured sputum

• Haemoptysis can occur either as blood-stained sputum or massive

haemorrhage

• Breathlessness may result from airflow limitation

 Investigations

• Chest X-ray: may be normal or may show dilated bronchi with

thickened bronchial walls and sometimes multiple cysts

• High-resolution CT scanning: shows bronchial dilatation with

loss of airway tapering at the periphery, bronchial wall
thickening and cysts at the end of the bronchioles with a
sensitivity of 97%

• Sputum examination: culture and sensitivity of the organisms

is essential for adequate treatment. The major pathogens
are Staph. aureus, Pseudomonas aeruginosa
Investigations

• Sinus X-rays: 30% have concomitant rhinosinusitis

• Serum immunoglobulins: 10% of adults with bronchiectasis have

antibody deficiency (mainly IgA)

• Sweat electrolytes – if cystic fibrosis is suspected

• Mucociliary clearance (nasal clearance of saccharin) - A 1 mm cube of

saccharin is placed on the inferior turbinate and the time to taste
measured (normally less than 30 minutes)
 Treatment

Postural drainage
• Postural drainage is essential and patients must
be trained by physiotherapists to tip themselves
into a position in which the affected lobe(s) are
uppermost at least 3 times daily for 10–20 minutes

• Most patients find that lying over the side of

the bed with head and thorax down is effective
 Treatment

Antibiotics
• Bronchopulmonary infections need to be eradicated if progression of the disease
is to be halted
• In mild cases, intermittent antibiotic therapy with cefaclor 500mg TDS or
ciprofloxacin 500 mg BD may be sufficient; Flucloxacillin 500 mg QID is needed if
S. aureus is isolated
• If sputum remains yellow or green despite regular physiotherapy and
intermittent antibiotic therapy, or if lung function deteriorates despite
treatment with bronchodilators, Pseudomonas aeruginosa infection is likely
• Treatment requires parenteral or aerosol chemotherapy at regular 3-month intervals
• Ceftazidime 2 g IV TDS or by inhalation (1 g BD) has been shown to be effective
• Ciprofloxacin 750 PO BD may work in the short term, but resistance can develop rapidly
 Treatment

Bronchodilators
• Bronchodilators are useful in patients with demonstrable airflow limitation

Anti-inflammatory agents
• Inhaled or oral steroids can decrease the rate of progression

Surgery
• Unfortunately, it is rare for bronchiectasis to be sufficiently localized for
resection to be practical
• Lung or heart–lung transplantation is sometimes required
 Complications

Haemoptysis
• Pneumonia
• Severe, life-threatening haemoptysis can also
• Pneumothorax occur, particularly in patients with cystic
• Empyema fibrosis
• Metastatic cerebral abscess • Massive haemoptysis originates from the high-
pressure systemic bronchial arteries and has
• Haemoptysis a mortality of 25%
• Other causes of massive haemoptysis include
• pulmonary tuberculosis (most common)
• Aspergilloma
• lung abscess
• Primary and secondary malignant tumours
Prognosis

• The advent of effective antibiotic therapy has greatly improved the

prognosis

• Ultimately, most patients with severe bronchiectasis will develop

respiratory failure

• Cor-pulmonale is another well-recognized complication

• The three pathogens that can cause infective episodes and are difficult
to eradicate are Pseudomonas aeruginosa, Aspergillus fumigatus and
MAI
LUNG ABSCESS
Outline

• Background
• Aetiology
• Clinical features
• Investigation
• Treatment
Background

• Refers to severe localized suppuration in the lung associated with cavity

formation on the chest X-ray, often with the presence of a fluid level, and
not due to tuberculosis
• There are many causes of lung abscess, but the most common is
aspiration, particularly amongst heavy alcohol users following aspiration
pneumonia
• Lung abscesses also frequently follow the inhalation of a foreign body
into a bronchus and occasionally occur when the bronchus is obstructed
by a bronchial carcinoma
• Chronic or subacute lung abscesses follow an inadequately treated
pneumonia
Background

• Abscesses also develop during the course of specific pneumonias,

particularly when the infecting agent is Staph. aureus or Klebsiella
pneumonia

• Septic emboli, usually staphylococci, result in multiple lung abscesses.

(Infarcted areas of lung occasionally cavitate and rarely become infected)

• Amoebic abscesses occasionally develop in the right lower lobe following

trans-diaphragmatic spread from an amoebic liver abscess
Aetiology
 Clinical Features

• The clinical features are persisting and worsening pneumonia associated with
the production of large quantities of sputum, which is often foul-smelling
owing to the growth of anaerobic organisms

• There is usually a swinging fever; malaise and weight loss occur

• The chest signs may be few but clubbing often develops if the condition is
not rapidly cured

• The patient is often anaemic with a high ESR and CRP

 Investigation
• Lung abscess can usually be detected with standard chest x-ray
• CT-scan is preferred for precise definition of the abscess and its
location, and possibly for detection of underlying lesions
• Bacteriological investigation of lung abscess and empyema is best
conducted on specimens obtained by transtracheal aspiration, bronchoscopy
or percutaneous transthoracic aspiration with ultrasound or CT guidance
• Bronchoscopy is helpful to exclude carcinomas and foreign bodies
• Microbiologic studies include stains and cultures of expectorated
sputum to detect aerobic bacterial pathogens
• In appropriate settings, it is important to consider cultures for fungi
and mycobacteria
Treatment

• Although anaerobic organisms are found in up to 70% of lung abscesses

there is usually a mixed flora
• Appropriate antibiotic treatment is given for up to 6 weeks
• Antibiotics should be given to cover both aerobic and anaerobic
organisms
• An appropriate initial choice is cefuroxime1 g i.v. 6-hourly and
metronidazole 500 mg i.v. 8- hourly for 5 days, followed by oral cefaclor
and metronidazole for a prolonged period depending on bacterial
sensitivities
EMPYEMA
Outline

• Introduction
• Aetiology
• Pathology
• Clinical features
• Investigations
• Treatment
 Introduction

• Empyema is the collection of pus within the pleural cavity

• The pus may be as thin as serous fluid or so thick that it is impossible to
aspirate even through a wide-bore needle
• This usually arises from bacterial spread from a severe pneumonia or after
the rupture of a lung abscess into the pleural space
• Empyema may involve the whole pleural space or only part of it
('loculated' or 'encysted' empyema) and is usually unilateral
• Typically an empyema cavity becomes infected with anaerobic organisms
and the patient is severely ill with a high fever and a neutrophil
granulocytosis
 Aetiology

• Empyema is always secondary to infection in a neighbouring structure,

usually the lung, most commonly due to the bacterial pneumonias and
tuberculosis
• Over 40% of patients with community-acquired pneumonia develop an
associated pleural effusion ('para-pneumonic' effusion) and about 15% of
these become secondarily infected
• Other causes are infection of a haemothorax following trauma or surgery,
oesophageal rupture and rupture of a subphrenic abscess through the
diaphragm
• Despite availability of antibiotics effective against pneumonia, empyema
remains a significant cause of morbidity and mortality even in developed
countries due delays in diagnosis or the initiation of appropriate therapy
Pathology

• Both layers of pleura are covered with a thick, shaggy inflammatory

exudate

• The pus in the pleural space is often under considerable pressure, and if
not adequately treated;
• pus may rupture into a bronchus causing a bronchopleural fistula and
pyopneumothorax
• pus may track through the chest wall with the formation of subcutaneous abscess or
sinus
 Pathology

• Empyema will only heal if infection is eradicated and empyema space is

obliterated, allowing apposition of visceral and parietal pleura
• This occur if re-expansion of the compressed lung is secured at an early
stage by removal of all pus from the pleural space
• Successful re-expansion and resolution will not occur if:
• the visceral pleura becomes grossly thickened and rigid due to delayed treatment or
inadequate drainage of infected pleural fluid
• pleural layers are kept apart by air entering the pleura through a bronchopleural
fistula
• there is underlying disease in the lung, such as bronchiectasis, bronchial carcinoma or
pulmonary TB preventing re-expansion
• In these circumstances an empyema tends to become chronic, and healing
will only occur with surgical intervention
Clinical Features

• Empyema should be suspected in patients with pulmonary infection if

there is persisting or recurrent pyrexia despite treatment with a suitable
antibiotic
• In other cases the primary infection may be so slight that it passes
unrecognised and the first definite clinical features are due to the
empyema
• Once an empyema has developed, systemic features are prominent:
• Pyrexia, usually high and remittent
• Rigors, sweating, malaise and weight loss
• Polymorphonuclear leucocytosis, high CRP
Clinical Features

Local features
• Pleural pain
• Breathlessness
• Cough and sputum production usually because of underlying lung disease
• Copious purulent sputum if empyema ruptures into a bronchus
(bronchopleural fistula)
• Clinical signs of pleural effusion
• Reduced expansion
• Stony dull percussion
• Abscent breath sounds
 Investigation
Chest X-ray
• The appearances may be indistinguishable from those of pleural effusion
• When air is present in addition to pus (pyopneumothorax), a
horizontal 'fluid level' marks the air/liquid interface
Ultrasound
• Shows the position of the fluid, the extent of pleural thickening and
whether fluid is in a single collection or multi-loculated by fibrin
and debris
CT Scan
• Gives information on the pleura, the underlying lung parenchyma
and patency of the major bronchi
 Investigation
Aspiration of fluid
• Ultrasound or CT is used to identify the optimal site to undertake
aspiration, which is best performed using a wide-bore needle
• If the fluid is thick and turbid pus, empyema is confirmed
• Other features suggesting empyema include;
• Fluid glucose < 3.3 mmol/L (60 mg/dL)
• LDH > 1000 U/L
• Fluid pH < 7.0 (H+ >100 nmol/L)
• The pus is frequently sterile on culture if antibiotics have already been
given
• The distinction between tuberculous and non-tuberculous disease can be
difficult and often requires pleural biopsy, histology and culture
 Treatment
Non-tuberculous empyema
• When the patient is acutely ill and the pus is thin, a wide-bore intercostal tube
should be inserted into the most dependent part of the empyema space and
connected to an underwater-seal drain system
• If the aspirate is turbid fluid or frank pus, or if loculations are seen on ultrasound,
the tube should be put on suction and flushed regularly with 20 mL normal saline
• An antibiotic directed against the organism causing the empyema should be given
for 2-4 weeks
• Empirical antibiotic treatment (e.g IV co-amoxiclav or cefuroxime with
metronidazole) should be used if the organism is unknown
• An empyema can often be aborted if these measures are started early
• When the pus is very thick or loculated, surgical intervention is required
 Treatment

Tuberculous empyema
• Anti-TB chemotherapy must be started immediately and the pus in the
pleural space aspirated through a wide-bore needle (or intercostal tube)
until it ceases to reaccumulate

• In many patients, no other treatment is necessary but surgery is

occasionally required to ablate a residual empyema space

• Fibrothorax, with restriction and encasement of the lung in thickened,

often calcified pleura is a late complication
Questions