Bronchiectasis, lung abscess, and empyema are chronic lung infections that can result from complications of pneumonia. They often occur in people with underlying lung disease or immune disorders. Key features include recurrent chest infections, coughing, sputum production, and life-threatening complications like respiratory failure. Treatment involves identifying and addressing the underlying cause, airway clearance techniques, long-term antibiotics, and surgery in some cases.

1. DR BABASHANI M.
MBBS,FWACP,FCCP
SUPPURATIVE LUNG
DISEASES

2. CHRONIC LUNG SEPSIS
BRONCHIECTASIS
LUNG ABSCESS
EMPYEMA

3. INTRODUCTION
• Lung abscess, bronchiectasis, and empyema represent
uncommon chronic lung infections and may reflect
complications of pneumonia.
• These pulmonary infections remain important clinical
entities and can occur in persons with structural lung
disease, genetic abnormalities, and disorders of innate or
acquired immunity.
• These chronic pulmonary infections can cause debilitating
and life-threatening medical complications.

4. BRONCHIECTASIS
 Definition- Irreversible abnormal dilatation of one
or more bronchi, with chronic airway inflammation
associated with chronic sputum production,
recurrent chest infections and airflow obstruction.
 Prevalence is unknown

5. Pathophysiology
 An initial damage to the airways
 Abnormal anatomical changes
 Accumulation of secretions and secondary infection,
ongoing inflammation and further airway damage.
 Mucosal oedema, inflammation and ulceration of major
airways.
 Obstruction of terminal bronchioles with secretions .
 Lung volume loss.
 Chronic inflammatory response ensues, with free radical
formation and the production of neutrophil elastase
contributing to further inflammatory process.
 Bronchial neovascularisation with hypertrophy and
tortuosity of vessels and subsequent haemoptysis.

7.  The most frequent pathogens isolated were
Haemophilus influenzae (55%), Pseudomonas spp.
(26%), and Streptococcus pneumoniae (12%)-
Angrill et al.
 Risk factors associated with bronchial colonization
by Pathogens including (1) diagnosis of
bronchiectasis before age 14 years; (2) FEV1 < 80%
predicted; and (3) presence of varicose or cystic
bronchiectasis. Patients colonized with Pathogens
demonstrated worse lung function compared with
patients not colonized .
Potential Pathogens

8. Role of Immune Function
 The role of host humoral deficiencies in the etiology of
bronchiectasis is unclear.
 Antibody deficiency was an uncommon etiologic or
underlying factor in the causation of bronchiectasis
beyond the fourth decade and that detailed investigation
of humoral immune status in bronchiectasis patients
may not be warranted.
 Allergic bronchopulmonary aspergillosis (ABPA)
patients with central bronchiectasis had higher IgE titers
and worse pulmonary function testing compared with
ABPA patients with no associated bronchiectasis.

9. Aetiology
Genetic
 Cystic fibrosis
Congenital
 Pulmonary sequestration
Post-infective
 Tuberculosis
 Whooping cough (if infection in a localized area).
 Non- Tuberculous Mycobacteria (NTM)- there is some
debate as to whether the bronchiectasis seen in
association with NTM (classically in elderly females) is
caused by, or secondarily infected by NTM.

10. Aetiology
Immune deficiency
 Primary- hypogammaglobulinaemia
 Secondary- HIV,CLL, nephrotic syndrome
excessive immune response.
Mucociliary clearance abnormalities
 Primary ciliary dyskinesia
 Kartagener’s syndrome
 Young’s syndrome (bronchiectasis, sinusitis and
azoospermia- i.e. clinical features identical to those
of CF)

11. Aetiology
Toxic insults
 Aspiration
 Inhalation (toxic gases, chemicals)
Mechanical insults
 Foreign body aspiration
 Extrinsic lymph node compression
 Intrinsic (intraluminal) obstructing tumor

12. Aetiology
Associations
 Bronchiectasis is associated with a number of systemic
diseases,
 Rheumatoid arthritis (up to 35% of RA patients have
bronchiectasis)
 Connective tissue diseases, e.g. Sjogren’s syndrome,
SLE.
 Ulcerative colitis and Crohn’s disease
 Chronic sinusitis
 Yellow nail syndrome
 Marfan’s syndrome

13. Clinical features
Symptoms
 Cough
 Chronic sputum production (typically tenacious, purulent,
and daily)
 Intermittent haemopytses
 Breathlessness
 Intermittent pleuritic pain (usually in association with
infections)
 lethargy)/malaise
Signs
 Coarse inspiratory and expiratory crackles on auscultation
 Airflow obstruction with wheeze
 Digital clubbing ,Anemia, Cyanosis

14. Investigations
Essentials
 HRCT chest is 97% sensitive in detecting disease.
 Typically shows airway dilatation to the lung periphery,
bronchial wall thickening and airway appearing larger
than its accompanying vessel (signet ring sign).
HRCT of the chest useful in:
 Confirming the diagnosis
 Identifying a treatable underlying cause for the
bronchiectasis (possible in about 40%)
 Optimizing management to prevent exacerbations and
further lung damage.

15. Investigations
 Airway obstruction best correlated with HRCT evidence for
bronchial wall thickening , and did not correlate with
endobronchial secretions.
 Negative correlation b/w severity of bronchial dilatation by
HRCT and airflow obstruction by Pulm. Function Tests.
 Airflow obstruction is linked to the disease of small and
medium airways and not to bronchiectatic abnormalities in
large airways, emphysema, or retained endobronchial
secretions.
 Severity of bronchial wall thickness is the primary
determinant of major decline in PFTs.

16. Investigations
 CXR sensitivity is only 50%, classically shows ‘ring
shadows 'and ‘tramlines’-indicating thickened
airways, and the ‘gloved finger’ appearance-
consolidation around thickened and dilated airways.
 Sputum microbiology standard M,C and S
(including for atypical organisms), acid fast bacilli
and Aspergillus.
 Pulmonary function tests with reversibility testing
 Aspergillus precipitins

17. Investigations
Second line investigations
 CF genotyping
 ANA, RF, ds DNA
 Vaccination response to tetanus, Haemophilus
influenzae, and pneumococcal antibodies, if
underlying immunosuppression suspected
 Skin tests/RAST to identify specific sensitizers
(Usually Aspergillus )
 Immunological investigation (including neutrophil
and lymphocyte function studies)
 Bronchoscopy

18. Investigations
 Nasal brushings/biopsy to access ciliary beat
frequency with video microscopy
 Saccharin test. The time for saccharin to be tested
in the mouth after deposition of a 0.5 mm particle
on the inferior turbinate of the nose. Normal is less
than 30 minutes.
 Alpha 1-antitripsin levels if deficiency
 Barium swallow/ oesophageal imaging if recurrent
aspiration suspected.

20. Bronchogram used historically to
diagnose bronchiectasis. There is
bronchial dilatation in the left lower
lobe in keeping with left lower lobe
bronchiectasis (one area is
arrowed).

21. Chest CT scan from a patient
with
tubular bronchiectasis, in
which the
bronchus has a thick wall a

22. CXR- bil cystic
bronchiectasis

23. A chest radiograph from a
patient
with cystic bronchiectasis,
showing
large thin walled cysts that
often
contain mucus.

25. Chest radiograph from a
patient
with cystic fibrosis and
bilateral
bronchiectasis.

26. Chest CT scan from a patient
with
cystic bronchiectasis,
showing cystic
lesions (one example is
arrowed) that
are often fluid filled.

27. Macroscopic picture of
lung tissue
with cystic bronchiectasis
(one
example is arrowed).

28. Lung with
bronchiectasis showing
dilatation of the airway with
inflammation in the
wall associated with fibrous
scarring

29. Gram stain of sputum samples
from two patients with cystic
bronchiectasis infected with mucoid
(right panel) and non mucoid (left
panel) Pseudomonas aeruginosa.
(Courtesy of Prof. J.Govan, University
of Edinburgh, Scotland.)

30. Management
 Main aims are:
 Treatment of any underlying medical condition
 Prevention of exacerbations and progression by
physiotherapy
 Options of airway clearance include:
 postural drainage
 active cycle of breathing technique- this involves
breathing control wt forced expiration (huffing)
using variable thoracic expansion
 Cough augmentation- using flutter valves/cough
insufflator /high frequency oscillation
 exercise regimes- important to prevent general
deconditioning

31. Aims of Mx –cont’d
 To reduce bacterial load and prevent secondary
airway inflammation and damage, with
antimicrobial chemotherapy
 To give treat associated airflow obstruction
 To optimize nutrition
 To refer to surgery if necessary for localized
resection of affected area
 To refer for transplantation if indicated

32. Antimicrobial therapy
 May be intermittent only ( mild ), or long term for more
severe disease
 Antibiotics may be oral, nebulized or intravenous
 Regular sputum microbial surveillance
 In vivo sensitivity may be different to in vitro sensitivity
 Higher antibiotic dose for longer duration (usually
minimum of 2wks)
 Choice of antibiotics depends on severity of disease
 Treatment response is usually assessed by a reduction in
sputum volume with improvement in systemic symptoms,
spirometric indices and CRP.

33. Bacterial colonization
 Pseudomonas colonized lungs have more frequent
exacerbations & worse CT scan appearances
 Different bacteria colonize the airways at different
stages of the disease.
 Eradication and suppressive treatment is vital .
 The usual freq of colonization is:
 Staph aureus
 Haemophilus influenzae
 Moraxella catarrhalis
 Pseudomonas species

34. Exacerbation
 A clinical diagnosis- increase in sputum volume and
tenacity & discoloration.
 Chest pain, haemoptysis and wheeze & systemic
symptoms- fever, lethargy and anorexia. Elevated CRP.
 Mild - antibiotics for exacerbation only (tailored to the
colonizing organism)
 Two-wk course of oral ciprofloxacin at 750mg bd if
Pseudo colonized
 If early relapse occur within 6-8wks, consider long term
oral antibiotics e.g. amoxicillin/ doxycycline

35. Severe Exacerbation
 Chronic suppressive AB to prevent progression
 Antibiotics for at least 2 days after sputum has cleared-
often 2 wks
 Intravenous may be required if oral AB fails .
 First isolation of Pseudomonas aeruginosa should be
treated aggressively
• Ciprofloxacin 750mg bd for 4- 6wks and,
• Concurrent nebulized Aminoglycoside e.g.
colomycin 1-2 mega units bd
• If this fails and Pseudomonas sputum culture +ve
give IV Aminoglycoside & anti pseudo penicillin for
min. of 2wks
• Long term therapy with nebulized Aminoglycosides

36. Further Mx
 Self management plan
 Treatment of associated airflow obstruction/wheeze with
inhaled steroids and/or bronchodilators(beta agonist,
anticholinergic)
 Anti-inflammatory –steroids,
 Β agonist may enhance Mucociliary clearance
 Nebulized DNase (Dornase alpha) for CF bronchiectasis
only
 N- acetylcysteine
 Annual influenza and pneumococcal vaccinations
 Osteoporosis prophylaxis if on long term steroids
 Treat Reflux if aspiration
 Immunoglobulin replacement

37. Further Mx
 Immunoglobulin replacement therapy.
 Surgery .
 Transplant.

38. Complications
 Infective exacerbation
 Haemoptysis-small volume (increases during
exacerbation)
 Massive haemoptysis- Life threatening emergency
 Pneumothorax
 Respiratory failure
 Brain abscess
 Amyloidosis

39. LUNG ABSCESS
 Definition- Necrosis of the pulmonary tissue and
formation of cavities containing necrotic debris or
fluid(suppuration) caused by microbial infection.
 Multiple (<2 cm) pulmonary abscesses is referred to as
necrotising pneumonia or lung gangrene.
 May be acute or chronic(>1 month)
 Primary or secondary
 Occur spontaneously , but often associated with
underlying disease
 May also be characterized based on resp. pathogen;
staph lung abscess or anaerobic or Aspergillus lung
abscess.
 Mortality- 20 to 30 % .

40. A thick-walled lung abscess

41. Pathophysiology
Aspiration of oropharyngeal flora
 Dental /periodontal sepsis
 Paranasal sinus infection
 Depressed conscious level
 Alcohol /sedative drug abuse
 Anesthesia
 Epilepsy
 Head injury
 Cerebrovascular accident
 Diabetic coma
 Other prostrating illness

42. Pathophysiology
 Impaired laryngeal closure
 Recurrent laryngeal nerve palsy
 Disturbances of swallowing
 Oesophageal stricture (benign or malignant)
 Oesopharyngeal motility disorders e.g. systemic sclerosis
 Neuromuscular disease, e.g. bulbar /pseudo bulbar palsy
 Achalasia
 Pharyngeal pouch
 Neck surgery
 Delayed gastric emptying/gastro-oesophageal reflux or
vomiting

43. Pathophysiology
Pneumonia
 Staphylococcus aureus
 Streptococcus milleri
 Klebsiella pneumoniae
 Pseudomonas aeruginosa
Hematogenous
 UTI
 Abdominal sepsis
 Pelvic sepsis
 Septic embolisation( R-sided Infective endocarditis)-IVDA
 Infected intravenous cannulae
 Septic thrombophlebitis

44. Pathophysiology
Structural lung disease
 Bronchiectasis
 Cystic fibrosis
 Bronchial obstruction
Tumour
foreign body
congenital abnormality
Infected pulmonary infarct
Trauma
Immunodeficiency -Primary or acquired

45. Pathophysiology
 Areas of necrosis develop within consolidated lung
 Coalesced areas form suppuration.
 With little or no treatment, inflammatory process
may progress into a chronic phase.
 Bronchial wall becomes eroded and the purulent
contents of the abscess may be expectorated as
foul sputum
 Fibrosis may occur and the abscess become
loculated and walled off
 Abscess may directly spread to adjacent
bronchus .

46. Pathophysiology
 Spillage of pus into the bronchial tree may also
serve to disseminate infection either to other parts
of the same lung or to the opposite lung
 Three quarters of lung abscess occur in the
posterior segment of the rt upper lobe or the apical
segments of either lower lobe.
 These segments are anatomically disposed to
accept the passage of aspirated liquid in the supine
position

47. Pathophysiology
 Lung abscess are usually close to the visceral
pleural, however spread of infection through the
membrane with resultant empyema is not the rule
 This occur in less than one-third of cases
 Lung abscess that occur as a result of
heamatogenous spread may be found in any part of
the lungs

48. Clinical
 Often insidious onset
 Productive cough ± haemoptysis
 Breathlessness, pleurisy
 Fevers, anorexia, wt loss
 Night sweats
 Non-specific features of infection – anemia, wt
loss, malaise (especially in the elderly)
 Expectorated sputum is foul smelling and bad
tasting.

49.  Oropharyngeal infection affecting young healthy adults.
 From jugular vein suppurative thrombophlebitis
 Rare pharyngeal infection caused by Fusobacterium
necrophorum.
 Presents with painful pharyngitis & bacteraemia
 Infection spreads to the neck and carotid sheath, leading to
thrombosis of internal jugular vein
 Septic embolisation to the lung with subsequent cavitation,
and abscess formation.
 Complications include empyema , abscesses in the bone,
joints, liver, and kidneys.
Lemierre’s syndrome (necrobacillosis)

50. Differential diagnosis of a cavitating mass
 Cavitating carcinoma- primary or metastatic
 Lymphoma(thick-walled)
 Parasitic- echinococcus,paragonimiasis, amoebiasis
 Cavitatory TB
 Wegener’s & churg-strauss granulomatoses
 Infected pulmonary cyst or bulla
 Fungal- aspergilloma, coccidioidomycosis
 Pulmonary infarction
 Rheumatoid nodule
 Sarcoidosis
 Bronchiectasis

51. Workup
 Microbiological culture ideally should be done before
commencement of antibiotics
 Exclude TB
 Blood culture
 History along with the appearance of a cavity with
associated air fluid level on CXR
 FBC
 Sputum or bronchoscopic specimen MCS
 Transthoracic Percutaneous needle aspiration (CT or US
guided) may provide samples.

52. Imaging
 Imaging helps to exclude aspirated foreign body,
underlying neoplasm, or bronchial stenosis and obstruction
 CXR may show consolidation, cavitation, air-fluid level.
 50% of abscesses are in the posterior segment of the R
upper lobe, or the apical basal segments of either lower lo
 CT is useful if the diagnosis is in doubt and can define the
exact position of the abscess which may be useful for
physiotherapy or surgery.
 CT is also useful to differentiate an abscess from a pleural
collection.
 An abscess appears as a rounded intrapulmonary mass.
 An empyema typically has a `lenticular` shape.

53. Pneumococcal
pneumonia
complicated by
abscess
formation

54. A lateral CXR
showing air-
fluid level in a
lung abscess

56. Microbiology
 Commonly mixed infection, usually anaerobes
 Organisms colonizing the oral cavity and gingival crevices-
Peptostreptococcus, Prevotella, Bacteroides,
Fusobacterium species
 Aerobes- Streptococcus milleri, Staphylococcus aureus,
Klebsiella species, Streptococcus pyogenes. Haemophilus
influenzae, Nocardia
 Non-bacteria pathogens-fungi (Aspergillus, Cryptococcus ,
Histoplasma, Blastomyces) and mycobacteria
 Immunocompromised - Nocardia, Mycobacterium,
Aspergillus

57. Management
Antibiotics
 To cover anaerobic and aerobic infection, including β - lactamase
inhibitors, e.g. co- amoxiclav and clindamycin
 Long courses are needed with risk of Clostridium difficile diarrhea
 Infections are usually mixed therefore antibiotics to cover these
 Metronidazole to cover anaerobes
 Ampicillin plus sulbactam is as effective as clindamycin +/-
cephalosporin in the treatment of aspiration pneumonia and lung
abscess.
 Moxifloxacin is as effective as ampicillin +sulbactam in asp
pneumonia & lung abscess
 Give intravenous therapy for 1-2 wks, with further oral antibiotics
for 2-6wks, often until out-patient clinic review.

58. Drainage
 Spontaneous drainage is common with production of
purulent sputum, augmented with postural drainage and
physiotherapy
 No data to support use of bronchoscopic drainage
 Percutaneous drainage with radiologically placed small
percutaneous drains for peripheral abscess may be useful in
those failing to respond to antibiotic.

59. Surgery
 Rarely needed.
 Indicated if no significant improvement after 6wks of
antibiotics.
Indications :
 Very large abscess (>6cm diameter)
 Resistant organisms
 Hemorrhage
 Recurrent disease
 Lobectomy or pneumonectomy is occasionally needed if
severe infection with an abscess leaves a large volume of
damaged lung that is hard to sterilize

60. Complications & Prognosis
Complications
 Hemorrhage , may be massive.
 Respiratory failure
 Bronchopleural fistula
 Pleural fibrosis
 Pleural cutaneous fistula
 Empyema
Prognosis
 85% cure rate in the absence of underlying disease
 Mortality is reported as high as 75% in the Immunocompromised
pts.
 The prognosis is much worse in the presence of underlying lung
disease, with increasing age, large abscesses (>6cm) and Staph
aureus .

61. THANK YOU