Suppurative lung diseases, Dr Inofomoh Francisca,

GRAND ROUND PRESENTATION
RESPIRATORY UNIT
JANUARY 2015.
26/06/2016INOFOMOH F.O.

Suppuration – “pus forming”
These are disorders associated with pus
formation within the lungs and are named
according to site;
 Bronchi---- bronchiectasis
 Lung parenchyma--- Lung abscess
 Pleural space- ---Empyema

 DEFINITION
 CLASSIFICATION
 EPIDEMIOLOGY
 AETIOLOGY
 PATHOPHYSIOLOGY
 CLINICAL FEATURES
 DIAGNOSIS/INVESTIGATIONS
 DIFFERENTIALS
 TREATMENT
 COMPLICATIONS
 PROGNOSIS

 This is as an abnormal irreversible,
dilatation of one or more bronchi or
bronchioles, large and small sized airways,
with destruction of their elastic and
muscular components,
 usually due to an acute or chronic infection
resulting in recurrent inflammation, airflow
obstruction and impaired clearance of
secretions.

 Bronchiectasis is a syndrome of chronic
cough and daily viscid sputum production
associated with airway dilatation and
bronchial wall thickening.
 Classified as an obstructive airway disease.
 May be focal or diffused.

 Currently there are no estimates of the
incidence but its prevalence varies by
country, region and underlying aetiology.
 Prevalence mirrors the socioeconomic
conditions of population under study.
 There is a decline in its prevalence in
developed countries with emergence of
vaccines and antibiotics in the 20th century.
 Overall it increases with age.
 More common in women than men.

 ADEBONOJO ET AL IN 1979 reported At UCH
54patients treated for bronchiectasis.
Also in 1982“Suppurative DISEASES of
the lung – a continuing challenge in
developing countries” 1,150patients
IN 2009, OLUFEMI DESALU ET AL reported
at FMC, Ido Ekiti 183 patients

 CONGENITAL CAUSES;
 CYSTIC FIBROSIS
 YOUNGS SYNDROME
 PRIMARY CILIARY DYSKINESIA
 KARTAGENERS SYNDROME
 ALPHA 1-ANTITRYPSIN DEFICIENCY
 PAN HYPOGAMMAGLOBULINEMIA
 WILLIAMS CAMPBELL SYNDROME
 MOORNIER- KUNN SYNDROME
 YELLOW NAIL SYNDROME
 AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY
DISEASE

 ACQUUIRED CAUSES
 POST INFECTIONS –Bacteria ;typical
organisms are
 Haemophilus influenzae
 St. pneumoniae
 Moraxella catarrhalis
 Pseudomonas aeruginosa
 Staph aureus

 Other bacteria causes includes;
 Mycobacterium tuberculosis
 Non-tuberculosis mycobacterium(MAC)
 Klebsiella spp
 Mycoplasma pnemonia
 Viral infections; measles, influenza,
whooping cough, herpes simplex, certain
types of adenovirus.
 Fungi- aspergillosis


 Diffuse disease of lung parenchyma; idiopathic
pulmonary fibrosis.
 Granuloma; sarcoidosis
 Mechanical obstruction ;intrinsic(foreign body
aspiration, insipatted mucus ,tumour
 Extrinsic (lymph node, tumour)
 Immune mediated diseases; ABPA, post lung
transplant.
 MIDDLE LOBE SYNDROME
 Autoimmune /rheumatologic diseases;
 Traction bronchiectasis
 Toxic gas exposure ; chlorine, ammonia gas.

1 ATELECTASIS:
2 TRACTION
3 MIDDLE LOBE SYNDROME
4 VISCIOUS CYCLE HYPOTHESIS

PATHOLOGICAL CLASSIFICATION
 Cylindrical or tubular bronchiectasis
 Varicose
 Saccular or cystic bronchiectasis

 A typical history of chronic cough productive
of thick tenacious sputum.
 Foetor Oris
 Fever
 Dyspnoea
 Wheezing
 Pleuritic chest pain
 Dizziness, weight loss.
 Haemoptysis

 No specific signs for diagnosis
 Pallor
 Cyanosis or plethora from chronic hypoxia
 Tachycardia
 Crackles/rales
 Respiratory failure
 Cor pulmonale
 Nb: In Acute exacerbation-

 COPD
 Bronchial asthma
 Empyema thoracis
 Lung abscess
 Recurrent pneumonia
 Bronchial tumour
 Tuberculosis
 GERD

 IMAGING;
 Chest X-ray;
 Thickened bronchial wall
 Tram track lines
 ring(signet)shadows
 Gloved finger appearance
 May be normal

Cystic spaces with peril-bronchial
fibrosis
ABPA, hyperinflation and proximal
mucus plugging
Multiple bibasal
air-fluid levels

Image modality of choice. It has largely
replaced bronchography It’s the gold
standard for detecting bronchiectasis.
97% sensitivity
93-100% specificity.
 It shows
 airway dilatation(tram track lines)
 Signet ring shadows(airway diameters at
least 1.5times >adjacent vessels.
 Lack of bronchial tappering
 Inspissated secretions(tree in bud

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

Cylindrical bronchiectasis Varicose bronchiectasis Saccular bronchiectasis

Signet ring appearance
Air-fluid level in cystic
bronchiectasis
Mucus plugging in ABPATree in bud appearance

 Pulmonary function test
 Complete blood count and differentials
 Gram stain and cultures for AFB,Fungi
 Quantitative immunoglobin levels
 Quantitative alpha 1-antitrypsin levels
 BAL for culture, stains
 Pilocarpine ionotophoresis(sweat test)+genetic
analysis
 Aspergillus precipitins and serum total IgE levels
 Autoimmune serological markers
 Electron examination of sperm, respiratory
epithelium

Goals of therapy:
 Eradication of infection
 Improve secretion clearance.
 Relieving airway obstruction
 Reducing complications
 Prevent exacerbations and improve
quality of life.

 MODALITIES;
 Antibiotics
 Bronchial hygiene
 Anti inflammatory
 Supportive therapy
 Surgical options

 A broad spectrum against most suspicious
pathogens.
 Guidelines says IV in acute exacerbation for
7-14days in high doses, or until symptoms
resolves or significant imaging resolution
 Most antibiotics recommended for post
infectious causes while waiting for
bacteriology results includes;

 Amoxicillin
 Amoxi/clavlanic
 Tetracycline
 Trimethoprim /sulfamethazole
 Azithromycin/clarithromycin
 A fluoroquinolone
 2nd generation cephalosporins
 For Pseudomonas aeuruginosa- IV gentamicin
+tobramycin+3rd generation cephalosporins.

 ‘Macrolides may have disease modifying
activity’
 Do not mix with IV aminoglycosides (increased
risk of auditory problems)
 For MAC, the ATS recommends 3-4 drug
regimen with clarithromycin, Rifampin,
ethambutol, streptomycin until cultures are
negative for 1yr.
 long term antibiotic regimen.
 Nebulised amoxicillin, azithromycin,
tobramycin.
Draft BTS Guidelines 2008

 HYDRATION
 MUCOLYTICS
 AEROSOLIZED BRONCHODILATORS
 HYPEROSMOLAR AGENTS
 CHEST PHYSIOTHERAPY
 DNASE for cystic fibrosis patient

 Mechanical chest percussion by hand
clapping of the chest.
 Use of oscillatory positive expiratory
pressure fluutter valve.
 Use of high frequency chest wall oscillation
vest.
 Short acting inhaled bronchodilators can be
given before physiotherapy, if there is an
asthmatic component.
 Oral indomethacin has also been shown to
reduce sputum volume but it has not been
approved.

 ANTI INFLAMMATORY
 Smoking ceasation
 Avoidance of secondary/ passive smokers
 Nutritional supplememts
 Immunization for influenza and
pneumococcal infections
 Oxygen therapy in severe cases
 NEW THERAPY Use of QBw251 drug that
increase activity of CFTR IN Cystic fibrosis

 Persistent infections in bronchiectatic area
refractory to medical treatment
 Massive haemoptysis; resection or bronchial
artery embolisation.
 Foreign body or localized tumour
 Lung transplantation; highly considered if
FEV1 is <30%of predicted, inan females, and
in younger patients.

 FOLLOWING SURGERY;
 EMPYEMA
 HAEMORRHAGE
 PNEUMOTHORAX
 LUNG ABSCESS
 MASSIVE HAEMOPTYSIS
 METASTATIC CEREBRAL ABSCESS
 ASPERGILLOMA
 MALIGNANT TUMOURS

 Life Threatening haemoptysis
 Bilateral lung involvement
 Associated lung abscess
 Malnutrition
 Chronic anaemia
 Frequency of exacerbation
 Specific pathogens; PAS ,Aspergillus, MAC

 Lung abscess is necrosis of
the pulmonary tissue and formation of
cavities (more than 2 cm) containing necrotic
debris or fluid caused by microbial infection.
 Lung gangrene refers to formation small
multiple abscesses(Necrotizing pneumonia).
 PUTRID are Anaerobic bacterial lung abscess
which are characterized by distinctive foul
smelling breath, sputum or empyema.

This pus-filled cavity is often caused by
aspiration, which may occur during
altered consciousness.

 Based on duration; Acute or Chronic
 presence or absence of underlying lesion;
primary(60%) or secondary
 Pathogen involved;
 staphylococcus lung abscess
 Anaerobic lung abscess
 Lemierre’s disease– fusobacterium
necrophorum.
 Aspergillus lung abscess
 Non specific lung abscess

47
Aspiration pneumonia from;
oropharyngeal flora
 Dental/periodontal sepsis
 Paranasal sinus infection
 Depressed conscious level
Alcohol/sedative drug abuse
Anaesthesia
Epilepsy
Head Injury
CVA/Coma

 IMPAIRED LARYGNEAL CLOSURE
Prolonged endotracheal intubation
Tracheostomy tube
Recurrent laryngeal nerve palsy
 DISTURBANCES OF SWALLOWING
Oesophageal stricture, Achalasia, Reflux dx
Oesophageal motility disorder eg systemic
sclerosis
Neuromuscular disease, eg
bulbar/pseudobulbar palsy

NECROTIZING PNEUMONIA
Staphylococcus aureus
Streptococcus milleri/intermedius
Klebsiella pneumoniae
Pseudomonas aeruginosa
HAEMATOGENOUS SPREAD FROM A DISTAL SITE
UTI
Abdominal sepsis AMEBIC LUNG ABSCESS
Pelvic sepsis SEPTIC EMBOLI
Infective endocarditis (right side)
METASTATIC LUNG ABSCESS

50
 Bacteria reaches lower airways, are not cleared by the
patient’s host defense mechanism
 Results in aspiration pneumonitis and progression to
tissue necrosis in 7-14 days later → lung abscess
 Other mechanisms:-
 Bacteremia – from area of focus of Gram-negative sepsis, or
anaerobic infection spread haematogeneously, septic emboli

 Pneumonitis
necrosis abscess
empyema
(if bronchopleural
fistula occurs or
infection extends
directly into
pleural space)
7-14 days
Pathophysiology

 It runs an indolent course especially in
aspiration pneumonia prone patients.
 History of periodontal infections.
 Symptoms and signs as essentially above.
 Pyoorhea, gingivitis
 Chills are uncommon.
 Lethargy,cachetic

 IMAGING;
 Chest X-ray, Bronchoscopy, HRCT Scan
 Abscess is often unilateral and single
involving posterior segments of the upper
lobes and the apical segments of the lower
lobes as these areas are gravity dependent
when lying down.
 Presence of air-fluid levels implies rupture
into the bronchial tree or rarely growth of
gas forming organism.
 NB;Lymphadenopathy

 Samples; sputum, BAL, transtracheal aspiration,
transthoracic needle aspiration under CT
guidance – all these specimens for
 Gram stain, cultures (aerobic and anaeroibic
bacteria, mycobacteria, fungi)
 Microscopic examination of aspirates
 OTHERS:
 Fibre optic bronchoscopy is often performed to
exclude obstructive lesion; it also helps in
bronchial drainage of pus.
 Raised inflammatory markers (high ESR, CRP)
but not specific.

 Cavitating carcinoma-primary or metastatic
 Lymphoma(thick-walled)
 Parasitic-echinococcus,paragonimiasis,
amoebiasis
 Cavitatory TB
 Wegener’s & churg-strauss granulomatosis
 Infected pulmonary cyst or bulla
 Fungal-aspergilloma, coccidioidomycosis
 Pulmonary infarction
 Rheumatoid nodule
 Sarcoidosis
 Bronchiectasis

 Broadspectrum antibiotic to cover mixed
flora is the mainstay of treatment.
 Pulmonary physiotherapy
 Postural drainage
 Surgical procedures are required in selective
patients for drainage or pulmonary resection.

 First drug of choice is Clindamycin with its
alternative being Penicillin+ metronidazole
 For Gram negatives, Cephalosporins,&
quinolones
 Standard therapy for anaerobes is IV
Clindamycin 600mg 8hrly then 150-300mg PO
 OR IV Amoxiclav or Carbapenems.
 For MRSA use Vancomycin 15mg/kg/12hrly
 OR IV Linezolid 600mg 12hrly.
 For Microaerophilic streptococci infections or
mixed flora, a combination of Metronidazole+
aminoglycoside + fluoroquinolone


 Persistence of fever beyond 5-7 days following
therapy.
 Progression of infiltrates
 Thick walled cavity
 Extremely large abscess >6cm in diameter
 Recurrent aspiration
 RULE OUT
 Obstruction
 Complicating Empyema
 Antibiotic resistant bacteria strains

Failed medical therapy
Suspected neoplasm
Congenital lung malformation
Bronhopleural fistula
Massive haemoptysis
OPTIONS: Lobectomy, pneumonectomy,
surgical drainage.

 INTRATHORACIC
 Rupture into pleural
space
 Pleural fibrosis
 Trapped lung
 Pleuro-cutaneous
fistula
 Respiratory failure
 Pyo pneumothorax
 haemoptysis
 EXTRATHORACIC
 Secondary
Amyloidosis
 Septicemia
 Metastatic brain
abscess

 Over 90% are cured with medical therapy
 Bronchial obstruction secondary to is
carcinoma is of bad prognosis
 Also bad in extremes of Age and other forms
of immunosuppression.

 This is defined as frank pus in the pleural
space. It is grossly purulent usually following
a parapneumonic effusion.
“ Pleural empyema (also known as
a pyothorax or purulent pleuritis) itself is
not a disease, but a condition often
complicating an underlying disease.
 Pus is thick, viscous and opaque with >15,000
neutrophils/ml.

 This is based on duration;
 Acute 6-8 weeks
 Chronic >3months
 OR based of Anatomy
 Loculated(focal) vs free(total)
 Closed or open(following a bronchopleural
fistula or a sinus track).

 PNEUMONIA of any origin causing a
parapneumonic effusion viz;
 Bacterial (accounts for 70% cases)
 3 most common isolated gram +ve aerobic orgs
are Streptococcus pneumonia, Streptococcus
milleri, Staphylococcus aureus)
 Most common gram –ve aerobes are klebsiella,
pseudomonas,haemophilus.
 Bacteriodes most common isolated anaerobes.

 Viral infections
 Atypical pneumonia
• Previous thoracic surgery (20%) ; chest drains,
percutaneous biopsy
• Blood or lymphatic seedling of the pleural
• Traumatic penetration.

 3 Stages are identified but they overlap.
 EXUDATIVE(0-2WKS)
 Interstitial fluid leakage / pus accumulatioin
 Initially sterile with low WBC, LDH, glucose and
pH within normal limits.
 It takes 2-5 days after onset of pneumonia.

 FIBRINOPURULENT PHASE(1-6WKS)
 Bacteria invasion of the pleural space
 Fibrin deposition
 Accumulation of PMN Leukocytes, bacteria
and debris.
 Tendency towards loculation and septation
 pH, glucose decreases as LDH levels rises.
ORGANIZATION PHASE(AS FROM 3WKS)
Fibroblast forms an inelastic membrane
called pleural peel.
- scarring of the pleural space may lead to lung
entrapment
- Presence of very thick pus

 ANAEROBICS;
 Subacute illness
 History of
predisposing factor
 Mild anemia
 Weight loss
 Brisk leukocytosis
 AEROBICS
 Acute onset of chest
pain
 Cough + sputuum
production
 primary infection
often due to
tuberculosis
 No prior history
suggesting
pneumonia

 Chest X-ray; appear as a cloudy or opaque area.
 Loculated or hydropneumothorax.
 C-T scan.
 Ultrasound scan
 Thoracentesis
 Pleural fluid Gram stain and
culture,biochemistry
 Assessment of bronchpleural fistula
 Histology
 Others


 Permits measurement of depth of location
from the chest wall.
 Purulent or viscous complex fluid have more
densities or shadows within the fluid.
 To differentiate loculated fluid from an
infiltrate, this has air bronchograms
intersparsed in it.
 Extent of pleural thickness, 56% exudative PF
 >86% thickness- Empyema

 This is a procedure which involves the
insertion of a needle into the pleural cavity
through the back between the ribs on the
infected side, and a sample of fluid is
withdrawn
 It is performed under local anesthetics
 Samples are sent for pleural fluid studies;
AFB, culture, bichemistry, cell count,
cytology, LDH levels, pH.

 In empyema, result shows
 Fulfills criteria for an exudate
 Wbc- >50,000cells/microL
 LDH>1000 U/L
 Ph < 7.2
 Glucose ,40mg/dl
 Pleural biopsy for histology may be needed , this
shows multiple granulocytes +/- necrotic debris.

 GOALS;
1. Control of infection and sepsis by
antibiotics.
2. Evacuation of pus from pleural space.
3. Obliteration of the empyema cavity.
Antibiotics- use – as above.IV FOR 2WKS.
 Delay in drainage increase mortality from
3.4% to 16%.
 Empyema is treated using a combination
of medications and surgical techniques

 Late-phase: continuous drainage or surgical
debridement & decortication.
 Performed under general anesthesia
 Done for the dependent rib
 Open all the intact cyst that leads to
conversion of empyema with free pus
 Then place intercostal tube for drainage and
close the wound
 Antibiotics should continue for 6 weeks

 Studies used Streptokinase or Urokinase,rTPA
or altepase
 Most effective in the early fibrinopurulent
stage and may make surgical drainage
unnecessary.
 CTScan predicts failure if pleural thickening
is <2mm.
 Potential adverse effects includes: Bleeding,
Bronchopleural fistula .

 Intercostal tube thoracostomy.
 Intrapleural instillation of streptokinase .
 Decortication
 Pleurectomy
 Videoscopic Assisted Thoracoscopy Surgery
(VATS)
 Rib Resection Drainage.
 OPEN drainage via Eloesser Flap

 Persistent indolent infections
 Osteomyelitis of the rib
 Tuberculous abscess
 Septicemia,septic shock
 Trapped lung.

 Respiratory infections remains a major
burden on our health infrastructure.
 Most common and earliest complaints is
productive cough, this should be properly
treated with prompt ,adequate and
appropriate antibiotics to avoid
complications of suppuration
 Consult a pulmonologist.

Suppurative lung diseases, Dr Inofomoh Francisca,

Suppurative lung diseases, Dr Inofomoh Francisca,

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