Suppurative Lung Disease

SUPPURATIVE LUNG DISEASE
SUPPURATIVE LUNG DISEASE

Bronchiectasis
Lung abscess
Empyema
Bronchiectasis
 Definition
Abnormal and permanent
dilatation of bronchi
Bronchiectasis
Focal
Airways supplying a limited region of
pulmonary parenchyma
Diffuse
More widespread distribution
Affects older individuals
2/3 women
Pathology
 Destructive and inflammatory changes
 Inflammation
 Neutrophils (elastase and matrix metalloproteinases)
 Normal wall structures destroyed /replaced by fibrous tissue
 Dilated airways
 Pools of thick, purulent material
 Peripherally occluded by secretions
 Obliterated and replaced by fibrous tissue
Pathology
 Microscopic
 Bronchial and peribronchial inflammation and fibrosis
 Wall ulceration
Squamous metaplasia
Mucous gland hyperplasia.
Parenchyma-fibrosis, emphysema,atelectasis
↑vascularity of the bronchial wall
Pathology
 Patterns
 Cylindrical
Uniformly dilated and end abruptly
 Varicose
Irregular or beaded resemble varicose veins.
 Saccular (cystic)
Ballooned appearance at the periphery, ending in blind sacs
Etiology and Pathogenesis
 Inflammation and destruction of the structural
components
 Infection -Inflammation
 Host inflammatory response induces epithelial

injury(mediators released from neutrophils)
 Vicious cycle
Inflammation → airway damage → impaired clearance
of microrganisms → further infection → inflammation
Infectious Causes
 Adenovirus and influenza virus
 Prulent bacteria-necrotizing organisms such as S.aureus,

Klebsiella, and anaerobes,no antibiotics/delayed
 B.pertussis, in childhood
 HIV infection- recurrent bacterial infection
 Tuberculosis, a major cause worldwide
 Direct damage/bronchostenosis or extrinsic compression by

lymph nodes
Infectious Causes
 Impaired host defense mechanisms
 Recurrent infections
 localized impairment of host defenses

 Endobronchial obstruction
 Bacteria and secretions poorly cleared

 Recurrent or chronic infection
Endobronchial neoplasms ( carcinoid tumors)
Foreign-body aspiration in children
Bronchostenosis, from impacted secretions/extrinsic compression
by enlarged L.N
Infectious Causes
 Generalized impairment of pulmonary defense
mechanisms
 IG deficiency
Primary ciliary disorders
Cystic fibrosis (CF)
Infections and bronchiectasis are often more

diffuse
Noninfectious Causes
 Toxic substance –severe inflammatory response
NH3 or aspiration of gastric acid +bacteria
 Immune response in the airway
In α 1-antitrypsin deficiency
Cigarette smoking
Clinical Manifestations
 Persistent /recurrent cough and purulent sputum
 Repeated, purulent RTI
 Hemoptysis (50–70%)- bleeding from friable, inflamed

mucosa
 Systemic Sx -fatigue, WT loss, myalgia
 Severe pneumonia followed by chronic cough and sputum

production
 Majority insidious onset of sx
 Asymptomatic /nonproductive cough, "dry" bronchiectasis

in an upper lobe
 Dyspnea , wheezing if widespread or underlying COPD
 Exacerbations of infection-↑amount of sputum, more

purulent,more bloody; systemic sx- fever, prominent
P/E finding :
Crackles, rhonchi, and wheezes , clubbing
Severe diffuse disease, with chronic hypoxemia, Cor

pulmonale and RVF
Clubbing of fingers
Metastatic abscess-brain abscess

DIAGNOSIS
 Radiology
CXR/CT
Nonspecific,Normal / prominent cystic spaces
Mimic bullous emphysema or honeycombing in severe ILD
 “Tram tracks“/ “Ring shadows"
Primary lesion/risk factors, Hilar L.N, complications

‘‘Signet ring’’ sign. Coned axial HRCT image shows a dilated
bronchus (arrow) in cross-section
Note that the internal diameter of the bronchus exceeds the
diameter o the adjacent pulmonary artery.
Coned axial HRCT image shows bronchial dilation with lack of
tapering (arrows). -varicose bronchiectasis .
(Left chest)A. Cylindrical bronchiectasis: Dilated and thickened airways.
B. (Right chest) Saccular or cystic bronchiectasis:Verydilatedairways
clustered into saccules, cysts, or grapelike clusters
Varicose bronchiectasis:
Dilated airways with irregular thickened mucosa
Cystic bronchiectasis
Axial HRCT imaging shows extensive bilateral
cystic bronchiectasis (arrows), consistent with the diagnosis
of tracheobronchomegaly. Note dilated trachea (T)
DIAGNOSIS
 HRCT, 1.0–1.5 mm thick
Currently gold standard
Site, extent
High cost
DIAGNOSIS
 Sputum -↑ neutrophils or organisms
Stain/culture- guide antibiotic therapy
Fiberoptic bronchoscopy underlying

endobronchial obstruction
DIAGNOSIS
CBC
Urinalysis
PFT- Diffuse bronchiectasis or associated
COPD
Workup should be dictated by a careful
assessment of the clinical scenario
Bronchiectasis: Treatment
 Major goals:
Treatment of infection, particularly in acute
exacerbations
Improved clearance of tracheobronchial secretions
Reduction of inflammation
Treatment of an identifiable underlying problem
Treatment
Antibiotics are the cornerstone
During acute episodes
 Choice - Gram's stain/culture of sputum, empiric

coverage
P. aeruginosa concern- poor outcome and worse

quality of life
10–14 day course or longer

Treatment
 Mechanical methods /positioning
 Mucolytic agents to thin secretions/allow better

clearance
 Bronchodilators
Treatment
 Surgery-Replaced by more effective antibiotic and
supportive therapy
 Indication
 Localized and the morbidity is substantial despite
adequate medical therapy
Massive hemoptysis
 Resection - localized,
 Embolization - widespread disease

Lung Abscess
 Definition
 Pulmonary parenchymal necrosis and cavitation from
infection
Lung abscess -high m.o burden/inadequate microbial

clearance
 Aspiration most common cause; (esophageal

dysmotility, seizure, and neurologic -bulbar dysfunction
Periodontal disease and alcoholism

Lung Abscess
 Microbiology
Anaerobic bacteria most common
Aerobic or facultative bac S. aureus, K.pneumoniae, Nocardia

sp., and Gm-VE organisms,nonbacterial- fungi and parasites
Immunocompromised host, aerobic bacteria and

opportunistic pathogens predominate
Multiple isolates –commonly when anaerobic and aerobic

cultures are done
 Typical -cough, purulent sputum production,

pleuritic chest pain, fever, and hemoptysis
 Anaerobic infection, insidous /asymptomatic
 Acute presentations are typical of infection with

aerobic bacteria
Physical exam often unrevealing
Rales or evidence of consolidation
Fetid breath and poor dentition-diagnostic clues
Clubbing or hypertrophic pulmonary osteoarthropathy

in chronic cases
Laboratory tests
 CXR
 Thick-walled cavities in dependent areas of the lung
 An air-fluid level
 CT of the chest
 Size and location /additional cavities/ presence of pleural dx
 Cavity in nondependent:other dx- malignancy
 Lab may reveal leukocytosis, anemia, elevated ESR
 Bronchoscopy to rule out airway obstruction, mycobacterial

infection, or malignancy
 Transtracheal or transthoracic aspiration

Lung Abscess: Treatment
 Antibiotics
Penicillin
Clindamycin (150 mg–300 mg every 6 h)
Metronidazole with penicillin
Choice guided by microbiologic result
Duration -4-6 weeks

Lung Abscess: Treatment
 Treatment failure - noninfectious etiology
 Surgery limited role in antibiotic era
 Surgical indications
Refractory hemoptysis
Inadequate response to medical therapy
Need for a tissue diagnosis(noninfectious)
EMPYEMA
 Definition
Pus collection in the pleural cavity
EMPYEMA
 The pathogenesis
 Empyema and lung abscesses are the same
 Shared presentations-
Indolent sx, fever, sweats, cough, dyspnea,weight loss, and pleurisy

Predisposing to aspiration(altered consciousness, dysphagia, and
gingivitis)
Foul odors of sputum or breath associatedwith anaerobic bacteriology.
EMPYEMA
 Clinical presentation
Depned on the underlying cause of infection.
1 to 3 weeks after aspiration pneumonia, sx of

pneumonia
High fever and leukocytosis.

Physical findings
Dullnes/ ↓ breath sounds
Localized in loculated fluid
Purulent fluid may be noted after treatment failure
Minimally toxic or severely ill, depending on the extent

of the infection and organisms present
Acute in staph/strep infections / rupture of hepatic

abscesses
EMPYEMA
 Parapneumonic Effusion
 Associated with bacterial pneumonia, lung abscess, or bronchiectasis
 Most common cause of exudative fliud
 Empyema - grossly purulent effusion
 Aerobic bacterial pneumonia and pleural effusion present with chest

pain, sputum p/n, and ↑WBC
 Anaerobic infections-subacute illness with weight loss, a brisk

leukocytosis, mild anemia, and a hx of some factor that predisposes
them to aspiration
 The presence of free pleural fluid can be demonstrated with a lateral

decubitus CXR, CT, or U/S
EMPYEMA
 Factors indicating the likely need for drainage
Loculated pleural fluid
Pleural fluid pH < 7.20
Pleural fluid glucose < 3.3 mmol/L (<60 mg/dL)
Positive Gram stain or culture of the pleural fluid
Presence of gross pus in the pleural space
EMPYEMA
 Repeat thoracentesis if fluid recur after initial
thoracentesis or above factors present
 Insert chest tube / fibrinolytic / thoracoscopy

with the breakdown of adhesions if repeated
thoracentesis fail
 Decortication if above Rx is ineffective

Diagnosis
 CBC/ESR
 CXR
 U/S -loculated
 PF analysis-exudative
 Low pH,glucose,↑LDH,↑protein
 CT
Treatment
Antimicrobial treatment
Identification and treatment of any anatomic processes
Drainage of the infected fluid
Based on the clinical status and microbiology
Gram’s stain predominant organism
Fastidious (S. pneumoniae, anaerobes) may be seen on
Gram’s stain but not isolated in culture
Antibiotic susceptibility guide therapy

Suppurative Lung Disease

Uploaded by

Copyright:

Available Formats

Suppurative Lung Disease

Uploaded by

Document Information

Original Description:

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Suppurative Lung Disease

Uploaded by

Copyright:

Available Formats

SUPPURATIVE LUNG DISEASE

SUPPURATIVE LUNG DISEASE

 Normal wall structures destroyed /replaced by fibrous tissue

 Host inflammatory response induces epithelial

 Prulent bacteria-necrotizing organisms such as S.aureus,

 HIV infection- recurrent bacterial infection

 Tuberculosis, a major cause worldwide

 Direct damage/bronchostenosis or extrinsic compression by

 localized impairment of host defenses

 Bacteria and secretions poorly cleared

Primary ciliary disorders

Cystic fibrosis (CF)

Infections and bronchiectasis are often more

 Toxic substance –severe inflammatory response

NH3 or aspiration of gastric acid +bacteria

 Immune response in the airway

In α 1-antitrypsin deficiency

 Repeated, purulent RTI

 Hemoptysis (50–70%)- bleeding from friable, inflamed

 Systemic Sx -fatigue, WT loss, myalgia

 Severe pneumonia followed by chronic cough and sputum

 Asymptomatic /nonproductive cough, "dry" bronchiectasis

 Dyspnea , wheezing if widespread or underlying COPD

 Exacerbations of infection-↑amount of sputum, more

Severe diffuse disease, with chronic hypoxemia, Cor

Metastatic abscess-brain abscess

Nonspecific,Normal / prominent cystic spaces

Mimic bullous emphysema or honeycombing in severe ILD

 “Tram tracks“/ “Ring shadows"

Primary lesion/risk factors, Hilar L.N, complications

Currently gold standard

Stain/culture- guide antibiotic therapy

Fiberoptic bronchoscopy underlying

Antibiotics are the cornerstone

During acute episodes

 Choice - Gram's stain/culture of sputum, empiric

P. aeruginosa concern- poor outcome and worse

10–14 day course or longer

 Mechanical methods /positioning

 Mucolytic agents to thin secretions/allow better

 Embolization - widespread disease

Lung abscess -high m.o burden/inadequate microbial

 Aspiration most common cause; (esophageal

Periodontal disease and alcoholism

Aerobic or facultative bac S. aureus, K.pneumoniae, Nocardia

Immunocompromised host, aerobic bacteria and

Multiple isolates –commonly when anaerobic and aerobic

 Typical -cough, purulent sputum production,

 Anaerobic infection, insidous /asymptomatic

 Acute presentations are typical of infection with

Rales or evidence of consolidation

Fetid breath and poor dentition-diagnostic clues

Clubbing or hypertrophic pulmonary osteoarthropathy

 Cavity in nondependent:other dx- malignancy

 Lab may reveal leukocytosis, anemia, elevated ESR

 Bronchoscopy to rule out airway obstruction, mycobacterial

 Transtracheal or transthoracic aspiration

Clindamycin (150 mg–300 mg every 6 h)