Lung Abscess
by |
Passant Abdul Nasser Dorgham
Definition:
• Microbial infection causes suppurative necrosis of
the lung parenchyma producing a cavity. Often
communicate with large airways resulting in cough,
expectoration of purulent sputum and AFL on
imaging studies .
• May be more than one cavity, but usually one is large
and dominant .
• More common in pre-antibiotic era with progression
bacterial pneumonia +/- empyema
• Necrotizing pneumonia:
often used to describe similar
pathologic process with multiple
small (<2cm) cavities in
contiguous areas of the lung .
• Hydatid cysts >> do not mistaken this for multiple
abscesses
No air fluid level
Classification
 Onset and duration :
 acute < 1month,
 chronic > 1 month
 Primary lung abscess or Secondary lung abscess :
o Primary lung
abscess:
used when abscess
develops in individuals
prone to aspiration or in
general good health
80% of lung abscess
is primary
o Secondary lung
abscess:
• obstructive airway
neoplasm
• treatment that
compromises host
immune defense
mechanisms
Microbiology :
 Bacteria
o Usually: mouthflora anaerobes, Most frequently isolated anaerobes:
• Peptostreptococcus,
• Fusobacterium nucleatum,
• Prevotella melaningogenica
o Less common:
• Staphylococcus aureus, . Streptococcus pyogenes,
• Pseudomonas aeruginosa, Klebsiella pneumoniae ,
• Streptococcus pneumoniae
• gram-negative bacilli, such as E. coli , Haemophilus influenzae type B
• Legionella,, Nocardia asteroides
Microbiology :
 Mycobacteria
• M. tuberculosis, M. avium complex,
• M. kansasii, other mycobacteria
 Fungi
• Aspergillus spp., Histoplasma capsulatum,
• Pneumocystis carinii, Coccidioides immitis,
• Blastocystis hominis , cryptococcus
 Parasites
• Entamoeba histolytica,
• Paragonimus westermani,
• Strongyloides stercoralis (post-obstructive)
Non-infectious Causes (cavity formation
causes):
 Neoplasms
Primary lung cancer(pulmonary adenocarcinoma),
metastatic carcinoma, Lymphoma
 Pulmonary infarction
Due to bland embolus (may be secondarily infected in <5%)
 Septic embolism
• Tricuspid endocarditis due to S. aureus
• jugular venous septic phlebitis due to Fuso-bacterium
necrophorum (Lemierre syndrome)
Non-infectious Causes (cavity formation
causes):
 Vasculitis
Wegener's granulomatosis,
rheumatoid lung nodule
 Airway disease
Bullae, blebs, or cystic bronchiectasis
 Developmental
Pulmonary sequestration
 Other
Sarcoidosis, transdiaphragmatic bowel herniation giving appearance of
cavity with airfluid level
Bronchiectasis (honey comb
appearance ) cavitations
Pathophysiology :
 Most occur as a complication of aspiration
pneumonia and are poly microbial due to anaerobic
bacteria that are normal oral flora
Initial aspiration lung insult may be due to direct chemical
injury from aspirated stomach acid or to areas of
obstruction due to aspirated particulate matter (food)
Following the obstruction the gases result from the putrifaction and the anaerobic
organisms will result in lung cavity which could be progressive
 Secondary bacterial infection then may occur.
 If the bacterial inoculum is large/virulent or lung defense
mechanisms (mucociliary apparatus,alveolar macrophages)
compromised, infection can occur without prior insult to the
lung .
studies of patients with known time of aspiration suggest that
tissue necrosis with lung abscess formation takes at least 1 week
and up to 2 weeks to develop.
 Aspirated bacteria are carried by gravity to dependent
portions of the lung.
 Due to bronchus/carina anatomy, occur most frequently in
posterior segment of RUL then posterior segment of LUL and
then the superior segments of RUL/LLL
 1/3 develop empyema due to
direct extension .
 Amebic lung abscess
typically occurs in RLL
due to direct extension of
liver abscess through the
diaphragm
Risk Factors for lung abscess:
 Predisposition to aspiration
 45% of health adults aspirate during sleep; 70% of patients with
AMS aspirate
 1ml of saliva with > 109 live bacteria.
 Patients with chronic COPD
 Poor dentition with gingivitis
 resulting in an unusually high density of oral anaerobic organism particular in
gingival crevices .
 Airway Obstruction
• Neoplasm: 50% of lung abscesses in patients >50 areassociated with lung carcinoma (post-
obstruction vs. necrotic tumor)
 Foreign bodies, extrinsic compression (enlarged lymph node)
 Patients with cell-mediated immunity (AIDS, transplant)
 Neutropenic patients
 Patients with prosthetic cardiac valves or vegetative
endocarditis
Clinical features : (symptoms )
• The onset may be abrupt or gradual.
• Symptoms include fever, sweating, cough and chest pain simulating
pneumonia.
• The cough is often non productive at first or may produce mucoid or
mucopurulent expectorate from bronchial inflammation close to the
abscess area and sometimes there is blood streaking.
• If this happens suddenly in large quantities, this denotes a rupture of
the abscess cavity into the bronchus and blood streaking is common.
• Pleuritic chest pain,
especially with coughing is
common because the
abscess is near to the
pleura.
• Weight loss, anaemia, and
clubbing or pulmonary
osteo arthropathy appear
when the abscess
becomes chronic (8-12
weeks after onset).
Signs :
 Consolidation due to pneumonia surrounding the abscess is
the most frequent finding.
 Inspiratory rales and pleural rub may be heard.
 Rarely the amphoric or cavernous breath sounds are heard
 Rupture into the pleural space produces signs of effusion or
hydro pneumothorax.
 Digital clubbing may develop rapidly.
 Then aspiration results will reveal the infecting organism.
Amebic lung abscess :
• Patients who develop an amebic lung abscess often have symptoms
• associated with a liver abscess.
• These may include right upper quadrant pain and fever.
• After perforation of the liver abscess into the lung, the patient may
develop a cough and expectorate a chocolate or anchovy paste–like
sputum that has no odor.
Radiological diagnosis :
• Consolidation due to pneumonia
surrounding the abscess is the most
frequent finding.
• A dense shadow is the initial finding
before rupture.
• Later this opacity develops a cavity
with fluid level. May have smooth and
regular walls.
• Chest films may also reveal
associated primary lesions,
(bronchogenic carcinoma).
• Malignant abcess shows eccenteric
cavitation with thick rough irregular
walls.
lateral view show Rt upper lobe consolidation
Contrast-enhanced (CT)
scan demonstrates large
focal area of decreased
attenuation with rim
enhancement (arrow)
characteristic of lung
abscess.
Lateral chest radiographs 3
weeks later show decreased
size of lung abscess and
development of cavitation with
fluid level .
The patient was a 43-year-old
woman with lung abscess
secondary to Haemophilus
infection
A cavity with an air
fluid level at apical
segment of upper
lobe of right lung due
to lung abscess.
Pneumococcal
pneumonia complicated
by lung necrosis and
abscess formation.
A lateral chest radiograph
shows air-fluid level
characteristic of lung abscess.
A 54-year-old patient
developed cough with
foul-smelling sputum
production. A chest
radiograph shows lung
abscess in the left
lower lobe, superior
segment.
Ultrasonography
 Peripheral lung
abscesses with pleural
contact or included
inside a lung
consolidation are
detectable using lung
ultrasonography
 Lung abscess
appears as a
rounded hypo-
echoic lesion
with an outer
margin.
Diagnostic material uncontaminated by bacteria colonizing the upper
airway may be obtained for anaerobic culture from the following:
Blood cultures are infrequently positive in patients with lung abscess.
Transtracheal aspirateBlood culture
Pleural fluid (if empyema present) Transthoracic pulmonary aspirate
Surgical specimens Fiberoptic bronchoscopy with
protected brush
Bronchoalveolar lavage with
quantitative cultures
Expectorated sputum and other methods of sampling the upper airway do not
yield useful results for anaerobic culture because the oral cavity is extensively
colonized with anaerobes.
Procedures:
Flexible fiberoptic bronchoscopy is performed to exclude bronchogenic
carcinoma whenever bronchial obstruction is suspected.
Laboratory Studies:
complete white blood cell count with differential may reveal leukocytosis.
Gram stain, culture, and sensitivity.
If tuberculosis is suspected, ZeilNelsen and mycobacterial culture is requested.
Routine investigations:
e.g blood glucose , liver functions tests , renal functions test, electrolytes
Complications of lung abscess :
 Rupture into pleural space causing empyema
 Pleural fibrosis
 Trapped lung
 Respiratory failure
 Bronchopleural fistula
 Pleural cutaneous fistula
In a patient with coexisting empyema and lung abscess,
draining the empyema while continuing prolonged antibiotic therapy is
often necessary.
Differential diagnosis:
 Cavitating lung cancer
 Localized empyema
 Infected bulla containing a fluid level
 Infected congenital pulmonary lesion,
• such as bronchogenic cyst or sequestration
 Pulmonary hematoma
 Cavitating pneumoconiosis
 Hiatus hernia
 Lung parasites (eg, hydatid cyst, Paragonimus infection)
 Actinomycosis
 Wegener granulomatosis and other vasculitides
 Cavitating lung infarcts
 Cavitating sarcoidosis
Treatment :
Several anaerobes may produce beta-
lactamase , develop resistance to penicillin.
Clindamycin is the treatment of choice
Flagyl as monotherapy is inferior to
clindamycin as it is not active against micro
aerophilic streptococci and anaerobic cocci
that are common constituents of anaerobic
lung infection (which are sensitive to
Penicillin)…. So we can combine flagyl with
penicilin.
Do not forget that treatment should continue from
4-6 weeks
Lung abscess

Lung abscess

  • 1.
    Lung Abscess by | PassantAbdul Nasser Dorgham
  • 3.
    Definition: • Microbial infectioncauses suppurative necrosis of the lung parenchyma producing a cavity. Often communicate with large airways resulting in cough, expectoration of purulent sputum and AFL on imaging studies . • May be more than one cavity, but usually one is large and dominant . • More common in pre-antibiotic era with progression bacterial pneumonia +/- empyema
  • 4.
    • Necrotizing pneumonia: oftenused to describe similar pathologic process with multiple small (<2cm) cavities in contiguous areas of the lung .
  • 5.
    • Hydatid cysts>> do not mistaken this for multiple abscesses No air fluid level
  • 6.
    Classification  Onset andduration :  acute < 1month,  chronic > 1 month  Primary lung abscess or Secondary lung abscess : o Primary lung abscess: used when abscess develops in individuals prone to aspiration or in general good health 80% of lung abscess is primary o Secondary lung abscess: • obstructive airway neoplasm • treatment that compromises host immune defense mechanisms
  • 7.
    Microbiology :  Bacteria oUsually: mouthflora anaerobes, Most frequently isolated anaerobes: • Peptostreptococcus, • Fusobacterium nucleatum, • Prevotella melaningogenica o Less common: • Staphylococcus aureus, . Streptococcus pyogenes, • Pseudomonas aeruginosa, Klebsiella pneumoniae , • Streptococcus pneumoniae • gram-negative bacilli, such as E. coli , Haemophilus influenzae type B • Legionella,, Nocardia asteroides
  • 8.
    Microbiology :  Mycobacteria •M. tuberculosis, M. avium complex, • M. kansasii, other mycobacteria  Fungi • Aspergillus spp., Histoplasma capsulatum, • Pneumocystis carinii, Coccidioides immitis, • Blastocystis hominis , cryptococcus  Parasites • Entamoeba histolytica, • Paragonimus westermani, • Strongyloides stercoralis (post-obstructive)
  • 9.
    Non-infectious Causes (cavityformation causes):  Neoplasms Primary lung cancer(pulmonary adenocarcinoma), metastatic carcinoma, Lymphoma  Pulmonary infarction Due to bland embolus (may be secondarily infected in <5%)  Septic embolism • Tricuspid endocarditis due to S. aureus • jugular venous septic phlebitis due to Fuso-bacterium necrophorum (Lemierre syndrome)
  • 10.
    Non-infectious Causes (cavityformation causes):  Vasculitis Wegener's granulomatosis, rheumatoid lung nodule  Airway disease Bullae, blebs, or cystic bronchiectasis  Developmental Pulmonary sequestration  Other Sarcoidosis, transdiaphragmatic bowel herniation giving appearance of cavity with airfluid level Bronchiectasis (honey comb appearance ) cavitations
  • 11.
    Pathophysiology :  Mostoccur as a complication of aspiration pneumonia and are poly microbial due to anaerobic bacteria that are normal oral flora Initial aspiration lung insult may be due to direct chemical injury from aspirated stomach acid or to areas of obstruction due to aspirated particulate matter (food) Following the obstruction the gases result from the putrifaction and the anaerobic organisms will result in lung cavity which could be progressive  Secondary bacterial infection then may occur.
  • 12.
     If thebacterial inoculum is large/virulent or lung defense mechanisms (mucociliary apparatus,alveolar macrophages) compromised, infection can occur without prior insult to the lung . studies of patients with known time of aspiration suggest that tissue necrosis with lung abscess formation takes at least 1 week and up to 2 weeks to develop.  Aspirated bacteria are carried by gravity to dependent portions of the lung.  Due to bronchus/carina anatomy, occur most frequently in posterior segment of RUL then posterior segment of LUL and then the superior segments of RUL/LLL
  • 13.
     1/3 developempyema due to direct extension .  Amebic lung abscess typically occurs in RLL due to direct extension of liver abscess through the diaphragm
  • 14.
    Risk Factors forlung abscess:  Predisposition to aspiration  45% of health adults aspirate during sleep; 70% of patients with AMS aspirate  1ml of saliva with > 109 live bacteria.  Patients with chronic COPD  Poor dentition with gingivitis  resulting in an unusually high density of oral anaerobic organism particular in gingival crevices .  Airway Obstruction • Neoplasm: 50% of lung abscesses in patients >50 areassociated with lung carcinoma (post- obstruction vs. necrotic tumor)  Foreign bodies, extrinsic compression (enlarged lymph node)  Patients with cell-mediated immunity (AIDS, transplant)  Neutropenic patients  Patients with prosthetic cardiac valves or vegetative endocarditis
  • 16.
    Clinical features :(symptoms ) • The onset may be abrupt or gradual. • Symptoms include fever, sweating, cough and chest pain simulating pneumonia. • The cough is often non productive at first or may produce mucoid or mucopurulent expectorate from bronchial inflammation close to the abscess area and sometimes there is blood streaking. • If this happens suddenly in large quantities, this denotes a rupture of the abscess cavity into the bronchus and blood streaking is common.
  • 17.
    • Pleuritic chestpain, especially with coughing is common because the abscess is near to the pleura. • Weight loss, anaemia, and clubbing or pulmonary osteo arthropathy appear when the abscess becomes chronic (8-12 weeks after onset).
  • 18.
    Signs :  Consolidationdue to pneumonia surrounding the abscess is the most frequent finding.  Inspiratory rales and pleural rub may be heard.  Rarely the amphoric or cavernous breath sounds are heard  Rupture into the pleural space produces signs of effusion or hydro pneumothorax.  Digital clubbing may develop rapidly.  Then aspiration results will reveal the infecting organism.
  • 19.
    Amebic lung abscess: • Patients who develop an amebic lung abscess often have symptoms • associated with a liver abscess. • These may include right upper quadrant pain and fever. • After perforation of the liver abscess into the lung, the patient may develop a cough and expectorate a chocolate or anchovy paste–like sputum that has no odor.
  • 20.
    Radiological diagnosis : •Consolidation due to pneumonia surrounding the abscess is the most frequent finding. • A dense shadow is the initial finding before rupture. • Later this opacity develops a cavity with fluid level. May have smooth and regular walls. • Chest films may also reveal associated primary lesions, (bronchogenic carcinoma). • Malignant abcess shows eccenteric cavitation with thick rough irregular walls.
  • 21.
    lateral view showRt upper lobe consolidation
  • 22.
    Contrast-enhanced (CT) scan demonstrateslarge focal area of decreased attenuation with rim enhancement (arrow) characteristic of lung abscess.
  • 23.
    Lateral chest radiographs3 weeks later show decreased size of lung abscess and development of cavitation with fluid level . The patient was a 43-year-old woman with lung abscess secondary to Haemophilus infection
  • 24.
    A cavity withan air fluid level at apical segment of upper lobe of right lung due to lung abscess.
  • 25.
    Pneumococcal pneumonia complicated by lungnecrosis and abscess formation. A lateral chest radiograph shows air-fluid level characteristic of lung abscess.
  • 26.
    A 54-year-old patient developedcough with foul-smelling sputum production. A chest radiograph shows lung abscess in the left lower lobe, superior segment.
  • 27.
    Ultrasonography  Peripheral lung abscesseswith pleural contact or included inside a lung consolidation are detectable using lung ultrasonography  Lung abscess appears as a rounded hypo- echoic lesion with an outer margin.
  • 28.
    Diagnostic material uncontaminatedby bacteria colonizing the upper airway may be obtained for anaerobic culture from the following: Blood cultures are infrequently positive in patients with lung abscess. Transtracheal aspirateBlood culture Pleural fluid (if empyema present) Transthoracic pulmonary aspirate Surgical specimens Fiberoptic bronchoscopy with protected brush Bronchoalveolar lavage with quantitative cultures Expectorated sputum and other methods of sampling the upper airway do not yield useful results for anaerobic culture because the oral cavity is extensively colonized with anaerobes. Procedures: Flexible fiberoptic bronchoscopy is performed to exclude bronchogenic carcinoma whenever bronchial obstruction is suspected.
  • 29.
    Laboratory Studies: complete whiteblood cell count with differential may reveal leukocytosis. Gram stain, culture, and sensitivity. If tuberculosis is suspected, ZeilNelsen and mycobacterial culture is requested. Routine investigations: e.g blood glucose , liver functions tests , renal functions test, electrolytes
  • 30.
    Complications of lungabscess :  Rupture into pleural space causing empyema  Pleural fibrosis  Trapped lung  Respiratory failure  Bronchopleural fistula  Pleural cutaneous fistula In a patient with coexisting empyema and lung abscess, draining the empyema while continuing prolonged antibiotic therapy is often necessary.
  • 31.
    Differential diagnosis:  Cavitatinglung cancer  Localized empyema  Infected bulla containing a fluid level  Infected congenital pulmonary lesion, • such as bronchogenic cyst or sequestration  Pulmonary hematoma  Cavitating pneumoconiosis  Hiatus hernia  Lung parasites (eg, hydatid cyst, Paragonimus infection)  Actinomycosis  Wegener granulomatosis and other vasculitides  Cavitating lung infarcts  Cavitating sarcoidosis
  • 32.
    Treatment : Several anaerobesmay produce beta- lactamase , develop resistance to penicillin. Clindamycin is the treatment of choice Flagyl as monotherapy is inferior to clindamycin as it is not active against micro aerophilic streptococci and anaerobic cocci that are common constituents of anaerobic lung infection (which are sensitive to Penicillin)…. So we can combine flagyl with penicilin. Do not forget that treatment should continue from 4-6 weeks