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Suppurative
Lung Diseases
-
-
-
Dr. Wondwossen M.
Introduction
• ↓ incidence after 1940s……..Penicillin
• Resurgence of lung abscess &
empyema
 Antibiotics resistant organisms
 ↑ immunosuppressed individuals
 Dv’t of drug abuse culture
 ↑ aging population
BRONCHIECTASIS
BRONCHIECTASIS
Abnormal & permanent dilatation of bronchi
• Classification
• Focal / Diffuse
• Cylindrical / Varicose / Saccular
Cylindrical bronchiectasis - bronchi appear as uniformly
dilated tubes
Varicose bronchiectasis – bronchi have irregular pattern
of dilatation
Saccular bronchiectasis - bronchi have a ballooned
appearance
INFECTIOUS
Viral
Bacterial
Mycobacterial
NON- INFECTIOUS
Inhalation of toxic
gas
Aspiration
Immune response
Congenital
Etiology
Pathogenesis
Is a consequence of inflammation & destruction of
of bronchial wall (major & minor bronchi)
INFLAMMATION (INFECTION)
 release of toxins & proteases
 bronchial wall damage
 impaired clearance of micro
organisms
 further chronic infection
more inflammation
 more airway destruction
• Persistent recurrent cough
• Copious production of foul smelling sputum
• Haemoptysis (50-70%)
• Halitosis
• P/E –crackles ,ronchi , wheezes reflect
damaged airways containing significant secretions
• - clubbing
- cor- pulmonale - pts with diffuse severe
disease particularly those with chronic hypoxemia
Clinical manifestations
• CBC
• Chest x-ray
• CT- scan
• Broncoscopy
• determine the specific segmental location of secretions
• detect foreign body, bronchial stenosis or neoplasm
• Sputum exam, staining & culture – may guide
antibiotic Rx
• Measurement of sweat chloride levels for cystic
fibrosis
Investigations
TREATMENT
1. Medical Rx
 Antibiotics
 Pulmonary toilet (postural drainage)
 Bronchodilators & steroids
 In patients with airflow obstruction, to enhance
airway patency
2. Surgical Rx
 Indicated for pts wit
 Localized (focal) bronchiectasis
 Proximal obstructive lesion
 Massive hemoptysis
 Recurrent infections
 Involves segmental resection of affected
area
THORACIC
EMPYEMA
THORACIC EMPYEMA
Defn-
 Presence of infected fluid or frank pus in
pleural cavity
 If not treated early
- pleural thickening surrounding the
walled of cavity + restricted lung mov’t
as a result of fibrosis
Etiology
1.Spread of infection from contagious
organs(2/3rd )
- Lungs-unresolved pneumonia, bronchiectasis, TB &
lung abscess
- Esophagus- perforations , post esophagectomy
- Spine & ribs – osteomyelitis
- Subdiaphragmatic – subphrenic & paracolic
abscesses
2. Direct inoculation (1/3rd )
- penetrating injuries of chest
- Iatrogenic infections – chest drains, post surgical
Bacteriology
Adults
- usually monomicrobial.
S. aureus, Strept. pneumonia, & Strept
pyogens
- In immunocompromised
Polymicobial & fungal infxn
children
<6 mths S. aureus
6/12 to 2 yrs S aureus, strept pneumonia & H. Inf
2 – 5yrs H. INFLUENZAE
Stages of Empyema
stage Main feature
I- Exudative phase Turbid thin fluid , minimal
pleural thickening &
mobile underlying lung
II- Fibropurulent Bacterial invasion of
effusion
Deposition of fibrin on
pleural surfaces
Loculation begins
III- Organizing Fibroblast proliferation &
scar formn. → lung
entrapment
Diagnosis
Assessment Finding
Clinical •Swinging pyrexia
•Cough, Dyspnoea
•chest pain
•Clubing & wt loss
•Signs of fluid
•Pus discharge
Laboratory Leukocytosis
↑ CRP & ESR
Radiology Abnormal PA & lateral CXR
U/S , CT
Treatment
Principle of Rx
> Control of infection – appropriate antibiotics
> Drainage of pus → lung expansion
Depends on the stage of Empyema
 Exudative phase  Antibiotic + thoracentesis
 Fibropurulent phase Chest tube + Antibiotic
 Organizing Phase Decortication
LUNG ABSCESS
LUNG ABSCESS
Defn:- A localized area of suppuration &
cavitation in the lung wit parenchyma
necrosis.
- Commonly affect
 Posterior segment of the
upper lobe
 Superior segment of lower
lobe
Risk factors
Dental caries & periodontal disease
Decreased state of consciousness
• Anesthesia
• Alcohol abuse
• Coma
• Convulsive disorders
Immunosupression
• Steroid Rx
• Malnutrition
• AIDS
Bacteriology
 Primary (aspiration, putrid, anaerobic)
Staphylococcus, peptococci, Bacteroides fragilis
 Immunocompromised
- Pseudomonas aeruginosa
- Proteus
- Aerobacter
- E Coli
- C albicans
- Legionella pneumophilia
Diagnosis
C/f - Sudden onset of cough, chest pain & fever
- Foul smelling sputum + haemoptysis
- Presence of contributing factor
Investigation
1. Sputum for gm stain/culture
2. CXR – cavitating shadow with air fluid level
3. CT–scan…… cavitation within an area of
consolidation
4. Bronchoscopy
TREATMENT
1. Conservative
 IV Antibiotics: PCN & metronidazole
- effective in 90% of cases
- for 4 -12 wks
 Internal drainage (Postural percussion,
coughing)
2. SURGERY
Indications:
• Failure of antibiotic therapy
• Massive hemoptysis
• Inability to rule out carcinoma
• Giant abscess (> 6cm in diameter)
• Rupture with a resultant empyema
Complications
 Pyopneumothorax rupture into pleura
cavity
 Metastatic intracranial abscess
 Septicemia
LUNG CANCER
Accounts for 90-95% of all lung tumors.
Leading common cancer in men & women.
• Accounts for 32% in men & for 25% of all cancer deaths
in women.
1.04 million new cases every year world wide.
Incidence: Males:80/100,000,Females:
40/100,000
80-90% of cases are inoperable at diagnosis &
86% of them die in the first years.
Highest incidence > 75
years, peaking at 80.
Male : female ratio - 1.14 : 1
Incidence rate has been
declining for men due to
reduction in smoking
Incidence increasing for
women due to increase in
cigarette smoking
Risk factors
SMOKING !!!
Age-Older age
Asbestos,
arsenic, mustard
Pulmonary
scar
Family history
Cigarette smoking
• Tobacco contains at least 55
known carcinogens.
• The cause in as many as 90%
of patients
• RISK 13.3x than Never-smoker
• Once a person quits smoking
• Risk gradually decreases
• Never returns to never-
smoker level
• Duration of smoking
• Numbers smoked
• Pattern of smoking
• Active Vs Passive
Active Vs Passive
Smoker
1 hr of hookah is equal to smoking 40-400
cigarettes.
1 hr of hookah exposes the smoker to 100-200x
the amount of smoke inhaled from 1 cigarette
WHO classification
Non-small cell carcinoma ~ 75%
• Adenocarcinoma
• Squamous cell carcinoma
• Large cell carcinoma
• Adeno-Squamous cell carcinoma
Small cell carcinoma ~ 25%
• Oat cell carcinoma
• Intermediate cell type
• Combined oat cell carcinoma
Adenocarcinoma
Accounts for 30-35% of
lung cancers
Most common type in
Non-smokers & Females
Often Peripheral Location
May arise from scars
“Scar carcinoma”
Squamous cell carcinoma
Accounts for 25-30%
of lung cancers
Essentially a
disease of Smokers
More common in
Males
Centrally Located
Small cell carcinoma
Accounts
for 15-25%
of lung
cancers
> 95% are
current or
past
Smokers
The Most
Malignant
type
Usually
central
Para-
neoplastic
syndrome
Clinical presentation
Manifestation depends on
1. Primary tumor location
• Peripheral
 Cough
 Dyspnea
 Pleural effusion
 Chest pain
• Endo –bronchial / Central
Cough, dyspnea
Hemoptysis
Atelectasis
Post-obstructive pneumonia
Wheezing
2. Extension into adjacent structures
• Pleural
effusion……………….........
• Hoarseness…………………
……………
• Dysphagia……………………
………….
• Diaphragm
paralysis……………..
• Rib
destruction……………………
…
• SVC
 Spread to the pleura
 RLN invasion
 Esophageal invasion
 Phrenic nerve invasion
 Chest wall invasion
 SVC compression
 Sympathetic ganglia
 Pericardial invasion
 C8-T2 invasion
3. Systemic effect due to hormonal
syndromes
• Typical for small cell cancers
 ADH…………………….Water Retention
 ACTH…………………..Cushing
Syndrome
 Parathyroid
Hormone………Hypercalcemia
4. Presence of metastases
• Lymphogenous:
 To regional lymph nodes
• Haematogenous:
 Liver 40%, Bones 40%, Brain 15%
• Tracheobronchial spread: uncommon
Diagnostic work up:
CBC,RFT,LFT
CXR
Sputum Cytology
CT- scan
Bronchoscopy
Bone & Brain scan
Treatment
Non small cell Lung Ca
• Surgery
• Radiotherapy
• Chemotherapy
Small cell Lung Ca
• Chemo-radiation
Solitary Pulmonary Nodule(SPN)
• SPN is defined radiographically as an
intrapulmonary lung lesion < 3 cm in diameter
that is not associated with adenopathy or
atelectasis.
• A lesion larger than 3 cm is considered a
mass.
• SPN should be considered malignant until
proved otherwise.
• Malignancy rate increases with age.
• Most are asymptomatic
• Nodules are benign if they;
 Are unchanged on CXR over 2 years
 < 2cms
 Have symmetrical patterns of calcification
 Well-circumscribed smooth borders
 Have Central fat on chest CT.
• Nodules are malignant if they:
 Growing
 > 2 cms
 Spiculated & irregular border
 Irregular eccentric calcification
 Older patients
 Smoking history
Differential diagnosis
Benign
Hamartoma
Tuberculosis
Histoplasmosis
Coccidioidomycosis
Malignant
• Bronchogenic Ca.
• Pulmonary adenoma
• Carcinoid tumor
• Metastasis
Thank
you

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Suppurative lung diseases & lung cancer

  • 2. Introduction • ↓ incidence after 1940s……..Penicillin • Resurgence of lung abscess & empyema  Antibiotics resistant organisms  ↑ immunosuppressed individuals  Dv’t of drug abuse culture  ↑ aging population
  • 4. BRONCHIECTASIS Abnormal & permanent dilatation of bronchi • Classification • Focal / Diffuse • Cylindrical / Varicose / Saccular Cylindrical bronchiectasis - bronchi appear as uniformly dilated tubes Varicose bronchiectasis – bronchi have irregular pattern of dilatation Saccular bronchiectasis - bronchi have a ballooned appearance
  • 5.
  • 6. INFECTIOUS Viral Bacterial Mycobacterial NON- INFECTIOUS Inhalation of toxic gas Aspiration Immune response Congenital Etiology
  • 7. Pathogenesis Is a consequence of inflammation & destruction of of bronchial wall (major & minor bronchi) INFLAMMATION (INFECTION)  release of toxins & proteases  bronchial wall damage  impaired clearance of micro organisms  further chronic infection more inflammation  more airway destruction
  • 8. • Persistent recurrent cough • Copious production of foul smelling sputum • Haemoptysis (50-70%) • Halitosis • P/E –crackles ,ronchi , wheezes reflect damaged airways containing significant secretions • - clubbing - cor- pulmonale - pts with diffuse severe disease particularly those with chronic hypoxemia Clinical manifestations
  • 9. • CBC • Chest x-ray • CT- scan • Broncoscopy • determine the specific segmental location of secretions • detect foreign body, bronchial stenosis or neoplasm • Sputum exam, staining & culture – may guide antibiotic Rx • Measurement of sweat chloride levels for cystic fibrosis Investigations
  • 10.
  • 11. TREATMENT 1. Medical Rx  Antibiotics  Pulmonary toilet (postural drainage)  Bronchodilators & steroids  In patients with airflow obstruction, to enhance airway patency 2. Surgical Rx  Indicated for pts wit  Localized (focal) bronchiectasis  Proximal obstructive lesion  Massive hemoptysis  Recurrent infections  Involves segmental resection of affected area
  • 13. THORACIC EMPYEMA Defn-  Presence of infected fluid or frank pus in pleural cavity  If not treated early - pleural thickening surrounding the walled of cavity + restricted lung mov’t as a result of fibrosis
  • 14. Etiology 1.Spread of infection from contagious organs(2/3rd ) - Lungs-unresolved pneumonia, bronchiectasis, TB & lung abscess - Esophagus- perforations , post esophagectomy - Spine & ribs – osteomyelitis - Subdiaphragmatic – subphrenic & paracolic abscesses 2. Direct inoculation (1/3rd ) - penetrating injuries of chest - Iatrogenic infections – chest drains, post surgical
  • 15. Bacteriology Adults - usually monomicrobial. S. aureus, Strept. pneumonia, & Strept pyogens - In immunocompromised Polymicobial & fungal infxn children <6 mths S. aureus 6/12 to 2 yrs S aureus, strept pneumonia & H. Inf 2 – 5yrs H. INFLUENZAE
  • 16. Stages of Empyema stage Main feature I- Exudative phase Turbid thin fluid , minimal pleural thickening & mobile underlying lung II- Fibropurulent Bacterial invasion of effusion Deposition of fibrin on pleural surfaces Loculation begins III- Organizing Fibroblast proliferation & scar formn. → lung entrapment
  • 17. Diagnosis Assessment Finding Clinical •Swinging pyrexia •Cough, Dyspnoea •chest pain •Clubing & wt loss •Signs of fluid •Pus discharge Laboratory Leukocytosis ↑ CRP & ESR Radiology Abnormal PA & lateral CXR U/S , CT
  • 18.
  • 19. Treatment Principle of Rx > Control of infection – appropriate antibiotics > Drainage of pus → lung expansion Depends on the stage of Empyema  Exudative phase  Antibiotic + thoracentesis  Fibropurulent phase Chest tube + Antibiotic  Organizing Phase Decortication
  • 21. LUNG ABSCESS Defn:- A localized area of suppuration & cavitation in the lung wit parenchyma necrosis. - Commonly affect  Posterior segment of the upper lobe  Superior segment of lower lobe
  • 22. Risk factors Dental caries & periodontal disease Decreased state of consciousness • Anesthesia • Alcohol abuse • Coma • Convulsive disorders Immunosupression • Steroid Rx • Malnutrition • AIDS
  • 23. Bacteriology  Primary (aspiration, putrid, anaerobic) Staphylococcus, peptococci, Bacteroides fragilis  Immunocompromised - Pseudomonas aeruginosa - Proteus - Aerobacter - E Coli - C albicans - Legionella pneumophilia
  • 24. Diagnosis C/f - Sudden onset of cough, chest pain & fever - Foul smelling sputum + haemoptysis - Presence of contributing factor Investigation 1. Sputum for gm stain/culture 2. CXR – cavitating shadow with air fluid level 3. CT–scan…… cavitation within an area of consolidation 4. Bronchoscopy
  • 25.
  • 26. TREATMENT 1. Conservative  IV Antibiotics: PCN & metronidazole - effective in 90% of cases - for 4 -12 wks  Internal drainage (Postural percussion, coughing) 2. SURGERY Indications: • Failure of antibiotic therapy • Massive hemoptysis • Inability to rule out carcinoma • Giant abscess (> 6cm in diameter) • Rupture with a resultant empyema
  • 27. Complications  Pyopneumothorax rupture into pleura cavity  Metastatic intracranial abscess  Septicemia
  • 29. Accounts for 90-95% of all lung tumors. Leading common cancer in men & women. • Accounts for 32% in men & for 25% of all cancer deaths in women. 1.04 million new cases every year world wide. Incidence: Males:80/100,000,Females: 40/100,000 80-90% of cases are inoperable at diagnosis & 86% of them die in the first years.
  • 30. Highest incidence > 75 years, peaking at 80. Male : female ratio - 1.14 : 1 Incidence rate has been declining for men due to reduction in smoking Incidence increasing for women due to increase in cigarette smoking
  • 31. Risk factors SMOKING !!! Age-Older age Asbestos, arsenic, mustard Pulmonary scar Family history
  • 32. Cigarette smoking • Tobacco contains at least 55 known carcinogens. • The cause in as many as 90% of patients • RISK 13.3x than Never-smoker • Once a person quits smoking • Risk gradually decreases • Never returns to never- smoker level
  • 33. • Duration of smoking • Numbers smoked • Pattern of smoking • Active Vs Passive
  • 35. 1 hr of hookah is equal to smoking 40-400 cigarettes. 1 hr of hookah exposes the smoker to 100-200x the amount of smoke inhaled from 1 cigarette
  • 36.
  • 37.
  • 38. WHO classification Non-small cell carcinoma ~ 75% • Adenocarcinoma • Squamous cell carcinoma • Large cell carcinoma • Adeno-Squamous cell carcinoma Small cell carcinoma ~ 25% • Oat cell carcinoma • Intermediate cell type • Combined oat cell carcinoma
  • 39. Adenocarcinoma Accounts for 30-35% of lung cancers Most common type in Non-smokers & Females Often Peripheral Location May arise from scars “Scar carcinoma”
  • 40. Squamous cell carcinoma Accounts for 25-30% of lung cancers Essentially a disease of Smokers More common in Males Centrally Located
  • 41. Small cell carcinoma Accounts for 15-25% of lung cancers > 95% are current or past Smokers The Most Malignant type Usually central Para- neoplastic syndrome
  • 42. Clinical presentation Manifestation depends on 1. Primary tumor location • Peripheral  Cough  Dyspnea  Pleural effusion  Chest pain • Endo –bronchial / Central Cough, dyspnea Hemoptysis Atelectasis Post-obstructive pneumonia Wheezing
  • 43. 2. Extension into adjacent structures • Pleural effusion………………......... • Hoarseness………………… …………… • Dysphagia…………………… …………. • Diaphragm paralysis…………….. • Rib destruction…………………… … • SVC  Spread to the pleura  RLN invasion  Esophageal invasion  Phrenic nerve invasion  Chest wall invasion  SVC compression  Sympathetic ganglia  Pericardial invasion  C8-T2 invasion
  • 44. 3. Systemic effect due to hormonal syndromes • Typical for small cell cancers  ADH…………………….Water Retention  ACTH…………………..Cushing Syndrome  Parathyroid Hormone………Hypercalcemia
  • 45. 4. Presence of metastases • Lymphogenous:  To regional lymph nodes • Haematogenous:  Liver 40%, Bones 40%, Brain 15% • Tracheobronchial spread: uncommon
  • 46. Diagnostic work up: CBC,RFT,LFT CXR Sputum Cytology CT- scan Bronchoscopy Bone & Brain scan
  • 47. Treatment Non small cell Lung Ca • Surgery • Radiotherapy • Chemotherapy Small cell Lung Ca • Chemo-radiation
  • 48. Solitary Pulmonary Nodule(SPN) • SPN is defined radiographically as an intrapulmonary lung lesion < 3 cm in diameter that is not associated with adenopathy or atelectasis. • A lesion larger than 3 cm is considered a mass. • SPN should be considered malignant until proved otherwise. • Malignancy rate increases with age. • Most are asymptomatic
  • 49. • Nodules are benign if they;  Are unchanged on CXR over 2 years  < 2cms  Have symmetrical patterns of calcification  Well-circumscribed smooth borders  Have Central fat on chest CT. • Nodules are malignant if they:  Growing  > 2 cms  Spiculated & irregular border  Irregular eccentric calcification  Older patients  Smoking history