the pneumonias

7/27/2019 The Pneumonias

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THE PNEUMONIAS

Associate Professor Dr. Laureniu orodoc


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DEFINITION Pneumonia is an acute inflammatory lung

disease, witch has infective or

noninfective etiology, characterized byexudative alveolitis and/or interstitial

inflammatory infiltration.


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CLASSIFICATIONI. Infectiv e:

1. Bacterial :Specific pneumonias: caused by microorganisms which can invade a

lung with intact

defense mechanisms.

1.Streptococcus pneumoniae

2.Staphylococcus aureus

3.Streptococcus pyogenes

4.Klebsiella pneumoniae and other gram-negative agents (Pseudomonas aeruginosa,

Escherichia coli, Proteus)5.Haemophilus influenzae

6.Bacteroides fragilis (and other anaerobe micro-organisms)

7.Mycobacterium tuberculosis

8.Yersinia pestis.

Non-specific pneumonias (aspiration pneumonias)- caused bymicroorganisms us

ually inhabiting the upper respiratory tract, which invade the

lung because its local defense mechanisms are impaired. Their common feature isthe absence of any specific pathogenic organism in the sputum and the existenceof some abnormality of the respiratory system which is predisposed to the invasionof the lung by organisms of relatively low virulence:

1.Streptococci.

2.Pneumococci (certain types)

3.Haemophilus influenzae.


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Infection may reach the lungs in various ways :

1. Aspiration from an infected nasal sinus or during

tonsillectomy, dental extraction (general anesthesia).2. Aspiration of the contents of the upper digestive

tract during anesthesia, coma or in sleep.

3. Gravity on air stream may carry microorganismfrom acute bronchitis, bronchiectasis or lung abscess.

Other causes that may predispose to thedevelopment of aspiration pneumonia:

1.Ineffective coughing due to post-operative or post-traumatic thoracic or abdominal pain; laryngealparalysis.

2.Bronchial obstruction ( ex: bronchial carcinoma) maydetermine inadequate ventilation of the lung beyondthe obstruction.


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2.Viral, Mycoplasmal, Fungal and Rickettsial

1.Inluenza, parainfluenza, respiratorysyncytial viruses, adenoviruses,enteroviruses.

2.Chlamidia (psittacosis, ornithosis)3.Mycoplasma pneumoniae (Eaton agent)

4.Candida albicans, Actinomices israeli,Aspergilus fumigatus, Histoplasma

capsulatum.5.Coxiella (Rickettsia) burneti Q fever

3.Protozoal: Pneumocystis carinii (AIDS)


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II. Chemical: war gasses and lipoidpneumonia

III. Physical: radiation

IV. Allergic:Loeffler`s syndrome


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CLASSIFICATIONSAnatomical classification

1. Lobar pneumonia

2. Broncho - pneumonia

Classification according to the situation in

which the pneumonia occurs

1.Community-acquired pneumonia

2.Nosocomial pneumonia

3.Pneumonia in the immunocompromised

host


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Pathogenic Classification

1. Primary pneumonia in healthy people

2. Secondary pneumonia complication ofpreexisting pulmonary diseases, viralinfections or pathological conditions thatgenerate local conditions (atelectasis,bronchial obstruction, pulmonary stasis,bronchoaspiration)

3. Metastatic pneumonia by haematogenicway


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PATHOGENYVACUUM

ORGANISMS COLONIZE

OROPHARYNGEAL

INHALATIONOF INFECTEDAEROSOLS

DISEMINATION

MARROW INFECTION

IN AN OUTBREAK

EXTRAPULMONARY

DIRECT INOCULATION

LUNG PATHOGENIC

MICROBIAL GERMS


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MECHANISMS OF DEFENSEAGAINST RESPIRATORY INFECTIONMECHANICAL

Nasal passage, nasal hairs, coughing, sneezing, muco-ciliary

clearance

SECRETORY

Mucus, lysozyme, lactoferrin, transferrin

Fibronectin, surfactant, complement

Immunoglobulins (secretory, Ig A, serum)

CELLULAR

Alveolar macrophages, inflammatory response (neutrophils,

monocytes)

Specific immune responses (humoral immunity, cell-mediated

T lymphocytes, cytokines)


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Predisposing Factors forRespiratory Infections:

Cigarette smoking, air pollution

Chronic alcohol consumption

Age > 65 years

Cold Bronchial obstruction

Lung stasis

Debilitating diseases (cirrhosis, diabetes, cancer)

or pathological conditions associated withimmunocompromised state

Prolonged treatments: antibiotics, cortisone,chemotherapy, respiratory intensive care measures


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Pneumococcal Pneumonia Lobar Pneumonia

Pathogeny1. Lobar homogenous consolidation, usually unilateral;

typically in the lower or posterior regions

2. The covering pleura, almost all the time shows acutepleurisy.

3. The disease passes through 3 stages:

Congest ion:congestion and minimal transudate in the alveoli

Hepatizat ion:The alveoli are filled with RBCs, WBCs, fibrin,germs.

Resolut ion:Clearance of the inflammatory debris bymacrophages and proteolytic enzymes. The alveoli becamefilled with watery exudate and few cells. The exudate isabsorbed through blood and lymph vessels.

N.B. Bacteremia and toxemia may occur.


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CLINICAL FEATURESI. General symptoms:

1. Sudden onset with high fever ( 39-40 in few hours), abrupt shakingchill.

2. Malaise, sweating, headache, insomnia, vomiting, sometimeconvulsions (children)

3. Upper abdominal pain ( due to pleurisy)

II. Chest symptoms:

1. Acute chest pain (due to pleurisy)

2. Dyspnea, sometimes severe

3. Cough :- dry - in early stage

- rusty sputum during hepatization

- copious productive sputum during resolution.


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Physical examination:

I. General signs:1. High, continuous fever ( 39 - 40) , lasts about 7 days, the offset is abruptly

2. Tachypnea( 30-40/ min)

3. Hot, pale and dry skin. Redness on the cheek (on the pneumonia side)4. Central cyanosis (severe cases)

5. Working alae nasi

6. Herpes simplex (around the lips and the nose)

7. Rapid pulse.

II. Chest signs:consolidation and pleurisyInspect ion: 1. Normal shape of the chest

2. Limitation of movements on the side of the lesion ( due to chest pain)

Palpation:

Tactile vocal fremitus is increased (this test is not in use anymore).

Percut ion:

1. Dullness consolidation

pleurisy

Auscul tat ion

1. Early - 24- 48 h fine inspiratory crepitations, without bronchial breathing

2. Hepatization : tubular type bronchial breathing + medium sizeconsonating crepitations

3. Resolution : Coarse crepitations

4. Pleural rub is usually present starting from the first day


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PARACLINICAL INVESTIGATION: 1. Blood picture: marked neutrophil leukocytosis : WBC

= 12.000 25.000 cells/mm; deviation to the left ofthe leukocyte formula.

2. Increase of acute phase reactants

3. Sputum examination: useful but not always strictlynecessary. Invasive methods of obtaining sputum

should be reserved for exceptional cases. 4. Blood culture: pneumococci are detected in up to

30% of cases.

5. X- ray: homogenous opacity localized to the affectedlobe or segment, appearing within 12 to 18 hours of theonset of the illness. It is usually triangular , the peak ison the hil and the basis is on the periphery . Hilar andmediastinal region are not changed.


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LOBAR PNEUMONIA


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DIFERENTIAL DIAGNOSISPulmonary disease with similar clinical and radiological picture : Tuberculosis pneumonia

Pulmonary infarction

Lung cancer

Limited lung atelectasis

Onset of tuberculosis pleurisy

Lung abscess before evacuation

Other etiologic types of pneumonia:

Klebsiella, Haemophilus, Streptococcus pyogenes, Staphylococcusaureus

Mycoplasma, rickettsia, viruses, fungus

Collagen diseases, vasculitis


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COMPLICATIONS:Evolution: The majority of cases recovered in 7-10 days. Any delay suggests complications.

A. Respiratory compl ications: 1. Unsolving pneumonia (more than 4 weeks)

Causes : a. Underlying disease: bronchiectasis or bronchial carcinoma

b. Tuberculosis pneumonia

c. Immune suppression (diabetes mellitus, renal failure, AIDS)

d. Occurrence of empyema or lung abscess

2. Post pneumonia lung abscess 3. Sero - fibrinous or purulent pleurisy

4. ARDS and multiple organ failure

5. Suprainfection E. Coli, Enterobacter, Proteus

6. Atelectasis by mucus plugs

B. General complicat ions : 1. Bacteremia may cause metastatic infection

* Meningitis * Endocarditis

* Pericarditis

* Peritonitis

* Suppurative arthritis

2. Toxemia - may cause miocarditis

3. Other complications: jaundice, glomerulonephritis, acute heart failure


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General Etiological Consideration:1. Causative micro-organisms:a. Staphylococcus pyogenes and aureus

b. Haemophilus influenze

c. Klebsiella pneumoniae

d. Streptococcus pneumoniae

2. Age : usually in children, old person and debilitated patients.

3. Often complicates other diseases:

In children: - Measles

- Whooping cough

- Typhoid fever

In adults: - Uremia- Acute or chronic bronchitis

- Influenza

- Surgical operation

- Heart failure


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Pathogeny :

1. Acute inflammation of the bronchi,especially the terminal bronchioles, field

with pus.2. Collapse and consolidation of the

associated groups of alveoli.

3. The distribution of the lesions is bilateralin small patches, which tend to becomelarger by confluence.

4. The lower lobes are more affected.


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Diagnostic Features1. Gradual onset, prolonged course (> 10 days ) and gradual offset in

lyses ; after 2-3 days of acute bronchitis, the temperature rises to ahigher level, the pulse and respiration rates increase, and dyspneaand central cyanosis appear.

2. The general condition of the patient is very affected. Specific featuresdepending on the causative organisms. Usually the cough is severewith purulent sputum and pleural pain is relatively uncommon.

3. Physical examination in early stages is like in acute bronchitis, but intime, crepitations become more numerous.

4. Chest X-ray film shows patchy opacities in both lung fields, mainly inlower zones.

5. Tendency t abscess formation, empyema, and fibrosis.

6. The mortality is higher at the extremes of life, especially in debilitatedpatients.


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BRONCHOPNEUMONIA

Bilateralmultifocal


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Main Differential Diagnosis FeaturesBetween Lobar Pneumonia andBroncho-pneumonia

Lobar Pneumonia Broncho-pneumonia

1.. Organisms2.Age3. Onset4. Offset5. Duration6. Localization7. Pathology8. Complications9.Empyema10. X-ray

Mainly pneumococci

15-45Acute

By crisis

1 week

LobarConsolidationLess commonMeta- pneumonic

Lobar

Staphyloc. and othersExtremesGradualBy lyses>2 weeksLobularConsolid. & bronchitisMore commonSyn - pneumonicPatchy infiltrates


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Staphylococcal Broncho-pneumonia1. Primary staphylococcal broncho-pneumonia is much

less frequent than pneumococcal pneumonia. Itcommonly occurs as a complication of influenza.

2. Secondary staphylococcal broncho-pneumonia is a

blood-borne infection from a staphylococcal lesionelsewhere in the body (osteomyelitis, genital infection,skin abscess).

3. There is a marked tendency of formation of thin-walled

abscesses which may rupture into the pleura leading toempyema or pyopneumothorax.


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Friedlander`s Pneumonia1. It is caused by Klebsiella pneumoniae.

2. There is tendency for affection of the apical parts of the lungs.

3. Massive consolidation and excavation of one or more lobes(simulating pulmonary tuberculosis).

4. Profound systemic disturbance.

5. The sputum is purulent and sometimes brick red in color, due topresence of blood.

6. The course is usually prolonged for months.

C it A i d P i


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Community-Acquired Pneumonia

ATS guideline - 2001

I. Outpatients with no history of cardiopulmonary disease,

and no modifying factors. Mortality


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Severe Community-Acquired

Pneumonia

The minor criteria: 1. Respiratory rate >30 /min

2. PaO2 / Fl O2 < 250

3. Bilateral or multilobar pneumonia

4. Systolic BP 90 mmHg

5. Diastolic BP 60mmHg.

The major criteria:

1. Need for mechanical ventilation

2. Increase in the size of infiltrates by >50% within 48 h

3. Septic shock or the need for pressors for > 4 h. 4. Acute renal failure ( urine output 2 mg/dl in the absence of chronicrenal failure)


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Hospital-Acquired Pneumonia

Etiology : 1. Pseudomonas aeruginosa (debilitated patients,

patients with previous antibiotic therapy, and thoserequiring mechanical ventilation)

2. Staphylococcus aureus 3. Enterobacter

4. Klebsiella pneumoniae

5. Escherichia coli

*Anaerobic organisms, mycobacteria, fungi,chlamydiae, viruses, rickettsiae and protozoalorganisms are uncommon causes of nosocomialpneumonia.


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Pathogeny : Nosocomial pneumonia groups under its clinical definition

(pneumonia occurring more than 48 hours after admission to the

hospital) several special pulmonary infections states, having incommon, apart from the site of occurrence, a high severityoutcome and, unfortunately, high mortality rates.

These particularities come from the significant resistance toantibiotics of the etiological microorganisms, and from the

particular disability state of the patients (malnutrition, advancedage, altered consciousness, swallowing disorders, and underlyingpulmonary and systemic diseases).

Therapeutical maneuvers and techniques are known to facilitateits occurrence, especially mechanical ventilation (ventilator-

associated pneumonia), and aspiration of infected. Lessimportant pathogenic mechanisms of nosocomial pneumoniainclude inhalation of contaminated aerosols and hematogenousdissemination of microorganisms.


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Pneumonia in the

Immunocompromised Host

1.Bacteria, mycobacteria, fungi, protozoa, helminthes orviruses may cause pneumonia in immunocompromisedpatients.

2. Humoral immunity defects predispose mainly to bacterial

infections.3. Defects in cellular immunitypredispose to infections with

viruses, fungi, mycobacteria and protozoa.

4. Chest radiographyis helpful for clarifying the differentialdiagnosis.

~ Diffuse infiltrates are usually seen withPneumocystis orviral pneumonia.

~ Bacterial and fungal infections are typicallyassociated with more localized infiltrates.


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5. Important data forestablishing the etiology ofpneumonia in immunocompromised patients comes

from the type of onset and the course of the clinicalfeatures, but sputum culture is always necessary for anappropriate therapy:

A fulminant pneumonia is probably caused by bacterialinfection.

An insidious pneumonia is suggestive for viral, fungal,protozoal, or mycobacterial infection.

Pneumonia occurring within 2-4 weeks after organtransplantation, is most likely to be bacterial.

Pneumonia occurring several months or more after

transplantation, is highly suggestive for infectioncaused by Pneumocystis carinii, viruses, and fungi.

6. AIDS is nowadays the major cause of Pneumocystiscarinii pneumonia.


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CURB - 65 SCORE (British Thoracic Society)


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General and SymptomaticTreatment of Pneumonia Oxygenotherapy 24-36 hours, in patients with toxicstate, extensive pneumonia, pulmonary disease

associated with hypoxemia.

Proper hydration (fever, sweating, vomiting)

Antipyretics aspirin, paracetamol

Pleural pain treatment aspirin, codeine

In alcoholics benzodiazepines prophylactic

General toxic syndrome - parenteral fluids, dopamine,3-5g/min/kg and / orHHC 100-200 mg i.v. every 6-8

hours


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2003 IDSA CAP Guidelines

Suspected aspiration

Clindamycin or Amoxicillin / clavulanate

Inpatient without recent antibiotic therapy (3 months)

Respiratory fluoroquinolone

Advanced macrolide plus beta-lactam

Advanced macrolide plus high-doseamoxicillin/clavulanate

Inpatient with recent antibiotic therapy (3 months)

Respiratory fluoroquinolone

Advanced macrolide plus beta-lactam


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Pathogens BL MAC FQ DOX

S. pneumoniae + + + +PCN-R + - +- + +-

Macro-R + - - + +-

H. influenzae + - +- + +

M. catarrhalis + + + +

Atypical agents 0 + + +

For S. pneumoniae with PCN MIC >2 mg/L, vancomycin, FQ, orketolides are probably the best option

BL-beta-lactam, MAC-macrolide, FQ-fluoroquinolone, DOX-

doxycycline


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ATS Guidelines for

Nosocomial PneumoniaPathogens Antibiotics

S. pneumoniae Ceftriaxone

H. influenzae or

Levofloxacin, Moxifloxacin,or

Ciprofloxacin or

Ampicillin / sulbactam

E. co li or

Enterobacter sp ErtapenemProteus sp

Am J Resp Crit Care Med 171:388-416, 2005


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Initially Empiric Therapy forNosocomial Pneumonia in Patientsat Risk for MDRCefipim (1-2 g every 8-12H) or Ceftazidim (2 g every 8H)

Imipenem (500 mg every 6H) or Meropenem (1g every 8H)

Piperacillin / Tazobactam (4.5 g every 6H)

Gentamicin or Tobramicin 7 mg/Kg/day

Amikacin 20 mg/Kg/day

Levofloxacin 750 mg/day or Ciprofloxacin 400 mg every 8H

Vancomycin 15 mg/Kg every 12H or Linezolid 600 mg every 12H

PLUS

PLUS


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Treatment of PneumocystisCarinii Pneumonia TRIMETOPRIM-SULFAMETOXAZOL

15-20 mg/kg/day every 6 hours i.v. or p.o.

PENTAMIDIN

3-4 mg/kg/day i.v.

Duration: 3 weeks


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Anaerobic Pneumonia and LungAbscess (Suppurative Pneumonia)Definition:

Suppurative pneumonia is the term used to

describe a form of pneumonicconsolidation in which the inflammatory

process destructs the lung parenchyma.

The lung abscess is a localized collection of

pus, or a cavity lined by chronicinflammatory tissue, from which pus has

ruptured into a bronchus.


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Pathogeny : May be produced in 2 ways :

I. Inhalation 2 factors are responsible:

a) Inhalation of septic material (vomitus during anesthesia or coma;foreign body or materials coming upper respiratory operations:nose, mouth, throat; periodontal disease).

b) Absent cough reflex (anesthesia, coma or prolonged

convulsions, alcohol abuse, or central nervous system disease).

* Aspiration of oropharyngeal secretions contaminated by anaerobicbacteria, particularly amongst alcoholics with periodontaldisease, is the typical example for this type of mechanism.

Aspiration type necrotizing pneumonia tends to prefer the

posterior segments of the upper lobes and superior and basilarsegments of the lower lobes.

The inhalation abscesses passes through 3 stages:

1. Pneumonic stage.

2. Stage of acute abscess.

3. Stage of chronic abscess.

II Secondary lung abscess:


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II. Secondary lung abscess:

1. Lung diseases:

Pneumonia, particularly when the infecting agent is

Staphylococcus pyogenes or Klebsiella pneumoniae and theinitial therapy was inadequate.

Bronchial carcinoma (bronchial obstruction)

Bronchiectasis

Lung collapse (infarcted areas of lung may occasionally cavitateand rarely become infected)

Infected lung cyst.2. Subdiaphragmatic diseases :

Liver abscess, especially amoebic, may spreadtransdiaphragmatically

Subphrenic abscess

3 .Mediastinal and thoracic wall disease: Mediastinal cancer invading the lung

Penetrating chest trauma

4. Pyaemia ( pyaemic abscess)- multiple, bilateral uniform in sizeabscess, usually with Staphylococcus aureus (bacteremicinfection septic emboli).


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Etiology: Anaerobic bacteria: About 2/3 of patients with

lung abscess and empyema are found to be

infected with multiple species of anaerobic

bacteria only. Prevotella melaninogenica

(formerly Bacteroides melaninogenicus),anaerobic streptococci and Fusobacterium

nucleatum are commonly isolated anaerobic

bacteria.

* Aerobic bacteria:Staphylococcus pyogenes

and aureus, Klebsiella pneumoniae.


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Clinical Findings


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Clinical FindingsI. Pneumon ic stage

1. General symptoms : fever, weight loss, malaise,prostration, sweating, chills.

2. Chest symptoms: pleuritic chest pain, dyspnea(consolidation), cough (first dry, later scanty rusty sputum or

fetid purulent sputum (anaerobic infection) not related toposture)

3. General signs: tachycardia, toxic facies, poor dentalhygiene

4. Chest signs: consolidation features +/- pleural rub


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II. Acute abscess stage:Symptoms:

1. After 9-12 days of evolution a severe attack of coughappears, with thick blood tinged sputum, followed byexpectoration of a huge amount of purulent fetidsputum.

2. Drop of fever + improvement of general condition ofthe patient.

3. Lying on the healthy side is determining cough withhuge expectoration.

4. While coughing accesses hemoptysis may occur.

Signs: 1. General : fever, tachycardia, sweating.

2. Cavity syndrome +/- pleural rub


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III. Chronic abscess stage :

Symptoms:

1. Progressive deterioration of the general condition:fatigue, malaise, and low-grade fever.

2. Suppurative syndrome symptoms.

Signs:1. General: osteoarthropaty, weight loss.

2. Chest: cavity syndrome +/- fibrosis:

Limitation of chest movement on the affected side.

TVF is increased.

Dullness over the site of the abscess.

Amphoric bronchial breathing.

Medium size consonating crepitations or coarsecrepitations.


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Laboratory Findings :Sputum is preferable to be collected only by transtracheal or

transthoracic aspiration, thoracentesis, or bronchoscopy, becausethese ways, the contamination with the normal existent mouthflora may be avoided. The bacteriological investigation is essentialnot only for diagnosis process, but most of all also for leading thefurther adequate therapy.

Chest X-ray: the different types of anaerobic pleuro-pulmonaryinfection are distinguished on the basis of their radiographicappearance.

~ Lung abscess appears as a thick-walled solitary cavitysurrounded by consolidation. An air-fluid levelis usually present.Other causes of cavitary lung disease (tuberculosis, mycosis,

cancer, pulmonary infarction) should be excluded.

~ Multiple areas of cavitation within an area of consolidationdistinguish necrotizing pneumonia.

~ Empyema is characterized by the presence of purulent pleural

fluid (on thoracentesis).


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LUNG ABSCESS


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Air-fluid level


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Positive Diagnosis: 1. Predisposition to aspiration. Poor dental hygiene. Fetid smelling

sputum.

2. Pneumonia features with important fever, weight loss, malaise. 3. Lung infiltrate, with single or multiple areas of cavitation, orpleural effusion.

Differential Diagnosis: other causes of suppurative syndrome.Clinically, in these cases, the excessive purulent expectoration is

related to posture:

1. Bronchiectasis continuous history (years) with winterexacerbations; early morning expectoration; the signs are mostlybilateral and basal; X-ray and bronchography confirm thediagnosis.

2. Bronchial carcinoma cavity.

3. Infected cystic lung.


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TREATMENT Goals:

Eradication of pathogenic bacterial

floraDrainage of abscess and of empyema

Surgical ablation of chronic lesions

Removing primary causes


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MEDICAL TREATMENT Antibiotics with broad spectrum , low toxicity, good penetrating

of necrotic areas, low cost.

PENICILLIN G10-20 mil u.i./day plus METRONIDAZOL 2 g/day

CLINDAMICIN 2,4 g/day

Broad spectrum betalactamine ( CARBENICILLIN 6-30g,TICARCILLIN 15g, MEZLOCILLIN 15-18g, PIPERACILLIN 12g)

CEFOXITIN the only active cephalosporin on B.fragi l is

IMIPENEM 1-2g

PENICILIN / BETA-LACTAMASE INHIBITORS


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The total duration of therapy 4-6 weeks

Efficacy criteria: Disappearance of purulent bronchial secretion

and of fetid sputum

Clarification of radiological opacity

Reduction and evacuation of cavities (complete

closure may last for 1-2 months)

Unsatisfactory response after 5-7 days: Inappropriate selection of drugs

Incorrect dosage

Association of pleural empyema, not evacuated

Severe infectious process

Associated diseases

Ineffective defense mechanisms


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In severe life- threatening cases:

PENICILLIN G plus METRONIDAZOL plusAMINOGLYCOSIDE

CARBENICILLIN plus METRONIDAZOL plus

AMINOGLYCOSIDE

In case of failure antibiotherapy guided by

antibiogram


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Postural drainage

In case of empyema - pleural

evacuation (thoracentesis) and pleural

lavage with saline solution or

pleurotomy and drainage.

In the case of inefficient postural

drainage - bronchoaspiration to 3-7

days Auxiliary treatment bronchodilators,

hydration, oxygenotherapy


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SURGICAL TREATMENT Indication: after at least 3 months of

ineffective medical treatment

- Lobar resection , segmental,

plurisegmental or lung resections

- Optimal time: The absence of acute clinical features

Stabilization of suppurative syndrome at alower level

Adequate cardio-respiratory function

Absence of organic disability

the pneumonias

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