THE PNEUMONIAS

Associate Professor Dr. Laureniu orodoc

DEFINITION
Pneumonia is an acute inflammatory lung disease, witch has infective or noninfective etiology, characterized by exudative alveolitis and/or interstitial inflammatory infiltration.

CLASSIFICATION
I. Infective: 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 by microorganisms usually inhabiting the upper respiratory tract, which invade the lung because its local defense mechanisms are impaired. Their common feature is the absence of any specific pathogenic organism in the sputum and the existence of some abnormality of the respiratory system which is predisposed to the invasion of the lung by organisms of relatively low virulence: 1.Streptococci. 2.Pneumococci (certain types) 3.Haemophilus influenzae.

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 microorganism from acute bronchitis, bronchiectasis or lung abscess.

Other causes that may predispose to the development of aspiration pneumonia: 1.Ineffective coughing due to post-operative or posttraumatic thoracic or abdominal pain; laryngeal paralysis. 2.Bronchial obstruction ( ex: bronchial carcinoma) may determine inadequate ventilation of the lung beyond the obstruction.

2.Viral, Mycoplasmal, Fungal and Rickettsial 1.Inluenza, parainfluenza, respiratory syncytial 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)

II. Chemical: war gasses and lipoid pneumonia III. Physical: radiation IV. Allergic: Loeffler`s syndrome

CLASSIFICATIONS
Anatomical 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

Pathogenic Classification
1. Primary pneumonia in healthy people 2. Secondary pneumonia complication of preexisting pulmonary diseases, viral infections or pathological conditions that generate local conditions (atelectasis, bronchial obstruction, pulmonary stasis, bronchoaspiration) 3. Metastatic pneumonia by haematogenic way

PATHOGENY
VACUUM ORGANISMS COLONIZE OROPHARYNGEAL

INHALATION OF INFECTED AEROSOLS

LUNG PATHOGENIC MICROBIAL GERMS

DISEMINATION MARROW INFECTION IN AN OUTBREAK EXTRAPULMONARY

DIRECT INOCULATION

MECHANISMS OF DEFENSE AGAINST RESPIRATORY INFECTION

MECHANICAL
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)

Predisposing Factors for Respiratory 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 with immunocompromised state Prolonged treatments: antibiotics, cortisone, chemotherapy, respiratory intensive care measures

Pneumococcal Pneumonia Lobar Pneumonia

Pathogeny
1. Lobar homogenous consolidation, usually unilateral; typically in the lower or posterior regions 2. The covering pleura, almost all the time shows acute pleurisy. 3. The disease passes through 3 stages: Congestion : congestion and minimal transudate in the alveoli Hepatization : The alveoli are filled with RBCs, WBCs, fibrin, germs. Resolution : Clearance of the inflammatory debris by macrophages and proteolytic enzymes. The alveoli became filled with watery exudate and few cells. The exudate is absorbed through blood and lymph vessels. N.B. Bacteremia and toxemia may occur.

CLINICAL FEATURES
I. General symptoms:
1. Sudden onset with high fever ( 39-40 in few hours), abrupt shaking chill. 2. Malaise, sweating, headache, insomnia, vomiting, sometime convulsions (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.

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 pleurisy

Inspection : 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). Percution: 1. Dullness consolidation pleurisy Auscultation 1. Early - 24- 48 h fine inspiratory crepitations, without bronchial breathing 2. Hepatization : tubular type bronchial breathing + medium size consonating crepitations 3. Resolution : Coarse crepitations 4. Pleural rub is usually present starting from the first day

PARACLINICAL INVESTIGATION:
1. Blood picture: marked neutrophil leukocytosis : WBC = 12.000 25.000 cells/mm; deviation to the left of the leukocyte formula. 2. Increase of acute phase reactants 3. Sputum examination: useful but not always strictly necessary. 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 affected lobe or segment, appearing within 12 to 18 hours of the onset of the illness. It is usually triangular , the peak is on the hil and the basis is on the periphery . Hilar and mediastinal region are not changed.

LOBAR PNEUMONIA

DIFERENTIAL DIAGNOSIS
Pulmonary 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, Staphylococcus aureus Mycoplasma, rickettsia, viruses, fungus Collagen diseases, vasculitis

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

A. Respiratory complications:
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 complications:
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

BRONCHO-PNEUMONIA
Definition: severe lung pneumonia preceded by bronchial infection, which accounts for the widespread patchy distribution of the lesions.

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

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 bilateral in small patches, which tend to become larger by confluence. 4. The lower lobes are more affected.

Diagnostic Features
1. Gradual onset, prolonged course (> 10 days ) and gradual offset in lyses ; after 2-3 days of acute bronchitis, the temperature rises to a higher level, the pulse and respiration rates increase, and dyspnea and central cyanosis appear. 2. The general condition of the patient is very affected. Specific features depending on the causative organisms. Usually the cough is severe with purulent sputum and pleural pain is relatively uncommon. 3. Physical examination in early stages is like in acute bronchitis, but in time, crepitations become more numerous. 4. Chest X-ray film shows patchy opacities in both lung fields, mainly in lower zones.

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

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

Bilateral multifocal

BRONCHOPNEUMONIA

Main Differential Diagnosis Features Between Lobar Pneumonia and Broncho-pneumonia

1.. Organisms 2. Age 3. Onset 4. Offset 5. Duration 6. Localization 7. Pathology 8. Complications 9. Empyema 10. X-ray
Lobar Pneumonia Mainly pneumococci 15-45 Acute By crisis 1 week Broncho-pneumonia

Lobar Consolidation Less common

Meta- pneumonic

Staphyloc. and others Extremes Gradual By lyses >2 weeks Lobular Consolid. & bronchitis More common Syn - pneumonic
Patchy infiltrates

Lobar

Staphylococcal Bronchopneumonia
1. Primary staphylococcal broncho-pneumonia is much less frequent than pneumococcal pneumonia. It commonly occurs as a complication of influenza. 2. Secondary staphylococcal broncho-pneumonia is a blood-borne infection from a staphylococcal lesion elsewhere 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 to empyema or pyopneumothorax.

Friedlander`s Pneumonia
1. 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 to presence of blood. 6. The course is usually prolonged for months.

Community-Acquired Pneumonia ATS guideline - 2001

I. Outpatients with no history of cardiopulmonary disease, and no modifying factors. Mortality <1- 5 %. II. Outpatients with cardiopulmonary disease (congestive heart failure or COPD) and/or other modifying factors (risk factors for DRSP or gram-negative bacteria). Mortality < 5 %. III. Inpatients, not admitted to the ICU, who have the following: a. Cardiopulmonary disease, and/or other modifying factors (including being from a nursing home); b. No cardiopulmonary disease, and no other modifying factors. Mortality < 5 25 %. IV. ICU-admitted patients who have the following: a. No risks for Pseudomonas aeruginosa b. Risks for Pseudomonas aeruginosa. Mortality up to 50%

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 <80 ml in 4h or serum creatinine >2 mg/dl in the absence of chronic renal failure)

Hospital-Acquired Pneumonia
Etiology :
1. Pseudomonas aeruginosa (debilitated patients, patients with previous antibiotic therapy, and those requiring mechanical ventilation) 2. Staphylococcus aureus 3. Enterobacter 4. Klebsiella pneumoniae 5. Escherichia coli *Anaerobic organisms, mycobacteria, fungi, chlamydiae, viruses, rickettsiae and protozoal organisms are uncommon causes of nosocomial pneumonia.

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 in common, apart from the site of occurrence, a high severity outcome and, unfortunately, high mortality rates. These particularities come from the significant resistance to antibiotics of the etiological microorganisms, and from the particular disability state of the patients (malnutrition, advanced age, altered consciousness, swallowing disorders, and underlying pulmonary and systemic diseases). Therapeutical maneuvers and techniques are known to facilitate its occurrence, especially mechanical ventilation (ventilatorassociated pneumonia), and aspiration of infected. Less important pathogenic mechanisms of nosocomial pneumonia include inhalation of contaminated aerosols and hematogenous dissemination of microorganisms.

Peculiarities of the Hospital Acquired Pneumonia

The clinical diagnosis of nosocomial pneumonia is based on the classic clinical features of pneumonia, adding a higher degree of symptoms and severity signs (high fever, toxemia). The radiological investigation shows nonspecific features (pulmonary infiltrates) imposing differential diagnosis with: atelectasis, pulmonary edema, aspiration, pulmonary hemorrhage, pleural effusion, and pulmonary embolism. Bronchoscopy allows bronchoalveolar lavage with quantitative cultures. Positive Diagnosis: A. Occurs more than 48 hours after admission to the hospital, especially in patients requiring intensive care and mechanical ventilation. B. Severe clinical findings (fever, cough, leukocytosis, purulent sputum). C. Pulmonary infiltrates on chest X-ray. Sputum culture and antibiogram identify resistant microorganisms. Course and Prognosis : high mortality rate (30 60 % ).

Pneumonia in the Immunocompromised Host

1.Bacteria, mycobacteria, fungi, protozoa, helminthes or viruses may cause pneumonia in immunocompromised patients. 2. Humoral immunity defects predispose mainly to bacterial infections. 3. Defects in cellular immunity predispose to infections with viruses, fungi, mycobacteria and protozoa. 4. Chest radiography is helpful for clarifying the differential diagnosis. ~ Diffuse infiltrates are usually seen with Pneumocystis or viral pneumonia. ~ Bacterial and fungal infections are typically associated with more localized infiltrates.

5. Important data for establishing the etiology of pneumonia in immunocompromised patients comes from the type of onset and the course of the clinical features, but sputum culture is always necessary for an appropriate therapy: A fulminant pneumonia is probably caused by bacterial infection. An insidious pneumonia is suggestive for viral, fungal, protozoal, or mycobacterial infection. Pneumonia occurring within 2-4 weeks after organ transplantation, is most likely to be bacterial. Pneumonia occurring several months or more after transplantation, is highly suggestive for infection caused by Pneumocystis carinii, viruses, and fungi. 6. AIDS is nowadays the major cause of Pneumocystis carinii pneumonia.

CURB - 65 SCORE (British Thoracic Society)

General and Symptomatic Treatment of Pneumonia

Oxygenotherapy 24-36 hours, in patients with toxic state, 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 / or HHC 100-200 mg i.v. every 6-8 hours

2003 IDSA CAP Guidelines

Previously healthy patients and no antibiotic therapy in last 3 months: Macrolide or Doxycycline Previously healthy patients and recent antibiotic therapy: respiratory fluoroquinolone advanced macrolide plus high-dose amoxicillin advanced macrolide plus high-dose amoxicillin- clavulanate Comorbidities (COPD, heart failure, diabetes) No recent antibiotic therapy advanced macrolide or respiratory uoroquinolone Recent antibiotic therapy (3 months) respiratory uoroquinolone or advanced macrolide plus a blactam
Clin Infect Dis 37:1405-1433, 2003

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-dose amoxicillin/clavulanate

Inpatient with recent antibiotic therapy (3 months) Respiratory fluoroquinolone Advanced macrolide plus beta-lactam

Pathogens S. pneumoniae PCN-R Macro-R H. influenzae M. catarrhalis Atypical agents

BL + ++++ 0

MAC + +++ +

FQ + + + + + +

DOX + +++ + +

For S. pneumoniae with PCN MIC >2 mg/L, vancomycin, FQ, or ketolides are probably the best option
BL-beta-lactam, MAC-macrolide, FQ-fluoroquinolone, DOXdoxycycline

ATS Guidelines for Nosocomial Pneumonia

Pathogens
S. pneumoniae H. influenzae

Antibiotics
Ceftriaxone or Levofloxacin, Moxifloxacin, Ciprofloxacin or Ampicillin / sulbactam or Ertapenem

or

E. coli Enterobacter sp Proteus sp

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

Initially Empiric Therapy for Nosocomial Pneumonia in Patients at Risk for MDR
Cefipim (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)

PLUS

Gentamicin or Tobramicin 7 mg/Kg/day Amikacin 20 mg/Kg/day Levofloxacin 750 mg/day or Ciprofloxacin 400 mg every 8H PLUS Vancomycin 15 mg/Kg every 12H or Linezolid 600 mg every 12H

Treatment of Pneumocystis Carinii 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

Anaerobic Pneumonia and Lung Abscess (Suppurative Pneumonia)

Definition: Suppurative pneumonia is the term used to describe a form of pneumonic consolidation in which the inflammatory process destructs the lung parenchyma. The lung abscess is a localized collection of pus, or a cavity lined by chronic inflammatory tissue, from which pus has ruptured into a bronchus.

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 anaerobic bacteria, particularly amongst alcoholics with periodontal disease, 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 basilar segments 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:

1. Lung diseases: Pneumonia, particularly when the infecting agent is Staphylococcus pyogenes or Klebsiella pneumoniae and the initial therapy was inadequate. Bronchial carcinoma (bronchial obstruction) Bronchiectasis Lung collapse (infarcted areas of lung may occasionally cavitate and rarely become infected) Infected lung cyst. 2. Subdiaphragmatic diseases : Liver abscess, especially amoebic, may spread transdiaphragmatically Subphrenic abscess 3 .Mediastinal and thoracic wall disease: Mediastinal cancer invading the lung Penetrating chest trauma 4. Pyaemia ( pyaemic abscess)- multiple, bilateral uniform in size abscess, usually with Staphylococcus aureus (bacteremic infection septic emboli).

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.

Complications:
Chest complications: # Pneumonia + spread to other parts of the lung # Fibrosis # Bronchiectasis # Pleurisy, pleural effusion, empyema, pyopneumothorax or pleural adhesions. General complications: 1. Toxaemia may lead to chronic inflammatory anemia or amyloidosis 2. Pyaemia causes metastatic abscesses.

Clinical Findings
I. Pneumonic 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 to posture) 3. General signs: tachycardia, toxic facies, poor dental hygiene 4. Chest signs: consolidation features +/- pleural rub

II. Acute abscess stage:

Symptoms: 1. After 9-12 days of evolution a severe attack of cough appears, with thick blood tinged sputum, followed by expectoration of a huge amount of purulent fetid sputum. 2. Drop of fever + improvement of general condition of the patient. 3. Lying on the healthy side is determining cough with huge expectoration. 4. While coughing accesses hemoptysis may occur. Signs: 1. General : fever, tachycardia, sweating. 2. Cavity syndrome +/- pleural rub

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 coarse crepitations.

Laboratory Findings :
Sputum is preferable to be collected only by transtracheal or transthoracic aspiration, thoracentesis, or bronchoscopy, because these ways, the contamination with the normal existent mouth flora may be avoided. The bacteriological investigation is essential not only for diagnosis process, but most of all also for leading the further adequate therapy. Chest X-ray: the different types of anaerobic pleuro-pulmonary infection are distinguished on the basis of their radiographic appearance. ~ Lung abscess appears as a thick-walled solitary cavity surrounded by consolidation. An air-fluid level is usually present. Other causes of cavitary lung disease (tuberculosis, mycosis, cancer, pulmonary infarction) should be excluded. ~ Multiple areas of cavitation within an area of consolidation distinguish necrotizing pneumonia. ~ Empyema is characterized by the presence of purulent pleural fluid (on thoracentesis).

LUNG ABSCESS

Air-fluid level

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, or pleural 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 winter exacerbations; early morning expectoration; the signs are mostly bilateral and basal; X-ray and bronchography confirm the diagnosis. 2. Bronchial carcinoma cavity. 3. Infected cystic lung.

TREATMENT
Goals: Eradication of pathogenic bacterial flora Drainage of abscess and of empyema Surgical ablation of chronic lesions Removing primary causes

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.fragilis

IMIPENEM 1-2g
PENICILIN / BETA-LACTAMASE INHIBITORS

 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

In severe life- threatening cases: PENICILLIN G plus METRONIDAZOL plus AMINOGLYCOSIDE CARBENICILLIN plus METRONIDAZOL plus AMINOGLYCOSIDE In case of failure antibiotherapy guided by antibiogram

 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

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 a lower level Adequate cardio-respiratory function Absence of organic disability