Dr Taher El NaggarProf of Pulmonary Medicine

Ain Shams University

taherelnaggar@gmail.com

SUPPURATIVE LUNG DISEASES

TYPES

1. ASPIRATION PNEUMONIA 2. NECROTISING/DESTRUCTIVE

PNEUMONIA ACUTE OR CHRONIC 3. LUNG ABSCESS 4. EMPYEMA 5. BRONCHIECTASIS  

All usually associated with aspiration Polymicrobial etiology, but anaerobes often involved (60-100%) Share many common features: -

i) Predisposition: - aspiration - decreased LOC - swallowing problem - dental sepsis - anaerobic infection else where - abnormal lung clearance (for. body, tumor, COPD)

ii) Purulent+++ sputum iii) Foul odour (sputum & breath) iv) Hemoptysis v) Chronicity vi) Site (posterior segment ULs, apical & basal segments

LLs)

Bronchiectasis The word bronchiectasis is derived from Greek

roots, bronchion meaning windpipe & ektasis a stretching out.

Bronkos + Ectasia = Bronchi + Dilatation

Definition:Permanent dilatation of bronchi with

destruction of elastic and muscular component of their, usually due to acute or chronic infection.

(AACP evidence base clinical practice guideline 2006)

Pathophysiology:

PathophysiologyBronchi and bronchioles involving a vicious cycle

of transmural infection and inflammation with mediator release.

(NEJM 2002 )

2 main insults - Infectious insult - Impairment of drainage, airway obstruction,

and/or a defect in host defense.

Pathophysiology

infectionRetained secretion and

inflammation

Airway destruction and

remodeling

Etiology & Pathogenesis:

Measles & Pertussis Adenovirus Pneumonia Tuberculosis Atypical mycobacteria

A) Infections::

Etiology & Pathogenesis:

α 1-Antitrypsin deficiency.Pulmonary agenesis.Sequestrated segment.Bronchomalacia..

B) Developmental defects:

Etiology & Pathogenesis:

Cystic fibrosis. Primary ciliary dyskinesia (Immotile cilia

syndrome & Kartagener’s syndrome). Human immunodeficiency virus infection (HIV). Immunoglobulin deficiency.

C) Primary impairment of mucus clearance:

Bronchiectasis

Focal bronchiectasisLocal or focal obstructive process of a lobe or

segment of a lung3 types of focal airway obstruction 1) luminal blockage by a FB, broncholith or

slowly growing tumor (usually benign) 2) extrinsic narrowing : Enlarged LN

Middle lobe syndrome 3) Twisting of displacement of the airway after a

lobar recretion

Diffuse presentationInvolving much of both lungs .

Often accompanied by other sinopulmonary disease e.g. sinusitis and asthma

Location Focal Disease

Morphological types of Bronchiectasis:

Cystic or Saccular

Cylindrical

Varicose

(Reid, Reid, 1950)1950)

AA

BBCC

Cylindrical/tubular bronchiectasisUniform luminal dilatation

The wall thickening is smooth

Cylindrical/tubular bronchiectasis

C haracterized by dilated airways alone and is s ometimes seen as a residual effect of pneumon

ia.

Cylindrical/tubular bronchiectasis

Varicose Bronchiectasis

Varicose bronchiectasisVaricose:Dilated,constricted,distorte

dirregular

Cystic/saccular bronchiectasisMost severe form of bronchiectasis

Cyst like.

Dilated, thick-walled bronchus terminates in a thick-walled cyst.

Cystic BronchiectasisBronchogram HRCT

Cystic/saccular bronchiectasis

Cystic/saccular bronchiectasis

Clinical manifestationCough (90 %)Daily sputum production (76%)Dyspnea (72%), WheezingHemoptysis (56%)Recurrent pleurisy Dry Bronchiectasis (sicca haemorrhagica )Acute exacerbationLate : hypoxemia and hypercapnia

Clinical manifestationAbnormal lung sound on auscultation (Crackles, wheezes, rhonchi)Clubbing of finger 3-24%

Clinical Features of Bronchiectasis

Symptomssputumchronic coughhemoptysisdyspneafeverchest pain

Signscracklesfinger

clubbingcyanosiscor pulmonale

Chest X ray : abnormal (>90%)Non specific : focal pneumonitis, scattered irre

gular opacities, linear - or plate like atelectasis

Specific : dilated and thickened airways that - appear as ring like shadows

Acute exacerbation of bronchectasis

Diagnosis and investigations:For the causeHistory.Investigations.

SputumCommon organisms:H.Infleunza.S.Pneumoniae.Pseudomonas.S.Aureus.TB .

RadiologyCXR.CT scan.

Laboratory investigationsCBC.Sweat chloride test.Spermatic count and function ,Serum Igs.In asthma: IgE, eosinophilia, +ve skin test,

aspergillus +ve precipitin test.

Functional impairment:

1.Measurement of ventilatory capacityAirway obstruction.Lung volumes and compliance.

2.Gas exchange studies

Decreased DLCO.Bronchopulmonary shunt.Abnormal V/Q scan.

AntibioticsIndications:1.Mucoid sputum muco-purulent sputum.2.Chronic muco-purulent or purulent sputum ↑

amount or purulence, change of color, systemic symptoms or worsening of lung functions.

Aim:1.Subjective improvement of symptoms.2.Objective improvement of PFT.

Choice of antibiotics:

1.According to culture and sensitivity.2.According to severity.3.According to chronicity.4.According to penetration of Abs.5.Duration: intermittent or long term.

Steps in using antibioticsStart with penicillin (amoxicillin)

If failed response try augmentin

If patient is allergic to penicillin give clarithromycin or azithromycin

Add antibiotics according to C &S

Failure of response to penicillin or those with serious condition from the start IM cefotaxime, anti-staph, or anti-pseudomonas treatment

Postural drainageValue:1.Mucociliary clearance2.Expectoration and mobilization of secretions3.Improvement of airway obstruction4.Improvement of V/ mismatchAim:Mobilization of secretions from the lung

periphery which is affected by the disease process to the hilum towards the more central unaffected segments in which cough reflex is intact and mucociliary function is preserved aided by gravity.

Technique:1.Determination of the affected lobe2.Position3.Before drainage:Humidification if inspired air BDDeep breathing for 10 minutesCough when it comes spontaneously4.PD techniqueForced expiration without closure of the glottisKetchup bottle techniqueChest wall percussion

Complications1. Infective exacerbations.2. Haemoptysis.3. Core pulmonale and P++.

4. Respiratory failure.5. Brain abscess.6. Amyloidosis. 7. Aspergillosis. 8. Lung cancer.

Lung Abscess & Necrotizing Pneumonia

Localized necrotic lesion of the lung parenchyma (≥ 2 cm) containing purulent material.

The formation of multiple small abscesses (<2 cm) is referred to as necrotizing pneumonia.

Both lung abscess & necrotizing pneumonia are Both lung abscess & necrotizing pneumonia are manifestations of a similar pathologic process.manifestations of a similar pathologic process.

AA

AFC

RB

EDAPM

BB

CC

Lung abscess. A, Cross-sectional view of lung abscess. AFC, Air-fluid cavity;

RB, ruptured bronchus (& drainage of the liquified contents of the cavity); EDA, early development of abscess; PM, pyogenic

membrane. Consolidation (B) & excessive bronchial secretions (C) are common secondary anatomic alterations of the lungs.

• Posterior segment of the upper lung lobe.• Apical segment of lower lung lobe.

Classification of Lung Abscess:

According o the duration:Acute abscesses : < 4 weeks Chronic abscesses: >4

weeks. .

According to the cause::Primary abscess: Aspiration or pneumonia in or pneumonia in

the healthy host.the healthy host.Secondary abscess:: Preexisting condition (e.g. Preexisting condition (e.g.

obstruction), spread, obstruction), spread, bronchiectasis & / or an bronchiectasis & / or an immunocompromised state. immunocompromised state.

Investigations:I. Blood picture: PMNL >20.000/mm3

High ESR Mild normocytic normochromic anaemiaII. Microbiological studies:1. Sputum Gram stain Culture AFB2. Blood culture

4. Specimens for anaerobic culture without oropharyngeal contamination

Transtracheal aspiration. Percutaneus needle aspiration. Protected sheathed brush.

III. Radiology:1. CXR.2. CT scan. 3. Esophagus.4. Bronchoscope.

EmpyemaDefinition:Pus in the pleural cavity

Etiology:1.Traumatic2.Non-traumatic

Common organisms:1.G-ve (30%).2.Staph (25%).3.Pneumococcus (15%).4.Strept. melleri.5.Anaerobes (11%).6.TB.7.Mixed.

Clinical picture:Symptoms

General: fever, headache, malaise and loss of weight

Local: Pain, dyspnea and cough sputumSignsGeneral: weight loss, fever, clubbing, mouth

for decaying teeth and groin & lumbar region for tracking pus

Local: pleural effusion or empyema necessitans.

ComplicationsRestrictive defectPleural calcificationsBronchopleural fistulaPleuro-cutaneous fistulaPleural thickening

Investigations:1. Blood and biochemical exam2. CXR3. CT scan4. Sputum culture5. Blood culture6. U/S guided thoracocenthesis: Chemistry Bacteriology Cytology8. Thoracoscope

Management(Abs + Drainage)

Antibiotics:

Non-tuberculous : : antibiotics should continue 2-3 wks after stoppage of drainage.

Tuberculous: anti-tuberculous treatment for 6-9 months according to the response.

Choice of antibioticsAnaerobesPenicillin+metronidazole-lactam+-lactamaseExtended spectrum penicillinCarbapenamsSecond generation cephalosporins.Clindamycin

PneumococciPenicillin(high dose) then amoxicillin If allergic: first generation cephalosporins or

macrolides

StaphFlucloxacillinAnti-staph penicillinVancomycin or Teicoplanin

Gram –ve Third generation cephalosporins + aminogycoside

• Hereditary disorder of infants, children & young adults characterized by widespread dysfunction of the exocrine glands leading to chronic pulmonary disease, pancreatic insufficiency & abnormally high levels of electrolytes in the sweat.

Autosomal recessive disease discovered in 1989, caused by mutation in the CFTR gene that produces the protein responsible for moving the chloride ions through the cell membranes.

11. . Sweat chloride testt > 60 mEq: confirmative 50 – 60 mEq: highly probable < 50 mEq: normal2. Chronic pulmonary disease2. Chronic pulmonary disease (99%) (99%)3. Pancreatic insufficiency3. Pancreatic insufficiency (80-90%) (80-90%)4. 4. CXR • increased interstitial marking (98%)• cystic bronchiectasis (64%)• hyperinflation (58%)

Characteristic Features of Cystic Fibrosis

Chronic Sinusitis Nasal Polyposis

Pancreatic Insufficiency

Adapted from Welsh and Smith. Sci Am. 1995;273:52-59.

Male InfertilityCholestasisCirrhosis

Obstructive Lung Disease

BronchiectasisChronic Infection

Bowel ObstructionMalnutrition High Cl- in Sweat