Suppurative lung diseases, Dr Inofomoh Francisca,

02/05/2023INOFOMOH F.O.

SUPPURATIVE LUNG DISEASES

GRAND ROUND PRESENTATIONRESPIRATORY UNIT

JANUARY 2015.


Suppuration – “pus forming”These are disorders associated with pus

formation within the lungs and are named according to site;

Bronchi---- bronchiectasis Lung parenchyma--- Lung abscess Pleural space- ---Empyema


BRONCHIECTASIS DEFINITION CLASSIFICATION EPIDEMIOLOGY AETIOLOGY PATHOPHYSIOLOGY CLINICAL FEATURES DIAGNOSIS/INVESTIGATIONS DIFFERENTIALS TREATMENT COMPLICATIONS PROGNOSIS


BRONCHIECTASIS This is as an abnormal irreversible,

dilatation of one or more bronchi or bronchioles, large and small sized airways, with destruction of their elastic and muscular components,

usually due to an acute or chronic infection resulting in recurrent inflammation, airflow obstruction and impaired clearance of secretions.


Bronchiectasis is a syndrome of chronic cough and daily viscid sputum production associated with airway dilatation and bronchial wall thickening.

Classified as an obstructive airway disease.

May be focal or diffused.



EPIDEMIOLOGY Currently there are no estimates of the

incidence but its prevalence varies by country, region and underlying aetiology.

Prevalence mirrors the socioeconomic conditions of population under study.

There is a decline in its prevalence in developed countries with emergence of vaccines and antibiotics in the 20th century.

Overall it increases with age. More common in women than men.


NIGERIA EXPERIENCE ADEBONOJO ET AL IN 1979 reported

At UCH 54patients treated for bronchiectasis.

Also in 1982“Suppurative DISEASES of the lung – a continuing challenge in developing countries” 1,150patientsIN 2009, OLUFEMI DESALU ET AL reported at FMC, Ido Ekiti 183 patients


AETIOLOGY

CONGENITAL CAUSES; CYSTIC FIBROSIS YOUNGS SYNDROME PRIMARY CILIARY DYSKINESIA KARTAGENERS SYNDROME ALPHA 1-ANTITRYPSIN DEFICIENCY PAN HYPOGAMMAGLOBULINEMIA WILLIAMS CAMPBELL SYNDROME MOORNIER- KUNN SYNDROME YELLOW NAIL SYNDROME AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY

DISEASE


ACQUUIRED CAUSES POST INFECTIONS –Bacteria ;typical

organisms are Haemophilus influenzae St. pneumoniae Moraxella catarrhalis Pseudomonas aeruginosa Staph aureus


Other bacteria causes includes; Mycobacterium tuberculosis Non-tuberculosis mycobacterium(MAC) Klebsiella spp Mycoplasma pnemonia Viral infections; measles, influenza,

whooping cough, herpes simplex, certain types of adenovirus.

Fungi- aspergillosis


Diffuse disease of lung parenchyma; idiopathic pulmonary fibrosis.

Granuloma; sarcoidosis Mechanical obstruction ;intrinsic(foreign body

aspiration, insipatted mucus ,tumour Extrinsic (lymph node, tumour) Immune mediated diseases; ABPA, post lung

transplant. MIDDLE LOBE SYNDROME Autoimmune /rheumatologic diseases; Traction bronchiectasis Toxic gas exposure ; chlorine, ammonia gas.


PATHOGENESIS1 ATELECTASIS:

2 TRACTION

3 MIDDLE LOBE SYNDROME

4 VISCIOUS CYCLE HYPOTHESIS


VISCIOUS CYCLE HYPOTHESIS

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PATHOLOGY

PATHOLOGICAL CLASSIFICATION Cylindrical or tubular bronchiectasis

Varicose

Saccular or cystic bronchiectasis


5/8/11Obaseki DO


CLINICAL PRESENTATION A typical history of chronic cough

productive of thick tenacious sputum. Foetor Oris Fever Dyspnoea Wheezing Pleuritic chest pain Dizziness, weight loss. Haemoptysis


No specific signs for diagnosis Pallor Cyanosis or plethora from chronic hypoxia Tachycardia Crackles/rales Respiratory failure Cor pulmonale Nb: In Acute exacerbation-


DIFFERENTIALS

COPD Bronchial asthma Empyema thoracis Lung abscess Recurrent pneumonia Bronchial tumour Tuberculosis GERD


INVESTIGATIONS

IMAGING; Chest X-ray; Thickened bronchial wall Tram track lines ring(signet)shadows Gloved finger appearance May be normal

X-RAY FINDINGS IN BRONCHIECTASIS

Cystic spaces with peril-bronchial fibrosis

ABPA, hyperinflation and proximal mucus plugging

Multiple bibasal air-fluid levels


HIGH RESOLUTION CT SCAN

Image modality of choice. It has largely replaced bronchography It’s the gold standard for detecting bronchiectasis.

97% sensitivity93-100% specificity. It shows airway dilatation(tram track lines) Signet ring shadows(airway diameters

at least 1.5times >adjacent vessels. Lack of bronchial tappering Inspissated secretions(tree in bud

appearance).


IChest CT scan from a patient with cystic P, showing cystic lesions (one example is arrowed) that are often fluid filled.

RHEUMATOID ARTHRITIS-DILATED BRONCHI=FIBROSIS

I -SARCOIDOSIS


TREE-IN- BUD APPEARANCE

I-CYSTIC FIBROSIS

Cylindrical bronchiectasis

Varicose bronchiectasis

Saccular bronchiectasis

CT FINDINGS IN BRONCHIECTASIS

Signet ring appearanceAir-fluid level in cystic bronchiectasis

Mucus plugging in ABPATree in bud appearance


OTHER INVESTIGATIONS Pulmonary function test Complete blood count and differentials Gram stain and cultures for AFB,Fungi Quantitative immunoglobin levels Quantitative alpha 1-antitrypsin levels BAL for culture, stains Pilocarpine ionotophoresis(sweat test)+genetic

analysis Aspergillus precipitins and serum total IgE levels Autoimmune serological markers Electron examination of sperm, respiratory

epithelium


TREATMENTGoals of therapy:

Eradication of infection

Improve secretion clearance.

Relieving airway obstruction Reducing complications Prevent exacerbations and improve

quality of life.


MODALITIES; Antibiotics Bronchial hygiene Anti inflammatory Supportive therapy Surgical options


ANTIBIOTICS

A broad spectrum against most suspicious pathogens.

Guidelines says IV in acute exacerbation for 7-14days in high doses, or until symptoms resolves or significant imaging resolution

Most antibiotics recommended for post infectious causes while waiting for bacteriology results includes;


Amoxicillin Amoxi/clavlanic Tetracycline Trimethoprim /sulfamethazole Azithromycin/clarithromycin A fluoroquinolone 2nd generation cephalosporins For Pseudomonas aeuruginosa- IV

gentamicin +tobramycin+3rd generation cephalosporins.

ANTIBIOTIC COMBINATIONS!

‘Macrolides may have disease modifying activity’

Do not mix with IV aminoglycosides (increased risk of auditory problems)

For MAC, the ATS recommends 3-4 drug regimen with clarithromycin, Rifampin, ethambutol, streptomycin until cultures are negative for 1yr.

long term antibiotic regimen. Nebulised amoxicillin, azithromycin,

tobramycin.

Draft BTS Guidelines 2008


BRONCHIAL HYGIENE

HYDRATION MUCOLYTICS AEROSOLIZED BRONCHODILATORS HYPEROSMOLAR AGENTS CHEST PHYSIOTHERAPY DNASE for cystic fibrosis patient


CHEST PHYSIOTHERAPY Mechanical chest percussion by hand

clapping of the chest. Use of oscillatory positive expiratory

pressure fluutter valve. Use of high frequency chest wall oscillation

vest. Short acting inhaled bronchodilators can be

given before physiotherapy, if there is an asthmatic component.

Oral indomethacin has also been shown to reduce sputum volume but it has not been approved.

CHEST PHYSIOTHERAPY

Vibration vest


OTHER SUPPORTIVE MEASURES ANTI INFLAMMATORY Smoking ceasation Avoidance of secondary/ passive

smokers Nutritional supplememts Immunization for influenza and

pneumococcal infections Oxygen therapy in severe cases NEW THERAPY Use of QBw251 drug

that increase activity of CFTR IN Cystic fibrosis


SURGERY Persistent infections in bronchiectatic

area refractory to medical treatment Massive haemoptysis; resection or

bronchial artery embolisation. Foreign body or localized tumour Lung transplantation; highly considered

if FEV1 is <30%of predicted, inan females, and in younger patients.


COMPLICATIONS

FOLLOWING SURGERY; EMPYEMA HAEMORRHAGE PNEUMOTHORAX LUNG ABSCESS MASSIVE HAEMOPTYSIS METASTATIC CEREBRAL ABSCESS ASPERGILLOMA MALIGNANT TUMOURS


PROGNOSIS Life Threatening haemoptysis Bilateral lung involvement Associated lung abscess Malnutrition Chronic anaemia Frequency of exacerbation Specific pathogens; PAS ,Aspergillus,

MAC


LUNG ABSCESS Lung abscess is necrosis of

the pulmonary tissue and formation of cavities (more than 2 cm) containing necrotic debris or fluid caused by microbial infection.

Lung gangrene refers to formation small multiple abscesses(Necrotizing pneumonia).

PUTRID are Anaerobic bacterial lung abscess which are characterized by distinctive foul smelling breath, sputum or empyema.

This pus-filled cavity is often caused by aspiration, which may occur during altered consciousness.


CLASSIFICATION Based on duration; Acute or Chronic presence or absence of underlying

lesion; primary(60%) or secondary Pathogen involved;

staphylococcus lung abscessAnaerobic lung abscessLemierre’s disease– fusobacterium

necrophorum.Aspergillus lung abscessNon specific lung abscess

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AETIOLOGYAspiration pneumonia from; oropharyngeal flora Dental/periodontal sepsis

Paranasal sinus infection

Depressed conscious levelAlcohol/sedative drug abuseAnaesthesiaEpilepsyHead InjuryCVA/Coma


IMPAIRED LARYGNEAL CLOSURE

Prolonged endotracheal intubation

Tracheostomy tube

Recurrent laryngeal nerve palsy

DISTURBANCES OF SWALLOWINGOesophageal stricture, Achalasia, Reflux dx

Oesophageal motility disorder eg systemic sclerosis

Neuromuscular disease, eg bulbar/pseudobulbar palsy


NECROTIZING PNEUMONIA

Staphylococcus aureusStreptococcus milleri/intermediusKlebsiella pneumoniaePseudomonas aeruginosa

HAEMATOGENOUS SPREAD FROM A DISTAL SITEUTIAbdominal sepsis AMEBIC LUNG ABSCESSPelvic sepsis SEPTIC EMBOLIInfective endocarditis (right side)

METASTATIC LUNG ABSCESS

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PATHOGENESIS

Bacteria reaches lower airways, are not cleared by the patient’s host defense mechanism

Results in aspiration pneumonitis and progression to tissue necrosis in 7-14 days later → lung abscess

Other mechanisms:- Bacteremia – from area of focus of Gram-negative

sepsis, or anaerobic infection spread haematogeneously, septic emboli

Pneumonitis

necrosis abscess

empyema(if bronchopleural fistula occurs or infection extends directly into pleural space)

7-14 days

Pathophysiology


CLINICAL FEATURES It runs an indolent course especially in

aspiration pneumonia prone patients. History of periodontal infections. Symptoms and signs as essentially

above. Pyoorhea, gingivitis Chills are uncommon. Lethargy,cachetic


INVESTIGATIONS IMAGING;

Chest X-ray, Bronchoscopy, HRCT Scan Abscess is often unilateral and single

involving posterior segments of the upper lobes and the apical segments of the lower lobes as these areas are gravity dependent when lying down.

Presence of air-fluid levels implies rupture into the bronchial tree or rarely growth of gas forming organism.

NB;Lymphadenopathy

DIAGNOSIS:


MICROBIOLOGIC STUDIES Samples; sputum, BAL, transtracheal

aspiration, transthoracic needle aspiration under CT guidance – all these specimens for

Gram stain, cultures (aerobic and anaeroibic bacteria, mycobacteria, fungi)

Microscopic examination of aspirates OTHERS: Fibre optic bronchoscopy is often performed

to exclude obstructive lesion; it also helps in bronchial drainage of pus.

Raised inflammatory markers (high ESR, CRP) but not specific.


DIFFERENTIAL DIAGNOSIS OF A CAVITATING MASS

Cavitating carcinoma-primary or metastatic Lymphoma(thick-walled) Parasitic-echinococcus,paragonimiasis,

amoebiasis Cavitatory TB Wegener’s & churg-strauss granulomatosis Infected pulmonary cyst or bulla Fungal-aspergilloma, coccidioidomycosis Pulmonary infarction Rheumatoid nodule Sarcoidosis Bronchiectasis

MANAGEMENT: Broadspectrum antibiotic to cover mixed

flora is the mainstay of treatment. Pulmonary physiotherapy Postural drainage Surgical procedures are required in

selective patients for drainage or pulmonary resection.


ANTIBIOTICS First drug of choice is Clindamycin with its

alternative being Penicillin+ metronidazole For Gram negatives, Cephalosporins,&

quinolones Standard therapy for anaerobes is IV

Clindamycin 600mg 8hrly then 150-300mg PO OR IV Amoxiclav or Carbapenems. For MRSA use Vancomycin 15mg/kg/12hrly OR IV Linezolid 600mg 12hrly. For Microaerophilic streptococci infections or

mixed flora, a combination of Metronidazole+ aminoglycoside + fluoroquinolone


TREATMENT FAILURE Persistence of fever beyond 5-7 days

following therapy. Progression of infiltrates Thick walled cavity Extremely large abscess >6cm in diameter Recurrent aspiration RULE OUT

Obstruction Complicating Empyema Antibiotic resistant bacteria strains


SURGICAL THERAPYFailed medical therapySuspected neoplasmCongenital lung malformationBronhopleural fistulaMassive haemoptysisOPTIONS: Lobectomy, pneumonectomy,

surgical drainage.


COMPLICATIONS INTRATHORACIC

Rupture into pleural space

Pleural fibrosisTrapped lungPleuro-cutaneous

fistulaRespiratory failurePyo

pneumothoraxhaemoptysis

EXTRATHORACICSecondary

AmyloidosisSepticemiaMetastatic brain

abscess


PROGNOSIS Over 90% are cured with medical

therapy Bronchial obstruction secondary to is

carcinoma is of bad prognosis Also bad in extremes of Age and other

forms of immunosuppression.


EMPYEMA This is defined as frank pus in the

pleural space. It is grossly purulent usually following a parapneumonic effusion.

“ Pleural empyema (also known as a pyothorax or purulent pleuritis) itself is not a disease, but a condition often complicating an underlying disease.

Pus is thick, viscous and opaque with >15,000 neutrophils/ml.



TYPES This is based on duration; Acute 6-8 weeks Chronic >3months OR based of Anatomy Loculated(focal) vs free(total) Closed or open(following a

bronchopleural fistula or a sinus track).


AETIOLOGY PNEUMONIA of any origin causing a

parapneumonic effusion viz;Bacterial (accounts for 70% cases) 3 most common isolated gram +ve aerobic

orgs are Streptococcus pneumonia, Streptococcus milleri, Staphylococcus aureus)

Most common gram –ve aerobes are klebsiella, pseudomonas,haemophilus.

Bacteriodes most common isolated anaerobes.


Viral infections Atypical pneumonia

• Previous thoracic surgery (20%) ; chest drains, percutaneous biopsy

• Blood or lymphatic seedling of the pleural• Traumatic penetration.


PATHOPHYSIOLOGY 3 Stages are identified but they overlap. EXUDATIVE(0-2WKS)

Interstitial fluid leakage / pus accumulatioin Initially sterile with low WBC, LDH, glucose

and pH within normal limits. It takes 2-5 days after onset of pneumonia.


FIBRINOPURULENT PHASE(1-6WKS) Bacteria invasion of the pleural space Fibrin deposition Accumulation of PMN Leukocytes, bacteria

and debris. Tendency towards loculation and septation pH, glucose decreases as LDH levels rises.ORGANIZATION PHASE(AS FROM 3WKS)

Fibroblast forms an inelastic membrane called pleural peel.

- scarring of the pleural space may lead to lung entrapment

- Presence of very thick pus


CLINICAL PRESENTATION ANAEROBICS;

Subacute illnessHistory of

predisposing factor

Mild anemiaWeight lossBrisk leukocytosis

AEROBICSAcute onset of

chest painCough + sputuum

productionprimary infection

often due to tuberculosis

No prior history suggesting pneumonia


INVESTIGATIONS Chest X-ray; appear as a cloudy or opaque

area. Loculated or hydropneumothorax. C-T scan. Ultrasound scan Thoracentesis Pleural fluid Gram stain and

culture,biochemistry Assessment of bronchpleural fistula Histology Others


CHEST X-RAY IN EMPYEMA


ULTRASONOGRAPHY Permits measurement of depth of

location from the chest wall. Purulent or viscous complex fluid have

more densities or shadows within the fluid.

To differentiate loculated fluid from an infiltrate, this has air bronchograms intersparsed in it.

Extent of pleural thickness, 56% exudative PF

>86% thickness- Empyema

ULTRASOUND IMAGE OF EMPYEMA


CT SCAN- LOCULATED EMPYEMA

CT Scan

http://upload.wikimedia.org/wikipedia/commons/e/e6/Hydro_pneumothorax.jpg

CALCIFIED EMPYEMA


THORACOCENTESIS This is a procedure which involves the

insertion of a needle into the pleural cavity through the back between the ribs on the infected side, and a sample of fluid is withdrawn

It is performed under local anesthetics Samples are sent for pleural fluid

studies; AFB, culture, bichemistry, cell count, cytology, LDH levels, pH.



THORACOCENTESIS


PLEURAL FLUID ANALYSIS In empyema, result shows Fulfills criteria for an exudate

Wbc- >50,000cells/microLLDH>1000 U/LPh < 7.2Glucose ,40mg/dlPleural biopsy for histology may be

needed , this shows multiple granulocytes +/- necrotic debris.



TREATMENT GOALS; 1. Control of infection and sepsis by

antibiotics.2. Evacuation of pus from pleural space.3. Obliteration of the empyema cavity.

Antibiotics- use – as above.IV FOR 2WKS. Delay in drainage increase mortality

from 3.4% to 16%. Empyema is treated using a combination

of medications and surgical techniques



DRAINAGE OF EMPYEMA

Late-phase: continuous drainage or surgical debridement & decortication.

Performed under general anesthesia Done for the dependent rib Open all the intact cyst that leads to

conversion of empyema with free pus Then place intercostal tube for drainage

and close the wound Antibiotics should continue for 6 weeks



ROLE OF INTRA PLEURAL FIBRINOLYTIC THERAPY Studies used Streptokinase or

Urokinase,rTPA or altepase Most effective in the early

fibrinopurulent stage and may make surgical drainage unnecessary.

CTScan predicts failure if pleural thickening is <2mm.

Potential adverse effects includes: Bleeding, Bronchopleural fistula .



SURGICAL OPTIONS

Intercostal tube thoracostomy. Intrapleural instillation of streptokinase .DecorticationPleurectomyVideoscopic Assisted Thoracoscopy

Surgery (VATS) Rib Resection Drainage.OPEN drainage via Eloesser Flap


Rib resection drainage

Eloesser Flap Drainage

Decortication


COMPLICATIONS Persistent indolent infections Osteomyelitis of the rib Tuberculous abscess Septicemia,septic shock Trapped lung.



CONCLUSION Respiratory infections remains a major

burden on our health infrastructure. Most common and earliest complaints is

productive cough, this should be properly treated with prompt ,adequate and appropriate antibiotics to avoid complications of suppuration

Consult a pulmonologist.


BREATH IS LIFE!!!

Devices & Hardware

Suppurative lung diseases, Dr Inofomoh Francisca,