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SUPPURATIVE LUNG DISEASES
GRAND ROUND PRESENTATIONRESPIRATORY UNIT
JANUARY 2015.
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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
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BRONCHIECTASIS DEFINITION CLASSIFICATION EPIDEMIOLOGY AETIOLOGY PATHOPHYSIOLOGY CLINICAL FEATURES DIAGNOSIS/INVESTIGATIONS DIFFERENTIALS TREATMENT COMPLICATIONS PROGNOSIS
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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.
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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.
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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.
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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
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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
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ACQUUIRED CAUSES POST INFECTIONS –Bacteria ;typical
organisms are Haemophilus influenzae St. pneumoniae Moraxella catarrhalis Pseudomonas aeruginosa Staph aureus
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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
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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.
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PATHOGENESIS1 ATELECTASIS:
2 TRACTION
3 MIDDLE LOBE SYNDROME
4 VISCIOUS CYCLE HYPOTHESIS
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VISCIOUS CYCLE HYPOTHESIS
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PATHOLOGY
PATHOLOGICAL CLASSIFICATION Cylindrical or tubular bronchiectasis
Varicose
Saccular or cystic bronchiectasis
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5/8/11Obaseki DO
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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
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No specific signs for diagnosis Pallor Cyanosis or plethora from chronic hypoxia Tachycardia Crackles/rales Respiratory failure Cor pulmonale Nb: In Acute exacerbation-
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DIFFERENTIALS
COPD Bronchial asthma Empyema thoracis Lung abscess Recurrent pneumonia Bronchial tumour Tuberculosis GERD
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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
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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).
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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
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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
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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
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TREATMENTGoals of therapy:
Eradication of infection
Improve secretion clearance.
Relieving airway obstruction Reducing complications Prevent exacerbations and improve
quality of life.
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MODALITIES; Antibiotics Bronchial hygiene Anti inflammatory Supportive therapy Surgical options
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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;
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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
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BRONCHIAL HYGIENE
HYDRATION MUCOLYTICS AEROSOLIZED BRONCHODILATORS HYPEROSMOLAR AGENTS CHEST PHYSIOTHERAPY DNASE for cystic fibrosis patient
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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
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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
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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.
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COMPLICATIONS
FOLLOWING SURGERY; EMPYEMA HAEMORRHAGE PNEUMOTHORAX LUNG ABSCESS MASSIVE HAEMOPTYSIS METASTATIC CEREBRAL ABSCESS ASPERGILLOMA MALIGNANT TUMOURS
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PROGNOSIS Life Threatening haemoptysis Bilateral lung involvement Associated lung abscess Malnutrition Chronic anaemia Frequency of exacerbation Specific pathogens; PAS ,Aspergillus,
MAC
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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.
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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
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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
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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
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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
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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:
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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.
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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.
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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
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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
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SURGICAL THERAPYFailed medical therapySuspected neoplasmCongenital lung malformationBronhopleural fistulaMassive haemoptysisOPTIONS: Lobectomy, pneumonectomy,
surgical drainage.
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COMPLICATIONS INTRATHORACIC
Rupture into pleural space
Pleural fibrosisTrapped lungPleuro-cutaneous
fistulaRespiratory failurePyo
pneumothoraxhaemoptysis
EXTRATHORACICSecondary
AmyloidosisSepticemiaMetastatic brain
abscess
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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.
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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.
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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).
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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.
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Viral infections Atypical pneumonia
• Previous thoracic surgery (20%) ; chest drains, percutaneous biopsy
• Blood or lymphatic seedling of the pleural• Traumatic penetration.
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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.
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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
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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
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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
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CHEST X-RAY IN EMPYEMA
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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
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CT SCAN- LOCULATED EMPYEMA
CALCIFIED EMPYEMA
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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.
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THORACOCENTESIS
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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.
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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
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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
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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 .
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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
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COMPLICATIONS Persistent indolent infections Osteomyelitis of the rib Tuberculous abscess Septicemia,septic shock Trapped lung.
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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!!!
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