7 SUPPURATIVE LUNG DISEASES.pptx88888888888

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1. SUPPURATIVE LUNG DISEASES DR S CONTEH 1

2. Introduction Suppurative lung diseases are a group of disorders which result in chronic lung infection, with pus in the lungs Individuals with suppurative lung diseases present with chronic purulent sputum and recurrent respiratory tract infections The aetiology of these conditions is variable and they include the following: Bronchiectasis Lung abscess Empyema 2

3. BRONCHIECTSIS 3

4. Outline Introduction Causes Pathophysiology Clinical features Investigations Treatment 4

5. Introduction Bronchiectasis refers to abnormal and permanently dilated airways The bronchial walls become inflamed, thickened and irreversibly damaged The mucociliary transport mechanism is impaired and frequent bacterial infections ensue Bronchiectasis shares many clinical features with COPD, including inflamed and easily collapsible airways, obstruction to airflow, and frequent clinic visits and hospitalizations 5

6. Causes of Bronchiectasis Congenital Deficiency of bronchial wall elements Pulmonary sequestration Mechanical bronchial obstruction Intrinsic: Foreign body Inspissated mucus Post- tuberculous stenosis Tumour Extrinsic: Lymph node Tumour Postinfective bronchial damage Bacterial and viral pneumonia, including pertussis, measles Aspiration pneumonia Granuloma Tuberculosis Sarcoidosis Diffuse diseases of the lung parenchyma Idiopathic pulmonary fibrosis Immunological over-response Allergic bronchopulmonary aspergillosis Post-lung transplant Immune deficiency Primary: Panhypogammaglobulinaemia Selective immunoglobulin deficiencies (IgA and IgG2) Secondary: HIV Malignancy 6

7. Causes of Bronchiectasis Mucociliary clearance defects Genetic: Primary ciliary dyskinesia ( Kartagener’s syndrome with dextrocardia and situs-inversus ) Cystic fibrosis Acquired: Young’s syndrome – azoospermia , sinusitis 7

8. Pathophysiology Bronchiectasis may result from congenital defect affecting airway ion transport or ciliary function (cystic fibrosis) It may be acquired; secondary to damage to the airways by a destructive infection, inhaled toxin or foreign body The result is chronic inflammation and infection in airways, then dilatation Localised bronchiectasis may occur due to accumulation of pus beyond an obstructing bronchial lesion; eg . enlarged tuberculous hilar lymph nodes, bronchial tumour or inhaled foreign body ( eg aspirated peanut) 8

9. Pathophysiology The bronchiectatic cavities may be lined by granulation tissue, squamous epithelium or normal ciliated epithelium There may also be inflammatory changes in the deeper layers of the bronchial wall and hypertrophy of the bronchial arteries Chronic inflammatory and fibrotic changes are usually found in the surrounding lung tissue, resulting in progressive destruction of the normal lung architecture in advanced cases 9

10. Clinical features Cough with production of large amounts of sputum With mild bronchiectasis sputum only becomes yellow or green sputum after an infection Localized areas of the lung may be particularly affected, and sputum production will depend on position As condition worsens, patient suffers from persistent halitosis, recurrent febrile episodes, malaise and pneumonia 10

11. Clinical features Clubbing occurs, and coarse crackles can be heard over the infected areas, usually the lung bases In severe cases there is continuous production of foul-smelling, thick, khaki-coloured sputum Haemoptysis can occur either as blood-stained sputum or massive haemorrhage Breathlessness may result from airflow limitation 11

12. Investigations Chest X-ray: may be normal or may show dilated bronchi with thickened bronchial walls and sometimes multiple cysts High-resolution CT scanning: shows bronchial dilatation with loss of airway tapering at the periphery, bronchial wall thickening and cysts at the end of the bronchioles with a sensitivity of 97% Sputum examination: culture and sensitivity of the organisms is essential for adequate treatment. The major pathogens are Staph. aureus , Pseudomonas aeruginosa 12

13. Investigations Sinus X-rays: 30% have concomitant rhinosinusitis Serum immunoglobulins : 10% of adults with bronchiectasis have antibody deficiency (mainly IgA) Sweat electrolytes – if cystic fibrosis is suspected Mucociliary clearance (nasal clearance of saccharin) - A 1 mm cube of saccharin is placed on the inferior turbinate and the time to taste measured (normally less than 30 minutes) 13

14. Treatment Postural drainage Postural drainage is essential and patients must be trained by physiotherapists to tip themselves into a position in which the affected lobe(s) are uppermost at least 3 times daily for 10–20 minutes Most patients find that lying over the side of the bed with head and thorax down is effective 14

15. Treatment Antibiotics Bronchopulmonary infections need to be eradicated if progression of the disease is to be halted In mild cases, intermittent antibiotic therapy with cefaclor 500mg TDS or ciprofloxacin 500 mg BD may be sufficient; Flucloxacillin 500 mg QID is needed if S. aureus is isolated If sputum remains yellow or green despite regular physiotherapy and intermittent antibiotic therapy, or if lung function deteriorates despite treatment with bronchodilators, Pseudomonas aeruginosa infection is likely Treatment requires parenteral or aerosol chemotherapy at regular 3-month intervals Ceftazidime 2 g IV TDS or by inhalation (1 g BD) has been shown to be effective Ciprofloxacin 750 PO BD may work in the short term, but resistance can develop rapidl 15

16. Treatment Bronchodilators Bronchodilators are useful in patients with demonstrable airflow limitation Anti-inflammatory agents Inhaled or oral steroids can decrease the rate of progression Surgery Unfortunately, it is rare for bronchiectasis to be sufficiently localized for resection to be practical Lung or heart–lung transplantation is sometimes required 16

17. Complications Pneumonia Pneumothorax Empyema Metastatic cerebral abscess Haemoptysis Haemoptysis Severe, life-threatening haemoptysis can also occur, particularly in patients with cystic fibrosis Massive haemoptysis originates from the high-pressure systemic bronchial arteries and has a mortality of 25% Other causes of massive haemoptysis include pulmonary tuberculosis (most common) Aspergilloma lung abscess Primary and secondary malignant tumours 17

18. Prognosis The advent of effective antibiotic therapy has greatly improved the prognosis Ultimately, most patients with severe bronchiectasis will develop respiratory failure Cor-pulmonale is another well-recognized complication The three pathogens that can cause infective episodes and are difficult to eradicate are Pseudomonas aeruginosa , Aspergillus fumigatus and MAI 18

19. LUNG ABSCESS 19

20. Outline Background Aetiology Clinical features Investigation Treatment 20

21. Background Refers to severe localized suppuration in the lung associated with cavity formation on the chest X-ray, often with the presence of a fluid level, and not due to tuberculosis There are many causes of lung abscess, but the most common is aspiration, particularly amongst heavy alcohol users following aspiration pneumonia Lung abscesses also frequently follow the inhalation of a foreign body into a bronchus and occasionally occur when the bronchus is obstructed by a bronchial carcinoma Chronic or subacute lung abscesses follow an inadequately treated pneumonia 21

22. Background Abscesses also develop during the course of specific pneumonias, particularly when the infecting agent is Staph. aureus or Klebsiella pneumonia Septic emboli, usually staphylococci, result in multiple lung abscesses. Infarcted areas of lung occasionally cavitate and rarely become infected Amoebic abscesses occasionally develop in the right lower lobe following trans-diaphragmatic spread from an amoebic liver abscess 22

23. Aetiology 23

24. Clinical Features The clinical features are persisting and worsening pneumonia associated with the production of large quantities of sputum, which is often foul-smelling owing to the growth of anaerobic organisms There is usually a swinging fever; malaise and weight loss occur The chest signs may be few but clubbing often develops if the condition is not rapidly cured The patient is often anaemic with a high ESR and CRP 24

25. Investigation Lung abscess can usually be detected with standard chest x-ray CT-scan is preferred for precise definition of the abscess and its location and possibly for detection of underlying lesions Bacteriological investigation of lung abscess and empyema is best conducted on specimens obtained by transtracheal aspiration, bronchoscopy or percutaneous transthoracic aspiration with ultrasound or CT guidance Bronchoscopy is helpful to exclude carcinomas and foreign bodies Microbiologic studies include stains and cultures of expectorated sputum to detect aerobic bacterial pathogens In appropriate settings, it is important to consider cultures for fungi and mycobacteria 25

26. Treatment Although anaerobic organisms are found in up to 70% of lung abscesses there is usually a mixed flora Appropriate antibiotic treatment is given for up to 6 weeks Antibiotics should be given to cover both aerobic and anaerobic organisms An appropriate initial choice is cefuroxime1 g i.v. 6-hourly and metronidazole 500 mg i.v. 8- hourly for 5 days, followed by oral cefaclor and metronidazole for a prolonged period depending on bacterial sensitivities 26

27. EMPYEMA 27

28. Outline Introduction Aetiology Pathology Clinical features Investigations Treatment 28

29. Introduction Empyema is the collection of pus within the pleural cavity The pus may be as thin as serous fluid or so thick that it is impossible to aspirate even through a wide-bore needle This usually arises from bacterial spread from a severe pneumonia or after the rupture of a lung abscess into the pleural space Empyema may involve the whole pleural space or only part of it (' loculated ' or 'encysted' empyema) and is usually unilateral Typically an empyema cavity becomes infected with anaerobic organisms and the patient is severely ill with a high fever and a neutrophil granulocytosis 29

30. Aetiology Empyema is always secondary to infection in a neighbouring structure, usually the lung, most commonly due to the bacterial pneumonias and tuberculosis Over 40% of patients with community-acquired pneumonia develop an associated pleural effusion ('para-pneumonic' effusion) and about 15% of these become secondarily infected Other causes are infection of a haemothorax following trauma or surgery, oesophageal rupture and rupture of a subphrenic abscess through the diaphragm Despite availability of antibiotics effective against pneumonia, empyema remains a significant cause of morbidity and mortality even in developed countries due delays in diagnosis or the initiation of appropriate therapy 30

31. Pathology Both layers of pleura are covered with a thick, shaggy inflammatory exudate The pus in the pleural space is often under considerable pressure, and if not adequately treated; pus may rupture into a bronchus causing a bronchopleural fistula and pyopneumothorax pus may track through the chest wall with the formation of subcutaneous abscess or sinus 31

32. Pathology Empyema will only heal if infection is eradicated and empyema space is obliterated, allowing apposition of visceral and parietal pleura This occur if re-expansion of the compressed lung is secured at an early stage by removal of all pus from the pleural space Successful re-expansion and resolution will not occur if: the visceral pleura becomes grossly thickened and rigid due to delayed treatment or inadequate drainage of infected pleural fluid pleural layers are kept apart by air entering the pleura through a bronchopleural fistula there is underlying disease in the lung, such as bronchiectasis, bronchial carcinoma or pulmonary TB preventing re-expansion In these circumstances an empyema tends to become chronic, and healing will only occur with surgical intervention 32

33. Clinical Features Empyema should be suspected in patients with pulmonary infection if there is persisting or recurrent pyrexia despite treatment with a suitable antibiotic In other cases the primary infection may be so slight that it passes unrecognised and the first definite clinical features are due to the empyema Once an empyema has developed, systemic features are prominent: Pyrexia, usually high and remittent Rigors, sweating, malaise and weight loss Polymorphonuclear leucocytosis, high CRP 33

34. Clinical Features Local features Pleural pain Breathlessness Cough and sputum usually because of underlying lung disease Copious purulent sputum if empyema ruptures into a bronchus ( bronchopleural fistula) Clinical signs of pleural effusion Reduced expansion Stony dull percussion Abscent breath sounds 34

35. Investigation Chest X-ray The appearances may be indistinguishable from those of pleural effusion When air is present in addition to pus ( pyopneumothorax ), a horizontal 'fluid level' marks the air/liquid interface Ultrasound shows the position of the fluid, the extent of pleural thickening and whether fluid is in a single collection or multiloculated by fibrin and debris CT Scan Gives information on the pleura, the underlying lung parenchyma and patency of the major bronchi 35

36. Investigation Aspiration of fluid Ultrasound or CT is used to identify the optimal site to undertake aspiration, which is best performed using a wide-bore needle If the fluid is thick and turbid pus, empyema is confirmed Other features suggesting empyema include; Fluid glucose < 3.3 mmol /L (60 mg/ dL ) LDH > 1000 U/L Fluid pH < 7.0 (H+ >100 nmol /L) The pus is frequently sterile on culture if antibiotics have already been given The distinction between tuberculous and non- tuberculous disease can be difficult and often requires pleural biopsy, histology and culture 36

37. Treatment Non- tuberculous empyema When the patient is acutely ill and the pus is thin, a wide-bore intercostal tube should be inserted into the most dependent part of the empyema space and connected to an underwater-seal drain system If the aspirate is turbid fluid or frank pus, or if loculations are seen on ultrasound, the tube should be put on suction and flushed regularly with 20 mL normal saline An antibiotic directed against the organism causing the empyema should be given for 2-4 weeks Empirical antibiotic treatment ( e.g IV co- amoxiclav or cefuroxime with metronidazole) should be used if the organism is unknown An empyema can often be aborted if these measures are started early When the pus is very thick or loculated , surgical intervention is required 37

38. Treatment Tuberculous empyema Anti-TB chemotherapy must be started immediately and the pus in the pleural space aspirated through a wide-bore needle (or intercostal tube) until it ceases to reaccumulate In many patients, no other treatment is necessary but surgery is occasionally required to ablate a residual empyema space Fibrothorax , with restriction and encasement of the lung in thickened, often calcified pleura is a late complication 38

39. Questions 39