1. Suppurative Lung Diseases
Author:
DR.N.C.GOWRISHANKAR
MD DCH DNB
Pediatric Pulmonologist & Bronchoscopist
Mehta Children’s Hospital, Chennai
Reviewers:
Dr. Subramanya N. K

2. Suppurative disease of the lung
Bronchiectasis
Lung abscess
Empyema
Time to develop suppurative disease -
Empyema –days
lung abscess -days to a week
bronchiectasis -few weeks to a month

3. Bronchiectasis
Bronchiectasis – first described- rené laennec (inventor – stethoscope)
Greek bronchion -windpipe ektasis stretched.
Age group 5-15
Causes
Congenital / Heriditary
Acquired

4. Bronchiectasis Definition :
Abnormal permanent dilatation of bronchi or subsegmental bronchi with inflammatory destruction of peribronchial tissue [muscle, cartilage] with accumulation of secretions in the dependent bronchi

5. Bronchiectasis In developing countries
Frequently sequelae of acute infection.
In developed world
in association with underlying disorders such as cystic fibrosis
immune deficiencies (including HIV)
primary ciliary dyskinesia
recurrent aspiration syndromes.

6. Bronchiectasis
End result of many pathophysiologic processes that make bronchial walls
weakened
easily collapsible
chronically inflamed
plugged with mucus secretions

7. Bronchiectasis - types
Classic ‘Reid’ classification (gross histological appearance) - three different patterns
Cylindrical bronchiectasis - mildly uniform airway dilation
Varicose bronchiectasis - focally dilated areas between narrowed segments
Saccular bronchiectasis - balloon-like airway dilation with more disruption of lung parenchyma

8. Bronchiectasis-Pathogenesis
Chronic infection – recruitment of neutrophils, T-lympho cytes, monocyte-derived cytokines with release of inflammatory mediators - elastases & collagenases
Loss of ciliated columnar epithelium
Micro-abscess in bronchial wall with peribronchial inflammation
Destruction -elastic & muscle tissue, cartilage of bronchus.
Endarteritis of pulmonary vessels
Bronchial arterial proliferation(predisposes to hemoptysis)

9. Bronchiectasis-Congenital causes
Structural –William campbell Syndrome, Mounier kuhn syndrome , airway malacia
Abnormal immune function – agammaglobulinemia, combined immunodeficiency, neutrophil function abnormalities
Cystic fibrosis (CF)
Ciliary abnormalities - Kartageners syndrome, Immotile cilia syndrome
Others – yellow nail syndrome, alpha 1 anti-trypsin deficiency, ataxia telangiectasia

10. Bronchiectasis-Acquired causes
Infection
Obstruction
Aspiration syndrome
BACTERIAL
Tb ,Pertussis, Mycoplasma
VIRAL
Measles, Viral Pneumonia,HIV
Chronic lung allograft rejection
Foreign body
Lymph nodes
Cardiomegaly
Tumours
Endobronchial TB
Inspissated mucus-[cystic fibrosis, Immotile cilia syndrome]
Near drowning Oropharyngeal surgery
General anesthesia
Dental extraction
GERD
Hydrocarbon poisoning

11. Bronchiectasis-clinical manifestations
Wide spectrum of disease severity
Intermittent symptoms cough and occasional lower respiratory tract infections.
Daily symptoms cough and copious purulent fetid sputum

12. Clinical manifestations-common
Most common symptom - persistent cough, typically "wet" or productive
Episodic exacerbations of infection-
Increased cough and sputum production
Fever
Pleuritic chest pain
Dyspnea
Absence of sputum production does not exclude bronchiectasis (younger children may not be able to expectorate sputum)

13. Clinical manifestations-uncommon
Hemoptysis - uncommon in children
Occurs - erosion of inflamed airway tissue adjacent to pulmonary vessels.
Bleeding
Mild, with blood streaked sputum
Profuse amounts of fresh bleeding if larger pulmonary vessels rupture.

14. Clinical manifestations-uncommon
Dyspnea and exercise intolerance
uncommon at presentation
may develop as disease progresses
may occur during acute exacerbation (intercurrent infection)

15. Clinical manifestations-uncommon
Cyanosis- severe bronchiectatic lung disease
Severe hypoxemia due to mismatched pulmonary ventilation and perfusion.
If hypoxemia - prolonged and profound- cause pulmonary hypertension & cor-pulmonale.

16. Clues for aetiology
Failure to thrive- cystic fibrosis (CF) and immunodeficiency disorders.
Chronic sinusitis – cystic fibrosis, ciliary dysfunction disorders, immunodeficiencies
Chronic ear infection with or without otorrhea -ciliary dysfunction.

17. Clues for aetiology Steatorrhea — suggests cystic fibrosis.
Choking history— foreign body aspiration or swallowing disorder with chronic aspiration of oropharyngeal contents.
Dextrocardia suggests primary ciliary dyskinesia.

18. Physical examination General physical examination Failure to thrive
Sinus and ear infections
Presence of congenital anomalies
Clubbing
Schamroth sign- obliteration of the quadrangular space when both fingers kept in unison
Distal phalangeal depth(DPD) to interphalangeal depth ratio(IPD) > 1

20. Clinical findings-common
clubbing
halitosis
growth retardation
Course leathery crackles - over the area of bronchiectasis

21. Goals of evaluation To confirm diagnosis of bronchiectasis
To identify underlying etiology & any potentially treatable causes
To assess severity of pulmonary disease

22. Diagnosis
Diagnosis depends on radiographically or anatomically visualizing abnormal dilatation of airways
Diagnostic procedure of choice high-resolution computed tomography (HRCT)scan
Other tests- diagnose underlying conditions.

23. Laboratory investigations
Complete blood count with differential
Sputum exam- volume, gram stain, C & S ,
Immunodeficiency- Total IgM, IgA and IgG
Tests for Tuberculosis –
Mantoux
Chest Xray
Resting Gastric juice for AFB
Test for cystic fibrosis (sweat chloride and/or DNA testing)

24. sputum When collected in conical flask -three layers Thin and frothy
Thick and mucopurulent
Opaque with dietrich’s plugs

25. Investigations Flexible bronchoscopy
shows structural alteration of bronchial tree
bronchoalveolar lavage - remove mucus plugs/ to obtain lower airway cultures.
If an airway foreign body is discovered-rigid bronchoscopy -for removal
HIV screening
Ciliary biopsy

26. Investigations
Test for GERD : 24 hour pH monitoring, upper gastrointestinal endoscopy and technetium milk scan scintigraphy.
Test for aspiration due to inadequate airway protective mechanisms during swallowing or dysphagia -evaluated by videofluoroscopy.

27. Investigations Pulmonary function tests -severity of lung disease
should be performed if the patient is able to do
useful tool to evaluate long-term progression of lung disease.
Most patients with bronchiectasis have features of obstructive lung disease (low FEV1 & FEV1/FVC ratio)

28. Laboratory investigations
Test for allergic bronchopulmonary aspergillosis
immunoglobulin E (IgE)
serum precipitins for Aspergillus species
sputum culture for fungus
aspergillus skin test

29. Imaging-Chest radiography
Dilated and thickened airways (tram-tracking or parallel lines)
Irregular peripheral opacities that represent mucopurulent plugs.
Loss of lung volume and peribronchial fibrosis

30. Imaging-Distribution of bronchiectasis
Cystic fibrosis - upper lobes
Allergic bronchopulmonary aspergillosis-Centrally located bronchiectasis
Bronchopulmonary sequestration-lower lobe and usually unilateral

31. Xray Chest PA view

32. Xray and CT chest – note the severity in CT chest

33. Bronchiectasis –Imaging -CT
Most sensitive -to detect bronchiectasis high resolution computed tomography (HRCT)
Internal diameter of airway - larger than diameter of adjacent artery
Airway wall thickening ("signet ring" shadows) with or without air fluid levels
Volume loss, mucus plugging and air trapping

34. CT Chest with bronchiectasis both lower lobes
CT Chest with bronchiectasis left lingular segment
CT Chest with bronchiectasis both lower lobes

35. CT Chest in ataxia telangiectasia
Telangiectatic vessel in conjunctiva
CT Chest in ataxia telangiectasia

36. Bronchiectasis-treatment
MEDICAL
SURGICAL
Ncgs -bronchiectasis

37. Bronchiectasis -Medical Treatment
Control infection
Physiotherapy
Nutritional support
Identify aetiology and treat accordingly

38. Bronchiectasis – Medical Management
Immediate
Medical treatment
Postural drainage
Relief of atelectasis
Treatment of associated problems
Long term
Continuation of postural drainage
Follow up for reversal

39. Chest Physiotherapy
Facilitate mucous expectoration - manual and mechanical interventions
Chest percussion
Vibration
Postural drainage
Cough-assist devices & airway oscillation-serve as adjuncts to cough (most effective and efficient manner of clearing airway) .

40. Bronchiectasis - Management
Treatment –any identified underlying disorder
Therapy
reduce airway secretions
facilitating their removal - with chest physiotherapy & mucolytic agents
Pharmacotherapy
to improve mucociliary clearance.
Antibiotics
prevent & treat recurrent infections
Surgery- if localised disease -may be considered.

41. Bronchiectasis- Surgical Treatment
Only in unilateral disease
Removal of affected segment/ lobe/lung
Surgery contraindicated if bilateral disease
Unilateral - surgical resection - good prognosis

42. Bronchiectasis - Complications
Broncho pneumonia
Empyema
Lung abscess
Hemoptysis
Metastatic abscess-brain
Osteomyelitis
Cor pulmonale
Amyloidosis

43. Syndromes with bronchiectasis
William campbell syndrome: defect of bronchial cartilage
Mounier khun syndrome : defect of muscular & elastic tissue of trachea & bronchi
Immotile cilia syndrome : Generalised ciliary dysfunction
Kartageners syndrome : Bronchiectasis, sinusitis and situs inversus
Yellow nail syndrome : yellow nail, bronchiectasis, pleural effusion &lymphoedema
Middle lobe syndrome : compression of middle lobe by enlarged lymph node causing bronchiectasis
Young syndrome

44. Prevention of Bronchiectasis
Childhood immunization for measles and pertussis
Screening for tuberculosis and treatment wherever needed
Aggressive appropriate therapy of lower respiratory tract infections
Therapy of child with chronic or recurrent respiratory problems due to recurrent aspiration and/or gastroesophageal reflux disease

45. Bronchiectasis- prognosis
Key to successful outcome -depend on etiology & treatment of underlying problem.
Growth of new pulmonary tissue in children proceeds rapidly until about age 6 years & then tapers off through childhood.
Injury at an early age may be compensated for by growth of normal healthy lungs in the absence of ongoing damage.
Overall - prognosis – good

46. Bronchiectasis- prognosis
In absence of an underlying condition-children with isolated bronchiectasis- good prognosis
Progressive bronchiectasis from underlying disease or ongoing pulmonary insult –causes progressive obstructive defect & ultimately, respiratory compromise

47. Lung abscess

48. Lung abscess
Definition -necrosis of pulmonary tissues by microbial infection and formation of cavities that contains pus (necrotic debris and fluid)
Acute or chronic -duration of symptoms prior to starting treatment
Acute -less than 4 to 6 weeks old
Chronic-longer duration.

49. Lung abscess “Primary lung abscess”
Abscesses caused by an infectious agent in a healthy host
“Secondary lung abscess"
Abscess caused by an infectious agent in children with decreased immune function
Pathogenesis- involves an area of initial pneumonitis that leads to necrosis, cavitation and abscess formation

50. Lung abscess-predisposing factors
Aspiration – when bacteria enter the pulmonary system.
Impaired or ineffective mucociliary defence mechanism
Underlying diseases such as pneumonia.
Children with neurocognitive impairment or disabilities

51. Lung abscess- symptoms
Cough
Fever +/- Chills
Pleuritic chest pain
Difficulty breathing
Diaphoresis
Foul-smelling, bloody, or purulent sputum

52. Lung abscess- course
May spontaneously rupture into pleural space - empyema, pyothorax or pneumothorax.
Connection between abscess cavity & pleural space may persist-formation of broncho- pleural fistula
Rupture into bronchus-drain out

53. Lung abscess-diagnosis
Basic diagnostic test- chest x-ray
- Air fluid level seen
CT chest rarely needed

54. Basic diagnostic test-chest xray Air fluid level seen

55. Lung abscess- management
Admission & IV antibiotic
Intravenous antibiotics-third-generation cephalosporin and clindamycin /vancomycin
Postural drainage –facilitate discharge- pus or necrotic material
Chest physiotherapy – includes coughing and deep breathing- facilitate expectoration - necrotic material
Surgical treatment- rarely needed

56. Lung Abscess Medical treatment (90% success)
Prognosis for children with primary lung abscess - favourable.
Radiological improvement may take longer than clinical resolution

57. Parapneumonic effusion and Empyema

58. Parapneumonic effusion and Empyema
Pleural effusion associated with pneumonia- Parapneumonic effusion (Effusion result - spread of inflammation & infection to pleura).
Presence of pus in pleural cavity- Empyema

59. Empyema is an accumulation of pus in the pleural space
Definition
Empyema is an accumulation of pus in the pleural space
Empyema can occur following:-
Bacterial Pneumonia
Penetrating trauma to chest
Oesophageal perforation
Surgery of the chest

60. Pleural space
Potential anatomic space - small amount of pleural fluid.
Pleural fluid- filtered by parietal pleura - absorbed by visceral pleura
Normally no extra fluid accumulates in pleural space.

61. Pleural fluid - physiology
Imbalance of hydrostatic & oncotic pressure between blood and pleural fluid - Fluid accumulates in pleural space
Lymphatic system removes small amounts of protein that ooze
If extra amounts of protein leak into pleural space (as in pneumonia) lymphatic system fails to cope up - exudative pleural effusion results

62. Streptococcus pneumoniae Staphylococcus aureus H. influenzae
Empyema-organisms
Common organisms
Streptococcus pneumoniae
Staphylococcus aureus
H. influenzae
Klebsiella
Group A streptococcus
Community acquired MRSA

63. Empyema – 3 phases Exudative phase Fibrinopurulent phase
Increased permeability of the inflamed pleura
Fibrinopurulent phase
By accelerated fibrin deposition leading to loculations and pus formation.
Organizational phase
Begins 1 week after infection
Multiloculated empyema and pleural peel with subsequent lung entrapment

64. Empyema- first and second phase
Pleural fluid charecteristics
Exudative phase
Fibrinopurulent phase
Glucose
Normal
Decreased pH
Cell count
Low
High
LDH
>1000
Duration
24-72 hours
7-10 days

65. Empyema- third phase Organizational - third stage
Fibroblasts grow on parietal and visceral pleural surfaces - form inelastic membrane - "pleural peel"
Lung reexpansion restricted & function impaired
Thoracocentesis -may yield a "dry tap“
Occurs 2-4 weeks after empyema develops

66. Empyema -Third stage - pleural peel

67. Empyema- symptoms Symptoms related to empyema Symptoms of pneumonia
Persistent fever
Malaise
Decreased appetite
Cough, chest pain, and dyspnea
Lie on affected side to splint the chest (provide temporary analgesia)
Weight loss if longer than one to two weeks.
Symptoms of pneumonia
But remain febrile or unwell 48 hours after initiation of antibiotic therapy for pneumonia

68. Empyema- signs Appear ill - rarely toxic Tachypnoeic Febrile
Shallow breaths (minimizes pain)
Scoliosis (child splinting affected side)
Mediastinal shift (tracheal deviation and apical impulse shift to opposite side)
Dullness to percussion
Absent breath sounds

69. Xray chest First investigation of choice
Shift of mediastinum to opposite side
Opaque hemithorax
Absence of normal bronchovascular markings
Widening of intercostal spaces

70. Xray chest Doesnot differentiate empyema from parapneumonic effusion
May reveal other findings
Cardiomegaly
Hilar lymphadenopathy
Bone lesions

71. Ultrasonography Confirms presence of fluid in pleural space
Detection of early loculations and septations
Quantification & determination –nature of effusion
Localise-optimal sites for thoracentesis / ICD
Limitations - Cannot distinguish between density of an early exudate and that of solid fibrin

72. Radiology in empyema Chest CT Failure to aspirate pleural fluid
Failure of medical management
Before surgery (thoracotomy or thoracoscopy)

73. Lab investigations CBC with differential
evidence of infection and/or anemia
helpful in monitoring progress
Blood cultures -all children with parapneumonic effusion
CRP- useful- monitoring progress
Serum LDH (pleural fluid LDH/serum LDH ratio > 0.6 – indicates empyema )
Serum electrolytes (to detect SIADH)
Secondary thrombocytosis ( >500,000/microL) and hypoalbuminemia - common

74. Pleural fluid Pleural tap pH, glucose,LDH & differential cell count
Before starting antibiotic therapy-single antibiotic dose can decrease the yield of culturing
Gram stain and bacterial culture ( aerobic and anaerobic culture)
Latex agglutination
Counterimmunoelectrophoresis
pH, glucose,LDH & differential cell count
PMN > 50,000 cells/microL - typical of complicated parapneumonic effusions

75. Diagnostic Thoracocentesis
Counter Immuno Electrophoresis or Latex Agglutination tests of Pleural fluid- may identify pathogens if infection by organisms with capsular polysaccharide antigen in antibiotic exposed cases.

76. Lung re-expansion after ICD
Empyema & ICD
Lung re-expansion after ICD
Empyema - right

77. Parapneumonic effusion
Different management strategies
At different stages
Hospitalization and IV antibiotics
Effusions-increasing/compromising respiratory function
Intercostal chest tube drainage- (ICD)
Left in place -fluid drainage -minimal(<15 ml/day)

78. Empyema- Principles of Therapy
Appropriate Antibiotic Therapy
Adequate drainage
Maintenance of Lung expansion

79. Empyema- Principles of Therapy
IV antibiotics with intercostal drainage tube placement
IV Co- amoxyclav (OR) IV 3rd generation cephalosporin (IV ceftriaxone ) with cloxacillin
Vancomycin - drug of choice to treat MRSA
IV antibiotics - up to two weeks
Antibiotic therapy –modified-sensitivity results
Oral antibiotics – at discharge
Duration of treatment 4- 6 weeks

80. Empyema- Principles of Therapy
Supportive care- antipyretics, analgesia, and early mobilization
Adequate analgesia-for pleuritic pain- prevent secondary scoliosis
IVFluids - poor intake and increased losses from fever and tachypnea

81. Instruments used for ICD

82. ICD Tubes

83. Intercostal tube with Under Water Seal
Drainage
Meticulous care is mandatory
Daily change of Sterile saline
Daily recording of nature and amount of discharge
Ensure air tight connection
Ensure inlet tube is well beneath the fluid level
Ensure that the outlet vent is not closed

84. Debridement of pleural space
Empyema
Surgical
If no improvement with medical management
Loculated or organized pleural effusion
Debridement of pleural space
Video assisted thoracoscopic surgery (VATS)
Thoracotomy - Open decortication

85. complications Bronchopleural fistula Lung abscess
Empyema necessitatis (perforation through the chest wall)

86. Broncho Pleural Fistula
Complication of Empyema
Should be suspected if air leak persists
Occasionally heralds cure by expectoration of pus through the bronchus which is coughed out
Resistant cases are treated by Surgery
Closure of stump
Reinforcement by Neuro vascular muscle pedicles

87. Thank you