1. Pneumonia & Other Patterns of Acute Lung Injury

2. Pneumonia Definition: Normal defence mechanisms: Nasal clearance
Inflammatory consolidation of the lung parenchyma caused by formation of intra-alveolar inflammatory exudate resulting from lung infection
Normal defence mechanisms:
Nasal clearance
Tracheobronchial clearance
Alveolar clearance

3. Predisposing Factors Local Factors Loss / impairment of cough reflex
(e.g. altered consciousness)
Impaired mucociliary elevator (e.g. smoking)
Impaired function of alveolar macrophages
(e.g. smoking, alcohol)
Accumulated / stagnant secretions (e.g. CF)
Oedema or congestion

4. Impaired Host Resistance
Predisposing Factors
Impaired Host Resistance
Chronic Disease
Malignancy
Immune Deficiency
Iatrogenic – immunosuppressive Rx

5. Pathogenesis Inhalation of air droplets
Aspiration of infected secretions or objects
Haematogenous spread

6. Classification Anatomic distribution Aetiology (microbiology)
Clinical classification
Nature of host inflammatory reaction

7. Anatomic Classification
Bronchopneumonia
patchy consolidation, usually extension of pre-existing bronchitis / bronchiolitis
Lobar (less frequent)
widespread fibrinosuppurative consolidation of a large portion of a lobe or an entire lobe

8. Aetiology Infectious: Aspiration (chemical & bacterial)
Acute Bacterial Pneumonia
NB Streptococcus pneumoniae = pneumococcus (>60%)
Staphyllococcus aureus
Haemophilius Influenza
Legionella pneumophilus
Klebsiella, Pseudomonas, E. coli, Proteus (Hospital-acquired)
Viral, Mycobacterial, Fungal, Parasitic (immunocompromised)
Aspiration (chemical & bacterial)

9. Nature of Host Response
Acute fibrinous
Granulomatous
Organizing
Interstitial
Eosinophilic

10. Bronchpneumonia
Infection centred on bronchi but extends into alveoli - patchy consolidation
Streptococcus pneumoniae, Haemophilus influenza, Staphylococcus aureus
Successive infection of conductive airways
Infants, debilitated young children, elderly, post-operative
‘Old man’s friend’

11. Widespread patchy areas of inflammation spreading from bronchitis and bronchiolitis
Lower lobes – larger and more numerous foci
Pale, slightly raised areas above the surface of the surrounding lung parenchyma

16. Acute Pneumonia
Alveolar Spaces filled by acute inflammatory cells (neutrophils)

17. Acute Pneumonia
Acute Inflammatory cells within alveolar spaces

18. Lobar Pneumonia Alcoholics Poor social/medical care
Otherwise healthy adults (20-50 yrs)
Usually Pneumococcus (90%) or Klebsiella
Abrupt onset
Pleuritic chest pain, rusty sputum
High fever, rapid & shallow breathing

19. Classic Stages of Lobar Pneumonia
1. Congestion
2. Red hepatisation
3. Grey hepatisation
4. Resolution

20. Congestion: Vascular engorgement Intra-alveolar fluid
Small numbers of neutrophils
Often numerous bacteria
Gross: heavy and hyperaemic lung

21. Red hepatisation: Vascular congestion persists
Extravasation of RBCs into alveolar spaces
Alveolar fibrinosuppurative exudate
Gross: solidification (consolidation) of the lung parenchyma with similar appearance to liver.

23. Grey hepatisation: Red cells disintegrate
Persistence of the neutrophils and fibrin.
Gross: The alveoli still appear consolidated, but grossly the color is paler (grey/brown).

25. Resolution:
Exudate is digested by enzymatic activity, and cleared by macrophages or by cough mechanism.

26. Primary Atypical Pneumonia
Inflammation of alveolar septa & interstitium
Fever, dry cough, dyspnoea but NO CONSOLDATION = atypical
Mycoplasma pneumoniae commonest
Others: viruses (e.g. Influenza virus), Chlamydia & Rickettsia.

27. R > L

29. Complications of Pneumonia
Abscess Formation
Organisation (fibrosis)
Empyema – suppurative pericarditis
Bronchiectasis
Bacteraemic dissemination to other organs (metastatic abscesses)
Endocarditis, Meningitis, Peritonitis & Suppurative arthritis
N.b. pneumonia is 6th leading cause of death (USA)

30. Lung Abscess Localized suppurative necrosis
Collection of pus that is walled off by chronic inflammatory / granulation tissue and fibrous tissue
Organisms commonly cultured:
Staphylococci
Streptococci
Gram-negative
Anaerobes
Frequent mixed infections
Pathogenesis:
Preceding pneumonia
Bronchial obstruction – tumour, foreign body, aspiration
Septic embolism

33. Diffuse Alveolar Damage (DAD)
Pathologic manifestation of Adult Respiratory Distress Syndrome (ARDS) / ‘Shock Lung’
Rapid onset respiratory failure and arterial hypoxaemia refractory to O2 therapy
End result of acute alveolar injury
Caused by a variety of toxic insults
Diffuse = damage to all parts of the alveolus: epithelium, endothelium and interstitium

34. Clinical Syndrome Acute onset of dyspnoea
Diffuse pulmonary infiltrates
Rapid development of respiratory failure
High mortality (50-60%)

35. Diffuse alveolar damage
Basic lesions: injury to pneumocytes & endothelial cells by:
Oxygen-derived free radicals
Activated neutrophils and macrophages
Loss of surfactant
Etiology:
Infections (viral)
Gas inhalation or liquid aspiration
Drugs, chemical, radiation
Shock, sepsis, trauma, idiopathic
Pathology:
Acute (exudative) stage
Proliferative or organizing stage
Exudative stage
Proliferative stage

36. Stages of DAD Early / Acute / Exudative Phase:
Day 1: Interstitial / alveolar haemorrhage & fibrin
Day 3-7: Hyaline membranes
Type II pneumocyte hyperplasia
Week 1: Interstitial inflammation
Late / Organizing / Proliferative Phase:
1-2 weeks: Fibroblast proliferation
Organization & fibrosis

40. Treatment & Prognosis ICU Overall 50-60% mortality
Continuous positive airway pressure (CPAP) ventilation?
Overall 50-60% mortality
20% morbidity in survivors