Pneumonia & Other Patterns of Acute Lung Injury

Pneumonia

• Definition:– 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

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

Predisposing Factors

Impaired Host Resistance

• Chronic Disease

• Malignancy

• Immune Deficiency

• Iatrogenic – immunosuppressive Rx

Predisposing Factors

Pathogenesis

• Inhalation of air droplets

• Aspiration of infected secretions or objects

• Haematogenous spread

Classification

• Anatomic distribution

• Aetiology (microbiology)

• Clinical classification

• Nature of host inflammatory reaction

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

• Infectious: – 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)

Aetiology

• Acute fibrinous

• Granulomatous

• Organizing

• Interstitial

• Eosinophilic

Nature of Host Response

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’

• 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

Bronchopneumonia

Gross appearanceof lung at autopsy -scattered, discreteyellowish areas oflung consolidationcentred around thebronchioles

Acute Pneumonia

Alveolar Spaces filled by acute inflammatory cells (neutrophils)

Acute Pneumonia

Acute Inflammatory cells within alveolar spaces

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

Classic Stages of Lobar Pneumonia

1. Congestion

2. Red hepatisation

3. Grey hepatisation

4. Resolution

• Congestion:– Vascular engorgement– Intra-alveolar fluid– Small numbers of neutrophils– Often numerous bacteria

– Gross: heavy and hyperaemic lung

• 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.

• 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).

• Resolution:– Exudate is digested by enzymatic activity, and cleared

by macrophages or by cough mechanism.

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.

Gross appearance and mechanism of localisation ofaspiration pneumonia in the lung

(a) supine (b) on side

a

b

R > L

• 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)

Complications of Pneumonia

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

EmpyemaPus filled pleural cavity is lined bythick granulation tissue(peeled back on leftside of photograph).This loculation of pusallows ongoing bacterial proliferation because access of antibiotics is denied. Empyematherefore must be drained before it can heal.

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

Clinical Syndrome

• Acute onset of dyspnoea

• Diffuse pulmonary infiltrates

• Rapid development of respiratory failure

• High mortality (50-60%)

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 stageExudative stage

Proliferative stageProliferative stage

Stages of DAD

Early / Acute / Exudative Phase: Day 1: Interstitial / alveolar haemorrhage & fibrinDay 3-7: Hyaline membranes

Type II pneumocyte hyperplasiaWeek 1: Interstitial inflammation

Late / Organizing / Proliferative Phase:

1-2 weeks: Fibroblast proliferation Organization & fibrosis

• ICU– Continuous positive airway pressure (CPAP)

ventilation?

• Overall 50-60% mortality• 20% morbidity in survivors

Treatment & Prognosis