Transcript PNEUMONIA AND OTHER PATTERNS OF ACUTE LUNG INJURY

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
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
Predisposing Factors
Impaired Host Resistance
•
•
•
•
Chronic Disease
Malignancy
Immune Deficiency
Iatrogenic – immunosuppressive Rx
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 preexisting bronchitis / bronchiolitis
• Lobar (less frequent)
– widespread fibrinosuppurative consolidation of
a large portion of a lobe or an entire lobe
Aetiology
•
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)
Nature of Host Response
•
•
•
•
•
Acute fibrinous
Granulomatous
Organizing
Interstitial
Eosinophilic
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, postoperative
– ‘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 appearance
of lung at autopsy scattered, discrete
yellowish areas of
lung consolidation
centred around the
bronchioles
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 of
aspiration pneumonia in the lung
R>L
a
(a) supine
(b) on side
b
Complications of Pneumonia
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•
•
•
•
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)
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
Empyema
Pus filled pleural
cavity is lined by
thick granulation tissue
(peeled back on left
side of photograph).
This loculation of pus
allows ongoing bacterial
proliferation because
access of antibiotics is
denied. Empyema
therefore 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
Exudative stage
• Pathology:
– Acute (exudative) stage
– Proliferative or organizing stage
Proliferative stage
Stages of DAD
Early / Acute / Exudative Phase:
Day 1:
Day 3-7:
Week 1:
Interstitial / alveolar haemorrhage & fibrin
Hyaline membranes
Type II pneumocyte hyperplasia
Interstitial inflammation
Late / Organizing / Proliferative Phase:
1-2 weeks:
Fibroblast proliferation
Organization & fibrosis
Treatment & Prognosis
• ICU
– Continuous positive airway pressure (CPAP)
ventilation?
• Overall 50-60% mortality
• 20% morbidity in survivors