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PNEUMONIA & other patterns of acute lung injury. PNEUMONIA DIFFUSE ALVEOLAR DAMAGE. PNEUMONIA. Inflammatory consolidation of the lung parenchyma NORMAL DEFENCES MECHANISMS Nasal clearance Tracheobronchial clearance Alveolar clearance. Local Factors Loss / impairment of cough reflex
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PNEUMONIA& other patterns of acute lung injury PNEUMONIA DIFFUSE ALVEOLAR DAMAGE
PNEUMONIA Inflammatory consolidation of the lung parenchyma NORMAL DEFENCES MECHANISMS • Nasal clearance • Tracheobronchial clearance • Alveolar clearance
Local Factors Loss / impairment of cough reflex Impaired mucociliary elevator Impaired function of alveolar macrophages Accumulated / stagnant secretions Impaired Host Resistance Chronic Disease Malignancy Immune Defficiency Iatrogenic – immunosuppressive Rx PNEUMONIA – why?
PNEUMONIA Classification Anatomic Distribution Aetiology Nature of host inflammatory reaction
PNEUMONIA- Anatomic Distribution Lobar vs. Bronchopneumonia • Lobar(less frequent) - widespread fibrinosuppurative consolidation of a large portion of a lobe or an entire lobe • Bronchopneumonia - patchy consolidation, usually extension of pre-existing bronchitis / bronchiolitis
PNEUMONIA - Aetiology • INFECTIOUS Acute Bacterial Pneumonia NB Streptococcus pneumoniae = pneumococcus The others: Staphyllococcus aureus Streptococcus pyogenes Haemophilius Influenza Klebsiella pneumoniae Legionella pneumoniae Viral, Mycobacterial, Fungal, Parasitic (NB in an immunocompromised population) • ASPIRATION • LIPID – endogenous vs. exogenous
PNEUMONIA - Nature of Host Response • Acute fibrinous • Granulomatous • Organizing • Interstitial • Eosinophilic
LOBAR PNEUMONIA • Abrupt onset • Pleuritic chest pain, rusty sputum • High fever, rapid & shallow resps, • Leucocytosis • Healing “by crisis”
LOBAR PNEUMONIA • Structural Changes: uniform • 4 Stages: Congestion Red Hepatization Grey Hepatization Resolution
BRONCHOPNEUMONIA • Successive infection of conductive airways • Infants, debilitated young children, elderly, post-operative • Insidious onset • Peripheral hypoxia • Slow healing, resolution “by lysis”
BRONCHOPNEUMONIA • Widespread patchy areas of inflammation spreading from bronchitis and bronchiolitis • Lower lobes – larger and more numerous foci • Pale areas raised above the surface of the surrounding lung parenchyma • Recovery – liquefaction – but also by fibrosis
Acute Pneumonia Alveolar Spaces filled by acute inflammatory cells (neutrophils)
Acute Pneumonia Acute Inflammatory cells within alveolar spaces
PNEUMONIA - Complications • Abscess Formation • Organization • Empyema – suppurative pericarditis • Bronchiectasis • Bacteraemic dissemination to other organs (metastatic abscesses) – endocarditis meningitis peritonitis suppurative arthritis
LUNG ABSCESS • Localized focus of suppuration consisting of a collection of pus that is walled off by chronic inflammatory / granulation tissue and fibrous tissue • Formation of an abscess entails necrosis and destruction of lung tissue • Causes – preceding pneumonia, bronchial obstruction – tumour, foreign body, aspiration, septic embolism
BRONCHIECTASIS • Permanent dilatation of the bronchi accompanied by inflammatory changes in their walls and surrounding parenchyma • Recurrent inflammation of bronchial walls & fibrosis in the surrounding parenchyma – traction on bronchi – dilatation • Divided into post-inflammatory, post-obstructive, and congenital / hereditary conditions • Cough, fever, foul sputum
BRONCHIECTASIS • Localized vs. widespread • Basal segments of LLs, RML & lingula • Gross: dilated bronchi exending to pleural surface, surrounding scarring • Microscopy: mucosal ulceration, submucosal CI & granulation tissue, adjacent OP • Complications: Cor pulmonale Brain abscess Amyloid
DIFFUSE ALVEOLAR DAMAGE (DAD) • Pathologic manifestation of Adult Respiratory Distress Syndrome (ARDS) • Sequence of events that follows acute lung injury caused by a variety of toxic insults • Diffuse = damage to all parts of the alveolus: epithelium, endothelium and interstitium
DAD - Clinical Syndrome • Acute onset of dyspnoea • Diffuse pulmonary infiltrates • Rapid development of respiratory failure • High mortality ~ 50%
DAD - Pathology Two Discrete but Overlapping Stages: Early and Late Acute and Organizing Exudative and proliferative
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
DAD has many Aetiolgies • Infection • Inhalants • Ingestants • Drugs • Shock • Sepsis • Radiation • Misc. • Idiopathic