Post on 02-Jan-2016
description
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
• INFECTIOUS Acute Bacterial PneumoniaNB 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 - Aetiology
• Acute fibrinous
• Granulomatous
• Organizing
• Interstitial
• Eosinophilic
PNEUMONIA - Nature of Host Response
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”
• 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
BRONCHOPNEUMONIA
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
Gross appearance and mechanism of localisation ofaspiration pneumonia in the lung
(a) supine (b) on side
a
b
• Abscess Formation• Organization• Empyema – suppurative pericarditis• Bronchiectasis• Bacteraemic dissemination to other organs
(metastatic abscesses) – endocarditis
meningitisperitonitissuppurative arthritis
PNEUMONIA - Complications
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
• 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
BRONCHIECTASIS
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)• 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 & fibrinDay 3-7: Hyaline membranes
Type II pneumocyte hyperplasiaWeek 1: Interstitial inflammation
Late / Organizing / Proliferative Phase:1-2 weeks: Fibroblast proliferation
Organization & fibrosis
• Infection
• Inhalants
• Ingestants
• Drugs
• Shock
• Sepsis
• Radiation
• Misc.
• Idiopathic
DAD has many Aetiolgies