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