dr robin smith dept of respiratory medicine l.
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Dr Robin Smith Dept of Respiratory Medicine. Interstitial and Occupational Lung Disease. Interstitial Disease. Any disease process affecting lung interstitium (ie alveoli, terminal bronchi). Interferes with gas transfer

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interstitial disease
Interstitial Disease
  • Any disease process affecting lung interstitium (ie alveoli, terminal bronchi).
  • Interferes with gas transfer
  • Restrictive lung pattern (may also have some airway obstruction if small airways involved)
  • Symptoms: breathlessness, dry cough
interstitial lung disease
Interstitial Lung Disease


  • Acute
  • Episodic
  • Chronic - part of systemic disease

- exposure to agent (e.g. drug, dust etc)

- idiopathic

acute ild
Acute ILD
  • Infection - usually viral
  • Allergy - eg drug reaction
  • Toxins - cytotoxic drugs, toxic fumes e.g. chlorine
  • Vasculitis - eg Wegener’s granulomatosis, Churg-strauss, SLE, Goodpasture’s syndrome
  • ARDS - trauma, sepsis
episodic ild
Episodic ILD
  • Pulmonary eosinophilia
  • Vasculitis (Churg-Strauss, Wegener’s, SLE)
  • Extrinsic Allergic Alveolitis
  • Cryptogenic Organising Pneumonia
chronic ild as part of systemic disease
Chronic ILD as part of systemic disease
  • Connective Tissue Disease (eg Rheumatoid arthritis, SLE, Systemic Sclerosis, Ankylosing Spondylosis)
  • Vasculitis (Churg-Strauss, Wegener’s, SLE)
  • Sarcoidosis
  • Cancer (lymphoma, lymphangitis carcinomatosis)
  • Miscellaneous - tuberose sclerosis, lipid storage disorders, neurofibromatosis, amyloidosis, miliary TB, bone marrow transplant)
chronic ild exposure to foreign agent
Chronic ILD - exposure to foreign agent
  • Fibrogenic inorganic dusts - coal, silica, asbestos, aluminium,
  • Non-fibrogenic dust - siderosis (iron), stannosis (tin), baritosis (barium)
  • Granulomatous/fibrogenic - berylliosis
  • Organic dusts - Farmer’s lung (Microsporylium), bagassosis (mouldy sugar cane), Bird fancier’s lung - (feather and dropping antigen)
chronic ild idiopathic
Chronic ILD - idiopathic
  • Idiopathic Pulmonary Fibrosis (IPF) – also known as Cryptogenic fibrosing alveolitis (CFA)
  • Cryptogenic organising pneumonia (COP)
  • Sarcoidosis
  • Alveolar proteinosis
  • Lymphangioleiomyomatosis (LAM)
  • many other rarer causes


  • Multiple-system disease:

common - lungs, lymph nodes, joints, liver, skin, eyes

less common - kidneys, brain, nerves, heart

  • non-caseating granuloma of unknown aetiology: probable infective agent in susceptible individual. Imbalance of immune system with type 4 (cell mediated) hypersensitivity


  • Acute sarcoidosis:

erythema nodosum, bilateral hilar lymphadenopathy, arthritis, uveitis, parotitis, fever.

  • Chronic sarcoidosis: lung infiltrates (alveolitis), skin infiltrations, peripheral lymphadenopathy, myocardial, neurological, hepatitis, splenomegaly, hypercalcaemia.


Differential diagnosis = TB (tuberculin test -ve), Lymphoma, Carcinoma, fungal infection.

  • Chest X-ray (BHL), CT scan of lungs (peripheral nodular infiltrate)
  • Tissue biopsy (eg transbronchial, skin, lymph node)  non-caseating granuloma.
  • Pulmonary function: Restrictive defect due to lung infiltrates.
  • Blood test:

- Angiotensin Converting Enzyme (ACE) levels as activity marker (NOT diagnostic test).

- raised calcium

- increased inflammitory markers

  • Acute: self-limiting condition.
  • Chronic: oral steroids if vital organ affected (eg lung, eyes, heart, brain).



  • Acute: self-limiting condition - usually no treatment

Steroids if vital organ affected (eg impaired lung function, heart, eyes, brain, kidneys)

  • Chronic: oral steroids usually needed

Immunosuppression (eg azathioprine, methotrexate)

monitor chest X-ray and pulmonary function for several years

often relapses


Bilateral hilar lymphadenopathy

and lung infiltrares -Sarcoidosis



  • Type III hypersensitivity (Immune complex deposition) reaction to antigen  lymphocytic alveolitis (hypersensitivity pneumonitis).
  • Aetiology: Microsporylium (farmers lung, malt workers, mushroom workers), avian antigens (bird fanciers lung), drugs (gold, bleomycin, sulphasalazine)
  • Can be ACUTE or CHRONIC
  • ACUTE: cough, breathless, fever, myalgia - several hours after acute exposure (flu-like illness)

Signs: +/- pyrexia, crackles (no wheeze!), hypoxia

CxR: widespread pulmonary infiltrates

Treatment: oxygen, steroid and antigen avoidance



CHRONIC:  repeated low dose antigen exposure over time  progressive breathlessness and cough

  • Signs: may be crackles, clubbing is unusual
  • CxR pulmonary fibrosis - most commonly in the upper zones
  • PFTs: restrictive defect (low FEV1 & FVC, high or normal ratio, low gas transfer - TLCO)
  • Diagnosis: history of exposure, precipitins (IgG antibodies to guilty antigen), lung biopsy if in doubt.
  • Treatment: remove antigen exposure, oral steroids if breathless or low gas transfer.


(also known as Cryptogenic Fibrosing Alveolitis)

Most common interstitial lung disease

  • Clinical presentation: progressive breathlessness, dry cough

OE: clubbing, bilateral fine inspiratory crackles,

Ix: restrictive defect (reduced FEV1 and FVC with normal or raised FEV1/FVC ratio, reduced lung volumes, low gas transfer CxR - bilateral infiltrates;

CT scan - reticulonodular fibrotic change, worse at the lung bases. The presence of “ground-glass” suggests reversible alveolitis; fibrosis is irreversible.

  • Causes: Primary (Idiopathic)

Secondary (eg rheumatoid, SLE, systemic sclerosis, drugs - amiodarone, busulphan, bleomycin, penicillamine, nitrofurantoin, methotrexate).



  • Differential diagnosis = exclude occupational disease (asbestosis, silicosis), mitral valve disease, left ventricular failure, sarcoidosis, extrinsic allergic alveolitis.
  • Ask about occupation (in depth), pets and drugs
  • Diagnosis: combination of history, examination and radiology tests
  • If the presentation is atypical then lung biopsy (either transbronchial or thoracascopic) is needed
  • Pathology: chronic inflammatory infiltrate (neutrophils and fibrosis in alveolar walls ± intra-alveolar macrophages.


  • Treatment: not clear if influences course of disease

oral steroids ± immunosuppressive drugs (eg azathioprine combined with N-acetyly cisteine) worth trying if patient is <75 years and evidence of acute inflammation on CT scan - some response in 30%.

NB treatment is aimed as slowing future progression rather than reversing established fibrosis.

Oxygen if hypoxic.

Lung transplantation in young patients

Future treatments: ?Anti-fibrotic agents


pulmonary artery vasodilators

  • Prognosis: most patients progress into respiratory failure and are dead within 5 years

DIP-pre steroids

Fibrosing Alveolitis



  • Simple pneumoconiosis - chest X-ray abnormality only (no impairment of lung function - often associated with chronic obstructive pulmonary disease).
  • Complicated pneumoconiosis - progressive massive fibrosis  restrictive pattern with breathlessness.
  • Chronic bronchitis (coal dust + smoking).
  • Caplan’s syndrome - rheumatoid pneumoconiosis (pulmonary nodules).


  • 15-20 years exposure to quartz (eg mining, foundry workers, glass workers, boiler workers).
  • Simple pneumoconiosis - chest X-ray abnormality only (egg-shell calcification of hilar nodes).
  • Chronic silicosis - restrictive pattern, pulmonary fibrosis.

ASBESTOS-related lung disorders

  • Mining, construction, shipbuilding, boilers and piping, automotive components (eg brake linings).
  • Pleural disease -

1- Benign pleural plaques - asymptomatic

2- Acute asbestos pleuritis - fever, pain, bloody pleural effusion

3- Pleural Effusion and Diffuse pleural thickening - restrictive impairment

4- Malignant Mesothelioma - incurable pleural cancer. Presents with chest pain and pleural effusion. No available treatment - fatal within two years.

  • Pulmonary Fibrosis - “Asbestosis” - heavy prolonged exposure. Diffuse pulmonary fibrosis and restrictive defect. Asbestos bodies in sputum. Asbestos fibres in lung biopsy.
  • Bronchial carcinoma - asbestos multiplies risk in smokers

Asbestos pleural plaques

and Bronchial Ca


Pleural effusion

due to mesothelioma



  • Sensitising agents - high molecular weight (eg bakers, enzymes, gums, latex) - low molecular weight (eg isocyanates, wood dust, glutaraldehyde, solder, flux, dye, adhesives, drugs).
  • Diagnosis: RAST test, provocation testing, PEFR at home/work.
  • Reactive airway dysfunction syndrome - acute episode of toxic gas or fume inhalation (eg chlorine or sulphur dioxide)  followed by persistent bronchial hyperreactivity.
hh http www radiology co uk srs x index htm guidelines
hhhttp://www.radiology.co.uk/srs-x/index.htm guidelines)

Useful clinical & X-ray teaching sites