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Hypersensitvity Pneumonitis/Extrinsic Allergic Alveolitis (Epidemiology,…
Hypersensitvity Pneumonitis/Extrinsic Allergic Alveolitis
Key Facts
Type of interstitial lung disease - distinct cellular infiltrates and extracellular matrix deposition in lung distal to the terminal bronchiole
ILD's are a group of lung diseases affecting the lung interstitial (the tissue and space around the air sacs of the lungs)
Previously called extrinsic allergic alveolitis
Epidemiology
Acute and subacute forms cause a pneumonitis which can be recurrent
Chronic disease can cause fibrosis, emphysema and permanent lung damage
There are acute, subacute and chronic forms
One of the most common causes worldwide is farmer's lung
Caused by an allergic reaction affecting the small airways and alveoli in response to an inhaled antigen or occasionally following the ingestion of a causative drug
Associated with may jobs and hobbies: farmer's lung, bird/pigeon fanciers lung, cheese-workers lung, malt-workers lung, humidifier fever
Usually a disease of adults
Risk Factors
Specific occupations including farmers, cattle workers, ventilation system workers, vets and those jobs that involve working with chemicals
Bird keeping
Pre-existing lung disease
Regular use of hot tubs
Pathophysiology
This attracts and activates alveolar & interstitial macrophages, which gives continued antigenic exposure, therefore progressive development of pulmonary fibrosis
In the acute phase; the alveoli are infiltrated with acute inflammatory cells
Some of the inhaled antigen may lead to inflammation by directly activating the alternate complement pathway
With chronic exposure, granuloma formation and obliterative bronchiolitis occur
The allergic response to the inhaled antigen involves both cellular immunity and the deposition of immune complexes (type III hypersensitivity reaction) resulting in inflammation through the activation of complement via the classical pathway
Clinical Presentation
Subacute
Occurs with intermittent or lower-level exposure
History or repeated acute attacks
Signs same as acute, symptoms less severe and more gradual onset
Can be present as recurrent pneumonia
Improvement is seen in weeks to months following removal from exposure
Chronic
Usually no history of preceding acute symptoms
If the source of antigen is removed only partial improvement of symptoms
Cyanosis and clubbing may develop
Weight loss
Increasing dyspnoea
Type 1 respiratory failure (low PaO2, normal/low PaCO2)
Acute (4-6hrs post-exposure)
Fever
Rigors
Myalgia
Dry cough
Dyspnoea
Crackles (no wheeze)
Chest-tightness
Patients may be mistakenly diagnosed with a chest infection
Symptoms related to level of exposure
Resolution occurs 24-48hrs following removal of antigen
Differential Diagnosis
Infection, connective tissue disorders causing interstitial lung disease, pulmonary fibrosis, asthma, drug-induced interstitial lung disease
Diagnosis
Full blood count (FBC)
Raised white cell count
Increased ESR (inflammatory marker)
Lung function test
Reversible restrictive defect
Reduced gas transfer during acute attacks
Chest X-ray
Fibrotic shadow in upper zone of lung (upper zone mottling/consolidation)
Diffuse small nodules and increased reticular shadowing may be present but not specific
Bronchoalveolar lavage
Analysis of lymphocyte count and CD4/CD8 ratio
Treatment
Acute
Give O2 (35-60%)
Oral prednisolone followed by reducing dose
Remove allergen
Chronic
Long term steroids can often achieve chest X-ray and physiological improvement
Corticosteroids e.g. prednisolone
Avoid exposure to allergen