Extrinsic Allergic Alveolitis

Still revising conditions. Still respiratory. So, here is another cause of interstitial lung disease.


Extrinsic Allergic Alveolitis

Definition: also known as Hypersensitivity Pneumonitis. Interstitial inflammatory disease characterised by a widespread diffuse inflammatory reaction in the alveoli and small airways of the lung as a response to inhalation organic dusts.

Aetiology/risk factors:

-Inhalation of allergens (fungal spores or avian proteins) provokes a hypersensitivity reaction in sensitized individuals. In the acute phase there is alveoli infiltration with acute inflammatory cells. With chronic exposure, granuloma formation and obliterative bronchiolitis occur.

Causes:

-Farmer’s lung = turning mouldy hay or other vegetable material (Micropolyspora faeni)

-Bird fancier’s and pigeon-fancier’s lung (proteins in bird droppings)

 -Mushroom worker’s lung = turning mushroom compost (Thermoactinomyces vulgaris)

-Malt worker’s lung = turning germinating barley (Aspergillus clavatus)

-Bagassosis or sugar worker’s lung (Thermoactinomyces sacchari)

-Cheese washer’s lung = mouldy cheese (Penicillium casei, Aspergilus clavatus)

-Wine maker’s lung = mould on grapes (Botrytis)

-Humidifier Lung = water containing bacteria and Naegleria (amoeba)

So, a full occupational history is really important. Also ask about pets and hobbies.

Epidemiology:

-Uncommon = 2% of occupational lung diseases

-By far, the most common cause is Farmer’s lung, affecting up to 1 in 10 of the farming community in poor wet areas around the world.   -50% cases affect farm workers

Symptoms:

4-6 h post-exposure: fever, rigors, malaise, myalgia, dry cough, dyspnoea

(Wheeze and productive cough may develop on repeat high level exposure).

Chronic: increasing dyspnoea, weight loss, exertional dyspnoea, decreased exercise tolerance, cough (exposure usually chronic, low level and may be no history of acute episodes).

Signs:

4-6 h post-exposure: fine end-inspiratory crackles, pyrexia, tachypnoea (rapid, shallow breathing), (no wheeze)

Chronic: fine end-inspiratory crackles, clubbing (rare),  cor pulmonale (right ventricular heave, raised JVP, peripheral oedema)

Investigations:

Acute:

FBC: neutrophilia, lymphopenia

-↑ESR

-Positive serum precipitins: = precipitating antibodies to specific causative antigens, indicate exposure only and not disease

ABG: ↓PO2 ↓PCO2

CXR: may be normal in acute episodes. May show upper-zone mottling/ consolidation, ground-glass appearance with alveolar shadowing or nodular opacities in the middle and lower zones, hilar lymphadenopathy (rare)

-Lung function tests: reversible restrictive defect (↓FVC and FEV1,, FEV1:FVC normal or increased) reduced gas transfer (TLCO/DLCO) during acute attacks

Chronic:

Blood tests: positive serum precipitins

Chest x-ray: upper-zone fibrosis (as opposed to idiopathic pulmonary fibrosis which tends to be bi-basal), honeycomb lung, cardiomegaly (if cor pulmonale)

 

Posteroanterior (PA) chest radiograph in a patient

PA CXR in a patient with chronic hypersensitivity pneumonitis- a pigeon fancier- shows reticular-nodular opacification

 

High resolution CT: reticular and nodular changes with ground-glass opacity

High-resolution CT (HRCT) scan in a man with a cli

HRCT scan in a man with a clinical diagnosis of hypersensitivity pneumonitis. Note the ground-glass appearance and small nodules.

Lung function tests: persistent restrictive changes (↓FVC and FEV1, FEV1:FVC normal or increased)

Bronchoalveolar lavage: fluid shows increased lymphocytes and mast cells

Management:

Acute:

-Remove allergen

-Give O2 (35-60%)

-Oral prednisolone (large doses-40mg/24h PO), followed by reducing dose (for about 2-4 wks) – may accelerate recovery

Chronic:

Avoid exposure to allergens or wear facemask or +ve pressure helmet

-Long-term steroids often achieve CXR and physiological improvement (trial of high dose oral prednisolone for 1 month, gradually reduced or stopped if no response).

-Compensation may be payable

Complications:

-progressive lung fibrosis

-type 1 respiratory failure

-pulmonary hypertension and cor pulmonale

Prognosis:

-the acute form generally resolves if further exposure is prevented

-with chronic disease some patients will improve while a minority progress to lung fibrosis

References: Cheese & Onion, Kumar and Clarke’s, Rapid Medicine
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