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.
-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.
-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.
-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
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).
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)
–FBC: neutrophilia, lymphopenia
-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
–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)
–High resolution CT: reticular and nodular changes with ground-glass opacity
–Lung function tests: persistent restrictive changes (↓FVC and FEV1, FEV1:FVC normal or increased)
–Bronchoalveolar lavage: fluid shows increased lymphocytes and mast cells
-Give O2 (35-60%)
-Oral prednisolone (large doses-40mg/24h PO), followed by reducing dose (for about 2-4 wks) – may accelerate recovery
–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
-progressive lung fibrosis
-type 1 respiratory failure
-pulmonary hypertension and cor pulmonale
-the acute form generally resolves if further exposure is prevented
-with chronic disease some patients will improve while a minority progress to lung fibrosis