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Hypersensitivity Pneumonitis

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1 Hypersensitivity Pneumonitis

2 INTRODUCTION HP known as extrinsic allergic alveolitis
Granulomatous, interstitial, bronchiolar and alveolar-filling lung diseases Caused by repeated exposure and subsequent sensitization to a variety of organic and chemical antigens.

3 ETIOLOGY Three main categories: Animal proteins Chemicals Bacteria
Microbial agents Bacteria Farmer’s lung Bagassosis Mushroom worker’s lung Fungi Wood pulp worker’s lung Cheese washer lung Ameba Humidifier lung Animal proteins Avian proteins Bird breeder’s lung Urine,Serum,Pelts Animal handler’s lung Wheat weevil Wheat weevil lung Chemicals Isocyanate TDI,MDI,HDI TMA Trimellitic anhydride


5 PATHOGENESIS Immunology: Cell-mediated immunity
Repeated inhalation of antigens → sensitization → immunology response(type III,IV) → influx of neutrophiles → shift T lymphocytes (~70%)(predominantly of CD8)(↓CD4/CD8 ) BAL → activated T lymphocytes Lung biopsy: Interstitial mononuclear cell infiltration Granulomatous inflammatory response Antibodies in HP are IgG class

6 PATHOGENESIS . . . Host factors: Exposure factors:
Host susceptibility or resistance factors may influence individual responses to inhaled antigens. Non smokers > smokers No association with HLA Exposure factors: Ag concentration Duration of exposure Frequency & intermittency of exposure Particle size Use of respiratory protection Farmer's lung disease: winter Bird breeder's lung: summer

Fever ,chills ,myalgia ,cough , dyspnea (4-12 h after heavy exp. ) Ph/E : basilar rales , peripheral leukocytosis Recurrent febrile episodes (most frequent presentation)

8 Subacute and chronic HP:
CLINICAL FEATURES . . . Subacute and chronic HP: Temporal relationship between symptoms and exposure is difficult to elicit. Insidious onset of respiratory symptoms Non-specific systemic symptoms Malaise, fatigue, weight loss, cough, dyspnea, low grade fever Ph/E: normal or basilar crackles & wheezing End-stage disease: cyanosis & right-sided HF

9 L/D ↑ Specific IgG ( no sensitive , no specific ) ↑ ESR & CRP
↑ IgM , IgA, IgG ↑ ACE ↑ ANA

10 PFT There is no single characteristic pattern of pulmonary function abnormalities . Acute HP : restrictive pattern Subacute and chronic HP : air way obstruction or mixed ↓ DLCO (most sensitive physiologic test in early HP ) Methacholine challenge test : increased non-specific bronchial hyper-reactivity

11 CXR Acute HP: Subacute HP: Chronic HP:
Diffuse ground glass opacification Fine nodular or reticulonodular pattern( lower lung field) Consolidation ( rarely ) Subacute HP: Reticulonodular pattern Chronic HP: Fibrosis with upper lobe retraction Reticular opacity Volume loss Honeycombing Mediastinal lymphadenopathy (up to 50%)

12 Ground glass pattern Most common in acute HP (but may also be seen in subacute and chronic HP) Middle lung zone PFT: restrictive , ↓DLCO May resolve with removal from exposure

13 Acute HP: pigeon breeder’s lung shows ground-glass haziness and associated air-trapping

14 Airspace consolidation
Only reported in acute HP Bilateral ill-defined areas of consolidation

15 Subacute HP: bilateral alveolar and reticular pattern

16 Centrilobular nodules
Round, poorly defined, less than 5 mm in diameter Typically centrilobular Profuse throughout the lung,but a middle to lower lung zone predominance. Most frequent HRCT finding in HP Centrilobular nodules + ground glass opacification are highly suggestive for HP. PFT : normal

17 Fibrosis Chronic HP (subacute HP) Irregular linear opacities
Traction bronchiectasis Honeycombing

18 Emphysema Chronic HP Emphysema occurred more commonly than fibrosis in chronic farmer’s lung.

19 Chronic HP: upper lobe fibrosis

20 Chronic HP: farmer’s lung disease showing bibasilar end-stage fibrosis

21 HRCT Sensitivity of HRCT is significantly better than CXR Ground glass
Centrilobular nodules Fibrosis Emphysema Mediastinal lymphadenopathy (> 20 mm )

22 Centrilobular ground-glass nodules uniformly distributed throughout the lung. Lobular air-trapping also frequently present.

23 Multiple low density ill-defined centrilobularnodules

24 Extensive areas of grand-glass attenuation
Extensive areas of grand-glass attenuation. Decreased perfusion (arrows)representing associated air-trapping.

25 Chronic HP: Honeycombing, intralobular and septal fibrosis, architectural distorsion

26 Mosaic pattern Patchwork of regions of differing attenuation
Due to patchy areas of ground glass or airtrapping

27 Histopathology Classic triad: Cellular bronchiolitis
Lympho-plasmocytic interstitial infiltration Non-necrotizing granulomas

28 Diagnosis Temporal relationship between symptoms and certain activities is often the first clue to the diagnosis of HP

29 Diagnostic criteria Required Supportive Recurrent febrile episodes
Appropriate exposure Dyspnea on exertion Inspiratory crackles Lymphocytic alveolitis Supportive Recurrent febrile episodes Infiltration on CXR Decreased DLCO Precipitating antibodies Granulomatous on lung biopsy Improvement with contact avoidance

30 DDx

31 Comparison HP& Inhalation fever

32 Comparison HP& Inhalation fever . . .

33 Comparison HP& Inhalation fever . . .

34 PROGNOSIS The clinical course of HP is variable
Acute HP generally resolves without sequelae But progressive impairment may occur with recurrent attacks or with a single severe attack. Subacute or chronic forms of HP present with insidious symptoms More subtle clinical abnormalities Frequently recognized later in the disease course Long-term mortality rates for patients with chronic HP range from 1% to 10%.

35 Prognostic factors Age Duration of exposure after onset of symptoms
Time of exposure prior to diagnosis

36 TREATMENT Cornerstone of therapy → removal from exposure
Respirators are used when removal from exposure is impossible. Oxygen (hypoxemic patients) Airflow limitation: Inhaled steroids β-agonists Oral corticosteroids (40–60 mg/day of oral prednisone) in severe or progressive disease. In refractory cases: Cyclophosphamide & Azathioprine


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