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Interstitial Lung Disease (ILD)
ILD is not one disease - it is a family of over 200 conditions that share a common thread: scarring, inflammation, or both occurring within the lung interstitium - the tissue and space around the air sacs. The consequences range from manageable inflammation that responds to treatment, to relentless progressive lung fibrosis that shrinks a person's world breath by breath. The tragedy of ILD in India is that it is typically diagnosed late - years after the first symptoms of breathlessness and dry cough - by which time significant irreversible fibrosis has already occurred. At Shree Hospitals, our interstitial lung disease treatment in Mumbai brings together the diagnostic tools and treatment pathways needed to identify ILD early, classify it precisely, and treat it with the intensity the diagnosis demands.
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Our Approach
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Our Approach in Managing Interstitial Lung Disease
The most important decision in ILD management is getting the diagnosis right at the start - because treating UIP/IPF with steroids not only fails, it may accelerate decline. And treating NSIP or COP without adequate immunosuppression equally fails the patient. Our ILD specialist pulmonologist team in Mumbai, India uses a multidisciplinary team (MDT) discussion model - pulmonology, radiology, and pathology together - before any treatment decision is finalised.
- Clinical Assessment & Exposure History
ILD diagnosis begins with a detailed history - not imaging.
- Onset and progression of breathlessness - gradual progressive dyspnoea is the cardinal symptom
- Dry cough - the second most common presenting complaint
- Occupational and environmental exposure history - asbestos, silica, bird feathers, mouldy hay, agricultural dusts
- Drug history - Methotrexate, Amiodarone, Nitrofurantoin, checkpoint inhibitors - all can cause ILD
- Connective tissue disease symptoms - joint pain, skin changes, dry eyes or mouth, Raynaud's - autoimmune ILD is a major category
- Family history - familial IPF accounts for 5% of cases; genetic testing emerging
- Fine end-inspiratory crackles on auscultation - the clinical hallmark of fibrotic ILD
- HRCT Pattern - The Diagnostic Cornerstone
HRCT pattern in ILD determines diagnosis, treatment, and prognosis more than any other single investigation.
- UIP pattern (Usual Interstitial Pneumonia) - basal predominant honeycombing ± traction bronchiectasis; characteristic of IPF; antifibrotic therapy, not steroids
- NSIP pattern (Non-Specific Interstitial Pneumonia) - ground-glass opacity with basal traction bronchiectasis; associated with connective tissue disease; responds to immunosuppression
- OP pattern (Organising Pneumonia) - consolidation with peribronchovascular distribution; responds dramatically to corticosteroids
- HP pattern (Hypersensitivity Pneumonitis) - centrilobular nodules, mosaic attenuation, fibrosis in upper and lower lobes; antigen identification and avoidance critical
- Sarcoidosis - upper and mid-lung lymphadenopathy, perilymphatic nodules, bilateral hilar adenopathy
- DIP/RB-ILD - smoking-related ILD; smoking cessation the primary intervention
- Bronchoalveolar Lavage & Lung Biopsy
- BAL (Bronchoalveolar Lavage) - lymphocytosis: HP or sarcoidosis; eosinophilia: eosinophilic pneumonia; macrophage predominance with lipid inclusions: aspiration-related ILD
- Surgical lung biopsy (VATS) - for ILD with non-diagnostic HRCT and uncertain clinical picture; provides histological diagnosis
- Transbronchial cryobiopsy - emerging less invasive alternative to surgical biopsy; higher diagnostic yield than conventional transbronchial biopsy
- Autoimmune ILD Workup
- ANA, anti-dsDNA, anti-Ro, anti-La, anti-Scl70, anti-Jo-1, anti-MDA5, RF, anti-CCP - comprehensive autoimmune panel
- Connective tissue disease-associated ILD (CTD-ILD) - RA-ILD, SSc-ILD, IIM-ILD - requires rheumatology co-management
- IPAF (Interstitial Pneumonia with Autoimmune Features) - incomplete CTD features; treated similarly to CTD-ILD
- SSc-ILD: Nintedanib (antifibrotic) approved for progressive SSc-ILD; Tocilizumab in selected patients
- Treatment - Disease Type Determines Everything
- IPF (Idiopathic Pulmonary Fibrosis): Antifibrotic therapy - Pirfenidone or Nintedanib - slows FVC decline; combined ICS and immunosuppression (Prednisolone, Azathioprine, N-Acetylcysteine) was shown to increase harm in the PANTHER trial; steroids alone are harmful in IPF
- CTD-ILD (NSIP pattern): Mycophenolate mofetil or Azathioprine ± low-dose Prednisolone; Rituximab for refractory cases
- Hypersensitivity Pneumonitis: antigen identification and avoidance; corticosteroids for acute or subacute HP; antifibrotics if chronic fibrotic HP
- Sarcoidosis: systemic corticosteroids for pulmonary stages II–IV with significant symptoms; Methotrexate for steroid-dependent cases
- Organising Pneumonia: dramatic response to oral Prednisolone; relapse common on tapering - slow taper essential
- Oxygen, Rehabilitation & Transplant
- Supplemental oxygen - for exertional or resting hypoxaemia; improves exercise tolerance and quality of life
- Lung rehabilitation programme - pulmonary rehabilitation produces meaningful improvements in exercise capacity and dyspnoea in ILD, though evidence less robust than in COPD
- Lung transplantation - the only intervention that improves survival in IPF; referral should begin when FVC <60% predicted or 6-minute walk distance <250m; bilateral lung transplant preferred
- Acute exacerbation of IPF - high mortality; high-dose corticosteroids, broad-spectrum antibiotics, ICU support; prognosis poor
Happy Patients & Their Case Stories
She had been treated for "chronic bronchitis" for three years with repeated antibiotic courses and bronchodilators. A chest X-ray at Shree Hospitals showed bilateral basal reticular shadowing. HRCT confirmed a UIP pattern with honeycombing. Autoimmune screen was negative.
Mrs. Darika ,L
Referred to Shree Hospitals with breathlessness, dry cough, and joint pains. HRCT showed bilateral ground-glass opacity with traction bronchiectasis in an NSIP pattern. Autoimmune workup revealed anti-Jo-1 antibody positivity - ILD associated with antisynthetase syndrome.
Mr. Arav . J
How to Identify the Cause of Interstitial Lung Disease?
ILD is diagnosed late in most patients because its symptoms develop slowly and are attributed to ageing, deconditioning, or other respiratory conditions.
Features that should prompt pulmonology evaluation and HRCT:
- Breathlessness on exertion that was not present two years ago and has gradually worsened without explanation
- Dry cough lasting more than 8 weeks without an identifiable cause - no reflux, no post-nasal drip, no ACE inhibitor use
- Fine crackling sounds at the lung bases - described as Velcro tearing - on a clinical examination
- Occupational history of dust, fibre, or mould exposure in someone with respiratory symptoms
- Rheumatoid arthritis, systemic sclerosis, polymyositis, or Sjögren's syndrome with new respiratory symptoms - autoimmune ILD must be excluded
- Drug exposure to known pulmonary toxins - Methotrexate, Amiodarone, checkpoint inhibitors
- Clubbing of the fingers - present in approximately 50% of IPF patients; a significant clinical pointer
Progressive lung fibrosis does not reverse. Antifibrotic therapy can slow it, immunosuppression can suppress the inflammatory component where it exists, and lung transplant can replace the lung - but none of these options work as well when the disease has been allowed to progress for years before diagnosis. Seek interstitial lung disease treatment in Mumbai as soon as the symptom pattern and HRCT raise the question - the earlier the MDT discussion, the better the options available.
Important FAQs : ILD
Is ILD the same as pulmonary fibrosis?
Pulmonary fibrosis is a type of ILD - specifically where scarring predominates. ILD is the broader category including inflammatory conditions like sarcoidosis and organising pneumonia, some of which have no fibrosis.
Can ILD be cured?
Organising pneumonia and some inflammatory ILDs respond very well to steroids and can achieve remission. IPF - the most common fibrotic ILD - is not curable, but its progression can be slowed with antifibrotic therapy.
How is IPF different from other ILDs?
IPF has a characteristic UIP pattern on HRCT, occurs in older adults, is not associated with autoimmune disease, and does not respond to - and may be worsened by - immunosuppression. This distinction determines treatment entirely.
How fast does ILD progress?
Highly variable. Some patients remain stable for years; others - particularly those with rapid FVC decline - deteriorate quickly. Regular 6-monthly FVC measurements are essential to track trajectory.
What is an acute exacerbation of IPF?
A sudden, unexplained worsening of breathlessness over days to weeks with new bilateral ground-glass opacity on CT, occurring without infection or other identifiable cause. It carries very high mortality.
Treatments for ILD at Shree Hospitals
Comprehensive fibrotic lung disease diagnosis and management in Mumbai from MDT diagnosis to antifibrotic therapy and transplant referral.
HRCT & MDT Diagnostic Programme
High-resolution CT with pattern analysis and multidisciplinary team discussion - pulmonology, radiology, and pathology - ensuring correct ILD subtype classification before any treatment decision is made.
Top ILD & Pulmonology Specialists in Mumbai
Dr. Jay Bhanushali
Pulmonologist
Dr. Tejal Shah
Interventional Pulmonology, Tuberculosis Management
Dr. Miti A Shah
Interventional Pulmonology, Pediatric Respiratory
Dr. Rishabh Raj
Interventional Pulmonology, Sleep Medicine
Every doctor and specialist at Shree Hospitals is board-certified and brings an average of 15 or more years of clinical experience in their area of subspecialty.
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