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Introduction to Interstitial Lung Disease(ILD) or Diffuse Parenchymal Lung Disease (DPLD)

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Introduction
Classification
Epidemiology
Pathogenesis
Clinical features
Investigation
Treatment

Published in: Health & Medicine
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Introduction to Interstitial Lung Disease(ILD) or Diffuse Parenchymal Lung Disease (DPLD)

  1. 1. DR MUHAMMED ASLAM MBBS MD PULMONARY MEDICINE facebook.com/medicalppt Interstitial Lung Disease(ILD) or Diffuse Parenchymal Lung Disease (DPLD)
  2. 2. OUTLINE • Introduction • Classification • Epidemiology • Pathogenesis • Clinical features • Investigation • Treatment
  3. 3. INTRODUCTION • Interstitial Lung Disease refers to a broad range of conditions that have common clinical, physiological, and radiological features. • ILD is not one disease but several diseases that do not necessarily share a common histopathological or pathophysiological basis
  4. 4. INTRODUCTION • By strict definition Interstitial lung disease involves abnormalities of the interstitium – “the potential space between the epithelium and capillary endothelial basement membrane within the alveolus”. HOWEVER…………..
  5. 5. INTRODUCTION • Interstitial is a misleading terminology because most of these disorders are associated with extensive alteration of airway and alveolar architecture in addition to changes in interstitial compartment. • For this reason Diffuse Parenchymal Lung Disease or DPLD is the better term.
  6. 6. CLASSIFICATION OF DPLD • DPLD : Two large groups (1)Idiopathic DPLD ( no known cause ) (2) Those with identifiable cause or occurs secondary to other diseases
  7. 7. IDIOPATHIC ILD 1.Idiopathic pulmonary fibrosis (IPF) – most common 2.Acute interstitial pneumonia (AIP) 3.Cryptogenic Organizing Pneumonia ( COP) / Bronchiolitis obliterans organizing pneumonia (BOOP) 4.Desquamative interstitial pneumonia (DIP) 5.Lymphocytic interstitial Pneumonia ( LIP) 6.Non specific interstitial Pneumonia (NSIP) 7.Respiratory bronchiolitis associated Interstitial lung disease (RBILD)
  8. 8. THOSE WITH IDENTIFIABLE CAUSE 1.Autoimmune- rheumatoid arthritis, S.L.E, Sarcoidosis, Scleroderma 2.Certain infections 3.Medications 4.Radiation 5.Occupational exposure :asbestos, coal, cotton, silica
  9. 9. CLASSIFICATION
  10. 10. EPIDEMIOLOGY • Incidence ranges from 3-26/1,00,000 per year. • Prevalence of preclinical and undiagnosed ILD is estimated to be 10 times that of clinical recognized disease. • IPF is the most common form representing at least 30 percent of the incident cases.
  11. 11. IPF - PATHOGENESIS VIDEO
  12. 12. NORMAL DPLD
  13. 13. RESPIRATORY SYMPTOMS Breathlessness (most common): Initially, dyspnea on exertion→ later at rest  Nonproductive cough  Pleuritic chest pain Wheeing  Hemoptysis
  14. 14. NON RESPIRATORY SYMPTOMS ASSOCIATED WITH DIFFERENT DPLDS • Arthritis • Ocular • Skin and muscle • GERD • Lower GI symptoms • Recurrent sinusitis • Neurological symptoms • Epilepsy & mental retardation • Diabetes inspidus
  15. 15. ONSET OF SYMPTOMS 1. Acute presentation (days to weeks)- eg: Acute idiopathic interstitial pneumoni,Hypersensitive pneumonitis 2. Sub-acute presentation (weeks to months)- eg: Sarcoidosis,Drug induced ILD ,Alveolar hemorrhage syndromes 3. Chronic presentation (months to years) – eg: IPF
  16. 16. ILD-HISTORY •Smoking •Medication history- Amiodorane, Methotrexate, •Occupational history •Environmental exposure history
  17. 17. OCCUPATIONAL HISTORY 􀂾 Pneumoconioses – miners 􀂾 Silicosis – sand blasters & granite workers 􀂾 Asbestosis – welders, electricians, mechanics, workers with brakes, shipyard workers 􀂾 Berylliosis – aerospace, nuclear, computer & electronic industries 􀂾 Hypersensitive pneumonitis – farm workers, poultry workers, bird breeders 􀂾 The degree of exposure, duration, latency of exposure, and the use of protective devices should be elicited
  18. 18. ENVIRONMENTAL EXPOSURE HISTORY • 􀂾 Exposures to pets (especially birds) • 􀂾 Air conditioners • 􀂾 Humidifiers • 􀂾 Hot tubs • 􀂾 Evaporative cooling systems
  19. 19. ILD-SIGNS • Crackles - Dry, velcro , end inspiratory, predominantly bibasilar • Inspiratory squeaks- Mid inspiratory, high pitched- Seen in Airway centred pathologies • Cor pulmonale features • Clubbing – IPF
  20. 20. EXTRA PULMONARY -SIGNS • Skin abnormalities • Lymphadenopathy • Hepatosplenomegaly • Maculopapular skin rashes • Erythema nodosum • Subcutaneous nodules • Proximal muscle weakness • Arthritis
  21. 21. INVESTIGATIONS
  22. 22. CHEST X RAY • Typically small lung volumes with Reticular , Nodular, or RETICULONODULAR shadow
  23. 23. HIGH-RESOLUTION COMPUTED TOPOGRAPHY (HRCT) • HRCT is more sensitive • Combinations of ground glass changes, reticulonodular shadowing, honeycomb cysts and traction bronchiectasis
  24. 24. PULMONARY FUNCTION TESTING • Objective assessment of Resp Symptoms • Grading the severity • Monitoring the response to therapy
  25. 25. PULMONARY FUNCTION TESTING • Restrictive Defect • ↓ Lung volumes (TLC, FRC,RV <80%) • ↓ FEV1, FVC With Normal or ↑FEV1/FVC • Reduced diffusing capacity (DLCO)
  26. 26. LABORATORY INVESTIGATIONS • Full blood count: lymphopenia in sarcoid; eosinophilia in pulmonary eosinophilias and drug reactions; neutrophilia in hypersensitivity pneumonitis • Ca2+: may be elevated in sarcoid • Serum angiotensin-converting enzyme: non-specific indicator of disease activity in sarcoid • ESR and CRP: non-specifically raised • Autoimmune screen: autoantibodies may suggest connectivetissue disease
  27. 27. OTHER INVESTIGATIONS • ARTERIAL BLOOD GAS ANALYSIS • Tuberculin test – negative in 2/3 of sarcoidosis patients • BRONCHOALVEOLAR LAVAGE- cellular profile , special stains or studies • Lung biopsy- TRANS BRONCHIAL BIOPSY , OPEN LUNG BIOPSY
  28. 28. MANEGEMENT PRINCIPAL AIMS: (1) to remove exposure to injurious agents (2) to suppress inflammation to prevent further destruction of the pulmonary parenchyma (3) to palliate the manifestations of these diseases.
  29. 29. CORTICOSTERIODS • Prednisone, 1 mg/kg • Gradually tapered (5 mg/week) over several months to a maintenance dose
  30. 30. IMMUNO SUPRISSIVE AGENTS Cytotoxic agents (Cyclophosphamide)or immunosuppressive agents (Azathioprine) may be used in patients who do not improve on steroid therapy or who cannot tolerate corticosteroids
  31. 31. N-ACETYL CYSTEIN • Antioxidant • 600 mg PO tid added to prednisone and azathioprine, preserves vital capacity and FVC and DLCO
  32. 32. PIRFENIDONE • Antifibrotic • Reduces acute exacerbations and reduction in FVC
  33. 33. OXYGEN THERAPY • F or pa tients w i t h d o c u m e nted h y p ox i a – S p O 2 <89% , P a O 2 <55m m H g • Improv e s e x e r c is e tolerance
  34. 34. CONCLUSION • DPLD is the better term , not a single disease • IPF is the most common DPLD • Restrictive Airway Disease • Main treatment aim is to suppress inflammation to prevent further destruction of the pulmonary parenchyma
  35. 35. Thank you !!

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