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Interstitial lung disease
The document presents an overview of interstitial lung disease (ILD), highlighting its diagnosis, evaluation, and occupational implications. It details various types of ILD, including pneumoconioses and hypersensitivity pneumonitis, while discussing the significance of occupational history and clinical evaluation in identifying the condition. Additionally, the document emphasizes the importance of accurately determining causation for effective management and treatment in workplace settings.
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Interstitial lung disease
- 1. INTERSTITIAL LUNG DISEASE Tee L.Guidotti, MD, MPH, DABT Medical Advisory Services OEMAC 2010
- 2. Benchmarks ACOEM PracticeGuidelines Authoritative guidance, updated, evidence-based Lung Disease Guidelines in progress Occupational Interstitial Lung Disease Airways Disorders ATS 2004 Revised Criteria for the Diagnosis of Non- Malignant Asbestos-Related Disease This presentation A general approach to ILD OILD Specific ILDs, esp. pneumoconioses Implications
- 3. Medical Evaluation ofOccupational Lung Diseases - Modalities Primarily diagnostic Chest film, CT Spirometry, DLCO Blood gases Methacholine challenge Biopsy (Ca, IPF, granulomatous disease) Primarily occupational Occupational history Impairment evaluation Provocative testing (rare) Serology (for HP) Biopsy (avoid) Cardiopulmonary exercise testing
- 4. What is theinterstitium? Fabric of connective tissue that supports its many structures Expands and contracts with ventilation Surrounds the air spaces, brings blood in close proximity to air with separation but minimal impedance to diffusion Serves as a conduit and fluid channel for lymphatic drainage and the migration of immune cells Collects and sequesters a fraction of insoluble particles that deposit in the lung
- 5. Interstitium and AlveolarWall Collagen bundles Fibroblasts Air space rbc
- 6. What is interstitialdisease? Acute Edema, per se or a stage on the way to alveolar edema Infection (e.g. mycoplasma) Inflammation Chronic Fibrosis, end stage of inflammation Often involves some degree of bronchiolitis.
- 7. Operational Classification Pneumoconioses Granulomatous disease Hypersensitivity pneumonitis Diffuse interstitial fibrosis Idiopathic pulmonary fibrosis (= “usual interstitial pneumonia”) Giant cell interstitital pneumonia (“GIP”) Other interstitial pneumonias
- 8. How is itdiagnosed? Usually, obvious because patient belongs to a high-risk group Demographics, family history (some IPF) Occupational history Exceptions: sarcoid, IPF Chest film – most often Restrictive pattern on PFTs Reduced FVC, preserved FEV1, decreased RV This is a late change, however. Biopsy – normally to be avoided!
- 9. Clinical Evaluation -History History of present illness Useful to rule out nonoccupational ILD Consider drug reactions, cancer, inflammatory bowel dz, rheumatologic/autoimmune/collagen vascular dz Time course may distinguish eosinophilic pneumonias, drug reactions, other diseases Not very useful for OILD Occupational history - essential
- 10. Clinical Evaluation – Symptomsand Signs Nonspecific SOB is disproportionate to PFTs! Cough Clubbing: suggests asbestosis, pigeon breeders’ HP, cancer Chest film PFTs: obstructive early → restrictive late
- 11. Chest film Plainfilm and digitized images B reader program Important features: Parenchyma (upper) Pleura Hilum Parenchyma (lower) Superimposition
- 12. Pulmonary Function Testingand Cardiopulmonary Evaluation Vital capacity Flow rates (e.g. FEV1) Lung Volumes and Diffusing Capacity (CO) Bronchodilators: Pre-, Post-Shift Bronchoprovocation Testing Methacholine Testing Specific Agents Metabolic Treadmill Oxygen Consumption Anaerobic Threshold Process leading to interstitial diseases may cause: • Airway irritation • Mild obstructive defect • Acute symptoms (cough) • Extrathoracic disease Interstitial Lung Disease itself causes: • Restrictive defect • Cough and SOB • Pulmonary hypertension • Shunting and V/Q mismatch • Abnormal CO diffusing cap • Desaturation with exercise • Clubbing (uncommon)
- 13. Restrictive Patterns Causes Extrathoracic Obesity Pregnancy Chest wall deformity Clothing or external device (e.g. corset, cuirass) Intrathoracic Pneumonectomy Pleural thickening Interstitial Fibrosis Indicators Restrictive Defects are usually identified by reduced Forced Vital Capacity (FVC) during spirometry However, FVC is effort dependent More conclusively measured by Total Lung Capacity (TLC)
- 14. Usually in medicine,diagnosis is primarily for treatment. Not here. Identification Diagnosis Causation Functional evaluation Treatment Prognosis sentinel event monitoring causation apportionment causal circumstances current impairment future impairment fitness to work
- 15. Challenges Occupational v.nonoccupational Identifying the responsible agent in a case of mixed-dust pneumoconiosis or hypersensitivity pneumonitis or when the history is unclear Ruling IPF in (it can’t be easily ruled out) Differentiating between sarcoidosis and beryllium disease
- 16. Approach to Evaluation Evidence of structural lesion consistent with the interstitial process (e.g. asbestosis) In practice, evidence of a structural lesion is usually demonstrated by chest film with or without CT Evidence of causation by an agent Evidence of causation by a particular agent may be more difficult but is usually satisfied by the occupational history Exclusion of alternative diagnoses may require additional clinical tests and even biopsy
- 17. ILD depends moreon structural features than functional assessment. Anatomical changes Histological changes Malignant potential Mechanical interference with function Markers of exposure Markers of effect Markers of outcome It’s the other way around with airways disease. However, causes of ILD may also cause some airways dysfunction.
- 18. Operational Classification Pneumoconioses Granulomatous disease Hypersensitivity pneumonitis Diffuse interstitial fibrosis Idiopathic pulmonary fibrosis (= “usual interstitial pneumonia”) Giant cell interstitital pneumonia (“GIP”) Other interstitial pneumonias
- 19. How Do YouKnow It is a Pneumoconiosis? Occupational history of exposure to a mineral or metal dust Organic dust pneumoconioses exist but are rare GIP is associated with exposure to “hard metal” (esp. W content) but is rare Compatible clinical and laboratory findings Diagnosis is primarily by chest film No alternative diagnosis likely This does not mean that it is a diagnosis of exclusion! Pneumoconiosis is a diagnosis of context!
- 20. Which Common PneumoconiosisIs It? Occupational history Silica Asbestosis Coal workers’ pneumoconiosis Chest film Rounded opacities and cardinal features of silicosis Irregular opacities and cardinal features of asbestosis Pathology biopsy rarely indicated asbestos bodies useful for identifying asbestosis
- 21. Silicosis Silicosis Simple Chronic nodular silicosis Accelerated silicosis Acute silicosis Silicotuberculosis Associated conditions Autoimmune disorders esp. systemic sclerosis Nephritis Lung cancer
- 22. Asbestos-Related Disorders Asbestosis Pleural plaques Rounded atelectasis Chronic obstructive airways disease Cancer Lung cancer Mesothelioma Larynx, colon, other If any occupational physician in this room cannot recognize this as advanced asbestosis, please recognize that you are in trouble!
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- 25. Which “Modern” PneumoconiosisIs It? Occupational history Hard metal, tungsten-cobalt (W, Co) steel alloy Beryllium (granulomatous) Mixed dust Chest film Pathology may be required to identify GIP, or in evaluation of suspected sarcoidosis Hard metal disease may be associated with cobalt- induced bronchoreactivity
- 26. Biopsy May berequired where there is a diagnostic dilemma: IPF v. sarcoid v. asbestos, silicosis (rarely and may carry risk) Diffuse ILDs Not acceptable just for medicolegal purposes Histology Pattern of fibrosis may suggest IPF Silicotic nodules, coal dust macules Asbestosis, asbestos bodies (not fibers), silica particles EDXA to identify composition of particles: may be important in mixed dust or unknown pneumoconiosis
- 27. Hypersensitivity Pneumonitis Typicalpresentation of farmer’s lung ≠ “silo-fillers’ disease” Infiltrate → fibrosis Cytokine-mediated disease Provoked by persistent antigen Often preceded by airways prodrome
- 28. Granulomatous Disease Sarcoidosisis the big differential diagnosis Eosinophilic granuloma possible but not without eos Miliary TB possible but would be clinically obvious Hypersensitivity pneumonitis causes lung granulomas Beryllium identified by occupational history Zirconium can also cause isolated granulomata Confirmation by Be lymphocyte proliferation test (available at National Jewish Hospital) Not a screening test
- 29. Which HP CouldIt Be? Occupational history of exposure to high MW, persistent antigen Agricultural settings, especially in wet climates R/O farmers’ lung Birds, esp. pigeons R/O “pigeon breeders’ lung” HVAC or older AC system, ventilation repairs R/O humidifier lung (diff includes Legionella) Rehabilitation of old buildings Serum antibody: “HP Panel” Farmers’ lung
- 30. HP Panel Usefulin presumptive, “classical” cases Range of specific antibody determinations limited Labs often offer secondary panels for less common antigen. These panels have been “abused” in fishing expeditions without good indications. HP Panel CPT Micropolyspora faeni IgG Thermoactinomyces vulgaris IgG Aspergillus fumigatusIgG 86606 Penicillium Chrysogenum/notatum IgG Alternaria tenuis/alternata IgG Tricoderma viride IgG Aureobasidium pullulans IgG Phoma betae IgG Related Tests & Panels: Bird Fancier’s Precipitin Panel I Bird & Mold Precipitin Panel II Bird Fancier’s Profile Panel III Other protein antigens & haptens The historically common hypersensitivity pneumonitides were: • Farmer’s lung • Pigeon breeders’s lung • Humidifier lung
- 31. Which “Modern” HPCould It Be? Occupational history of exposure to low MW antigen Isocyanate Trimellitic anhydride Pyrethrum powder (pesticide) Harder to diagnose Requires high index of suspicion Compatible history of exposure No HP panel available or practical TDI-induced HP
- 32. Diffuse Interstitial Disease Giant cell interstitial pneumonia Most often seen in grinding, toolmaking with hard metal Uncommon Deep lung injury with honeycombing Catastrophic event, so history is known Bronchiolitis obliterans Idiopathic pulmonary fibrosis (= UIP) Resembles asbestosis, pathologically distinct Sporadic (older) or hereditary (younger) forms Elevated cancer risk Generally requires biopsy Many other interstitial pneumonias (nomenclature issues) “Other” – many but individually uncommon! Occupational Nonoccupational
- 33. Differential Diagnosis ofDiffuse ILDs Infection AIDS Mycoplasma Mycobacteria Legionella (humidifier lung) Psittacosis (pigeon breeders’ lung) Cryptococcosis (bird source) Drug reaction Autoimmune, rheumatological, collagen-vascular disorders Post-radiation (therapeutic) Graft v. host Paraquat toxicity (suicide) Storage diseases Gaucher’s disease Amyloidosis Tuberous sclerosis Infection Whipple’s disease Lymphangiitic spread of cancer (rare in this presentation) Not Rare but Uncommon Rare
- 34. Principles of Management When an OILD is suspected: Diagnosis first Document level of impairment, track Treat according to condition Protection at workplace to prevent progression Pneumoconioses: removal not indicated if <OEL Be disease: removal from exposure required HP: removal or effective protection essential Otherwise, symptomatic treatment once fibrosis is established
- 35. Essential Questions Whatis the nature of the process? What exposure in the worker’s employment history may have been responsible? What permanent level of impairment can be predicted? What can be done to control or limit the disease process? Are other people in the workplace likely to be affected, now or in the future?
- 36. Causation Specific, responsible exposure Work relationship Circumstances of exposure Possible interactions Interpretation: underlying cause proximate cause aggravation Cannot/should not use epidemiological principles for the individual case: Patients ≠ populations Hill criteria do not apply. Epi inferences are post hoc, single cases are Bayesian. Standard of certainty is not the same. WC Acts are clear.
- 37. Social function sentinelevent monitoring Causation/causality apportionment causal circumstances current impairment future impairment fitness to work Workers’ compensation Occupational health regulation Employer responsibility (Public health) (Human rights) Specific Functions Institutions ?
- 38. Social dimension: whyaccurate diagnosis, causality is important. Equity Fairness (Justice) Sufficiency Transparency Standardization Consistency Predictability Reliability Rapidity Validity Values Means