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Occupational Lung Disease
By John J. Beneck MSPA, PA-C
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Occupational Lung Disease
Interstitial Lung Disease Coal Worker’s Pneumoconiosis (black lung) Silicosis Asbestosis Hyersensitivity Pneumonitis (allergic rxn) Smoke Inhalation Tissues of the lung
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Abbreviations ARDS-Acute respiratory distress syndrome
a/w-Associated with COPD-Chronic obstructive lung disease CRP-C reactive protein CTD-Connective tissue disease Cx-Culture CXR-Chest Xray DLCO-Diffusion capacity of the Lung for Carbon Dioxide d/t-Due to Dx-Diagnosis ESR-Erythrocyte sedimentation rate FEV1-Forced expiratory volume in 1 second FVC-Forced vital capacity HJR-Hepato-jugular reflux ILD-Interstitial lung disease JVD-Jugular venous distension LDH-Lactate dehydrogenase LL-lower lobe ML-Middle lobe OLD-Occupational lung diseasePFTs-Pulmonary Function tests PEEP-Positive end expiratory pressure PMN-Polymorphonuclear leukocyte PPD-Positive protein derivative PRN-As needed Pt-Patient Q-Every RF-Rheumatoid factor s/a-Same as Sx-Symptoms TB-Tuberculosis TLC-Total lung capacity VC-Vital capacity
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Objectives for Discussion
Etiology/Pathology Epidemiology Clinical Presentation Clinical Course/Prognosis Diagnostic Studies Clinical Interventions/Therapeutics Patient Education/Health Maintenance
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Interstitial Lung Disease A.K.A.-Interstitial Pulmonary Fibrosis
Multitude of Parenchymal lung diseases Coal worker’s pneumoconiosis Silicosis Asbestosis Hypersensitivity pneumonitis Other exposures Granulomatous disorders Idiopathic… ILD – A.K.A. Interstitial Pulmonary Fibrosis
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Interstitial Lung Disease
Similar Clinical presentation Chest Xray findings Progression Pathology Involve Alveolar changes Airway changes Involve changes throughout the lung tissue
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ILD - Epidemiology Inorganic Dust Exposure Organic Dusts
Silicates Silica Asbestos Carbon Coal Graphite Organic Dusts Hypersensitivity Pneumonitis Chemical Exposure Auto Immune Unknown
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sources
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ILD - Clinical Presentation
Progressive DOE to SOB Frequently Insidious Onset Disease Specific Sx Ex: Conn Tissue Diseases Abnormal Chest X ray Abnormal PFTs CTDs – Lupus, Scleroderma, RA… Comes on very slowly that they barely notice it, almost tolerant of it. May have altered lifestyle in small ways that keep them from getting sob.
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ILD - Evaluation Initial: Secondary Complete History & Physical Exam
Routine Labs CXR Secondary Serologies PFTs ABG High Resolution Chest CT Hx is the key as to where it came from and what is going on. If someone has a breathing prob that we don’t know what it is, get a CXR
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History Age Gender Smoking Hx Duration of Sx Prior Med Usage
Pt and spouse /family Duration of Sx Prior Med Usage R.E. – Autoimmune, CTD, Idiopathic Age can also tell us about possible exposures
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Further History Occupational History Environmental Exposures Work Home
Family
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Symptoms Dyspnea Dry Cough Typically
No Wheeze b/c lg airways not involved No Chest Pain with ILD Secondary to O.L.D.
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Exam NONSPECIFIC Crackles
Bronchovesicular Breath Sounds – hear high pitch sounds over r/l main bronchi – overwhelms regular vesicular sounds Occasional Digital Clubbing
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Clubbing
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Coal Worker’s Pneumoconiosis (Black Lung)
“The accumulation of coal dust and the tissue’s reaction to its presence.” Particles overwhelm cilia or they are so small they go past them.
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CWP Types: Simple (SCWP)
Complicated (CCWP) or Progressive Massive Fibrosis (PMF)
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CWP Epidemiology Location - Coal Country Length of Exposure
Pa, Md.,WV, Va, Ky Length of Exposure Type of Coal Dust Overall, 16% Miners in U.S. and Great Britain (Wales) Progress to Interstitial Fibrosis
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Risk Factors Type of Coal Dust: Anthracite Worst coal dust for CWP
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Other Types of Coal Bituminous
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Other Types of Coal Lignite
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Other Risk Factors Age at First Exposure Duration/Type of Exposure
Smoking Particle Size Possible Silica Exposure Some went in at very young age. 5 microns or less can make it to the alveoli
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CWP Pathology Anthracosis Coal Workers City Dwellers Smokers
Accumulation of carbon dust in the lung/ typically asymptomatic. First stage of development for CWP
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CWP Path (Cont.) Dust 2-5 µm Phagocytosis of Carbon Pigment
Expulsion through Mucociliary Escalator or lymphatics – problem is that they are too small or overwhelm system System Overwhelmed Macrophages accumulate Immune Response
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Immune Response Fibroblasts secrete Reticulin Macrophage is enveloped
Possibly Lyses Increased Lysis if Coal Contains Silica ↑ Fibroblast response over time leads to ↑ Collagen Deposition – more scaring in lung Fibrosis Occludes Lymphatics, Arterioles Ischemic Necrosis Reticulin – collagenous fibrous stuff that builds scar tissue/fiber.
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CWP Formation of Coal Macules (what they grow into)
Extension Coalescence Bronchiole Distention – forms little ballons- Focal Emphysema Role of CWP and Rheumatoid Factor Caplan Syndrome PMF Caplan’s syndrome – In pts w/ both pneumoconiosis and RA, the development of mult peripheral basilar nodules w/ mild airflow obstruction. Similar to Rheum nodules but surrounded by pigmented cells. No tx but prognosis is good. Rare in U.S.
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CWP Presentation SCWP - Asymptomatic CCWP Cough Dyspnea
Decreased Lung Function RV Failure Late Lungs become stiffer – affects right heart when distal arteries are occluded
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CWP - Course Variably Progressive Worse With: High Level Exposure
Long Duration Smoking Caplan Syndrome (positive RF or dx of RA)
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CWP - Diagnostics CBC Sputum Cx if Infection Suspected
CXR – reticular opacities PFTs Chest CT
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ILD - Reticular CXR Sharp thick linear markings. Doesn’t get a lot thicker as it goes inferior (we expect bottom to be more opaque than top half)
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ILD - CT Look at slice a and p to make sure that you are really looking at nodules (won’t be on other slices)
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CWP - Treatment Symptomatic Monitor Progression CXR Q 5 Years
Smoking Cessation O2/Bronchodilators PRN Immunizations – want flu and other vaccines to limit sec infections Monitor for Secondary Infection
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Asbestos Fibers Amphibole (thin and straight) – goes down and stabs alveoli Bad Serpentine (Chrystotile) (Curved) Not quite so bad
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Asbestosis Pneumoconiosis Associated with Exposure to Asbestos Fibers
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Spectrum Asbestosis – around areas in lung Pleural Plaque Malignancies
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Asbestosis Plaques Well demarcated area. Know they are on pulm membrane and not in lung by looking at it from a different angle as well
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Occupational Exposure
Fiber Mining and Milling Industrial Application Non-Occupational Airborne Exposure
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Pathology Exposure Prolonged Latency Period
Partial or complete phagocytosis of Fiber Attempted expulsion through Mucociliary Escalator or lymphatics Macrophages accumulate Immune Response These are sharp and they stick. Makes it hard to remove them from body. Same process as for CWP
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Immune Response Macrophage is enveloped Fibroblast response
Fibroblasts secrete Reticulin Collagen Deposition
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Asbestosis Grading
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Normal Lung
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Asbestosis with ILD & Pna
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Grade IV Asbestosis
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Clinical Presentation
DOE Progressive DOE Rare: Cough Sputum Wheeze Typically no cough.
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Exam Bibasilar Crackles Late Cor Pulmonale Edema JVD
HJR – hepatojugular reflex (lie flat and they don’t have it. IF you compress liver it will cause distention of JV S3 Gallop – implies ht failure
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Diagnostics CBC Serologies Sputum Cx if Infection Suspected CXR PFTs
DLCO – how thick alveolar walls are TLC, VC No Obstructive Pattern/it’s restrictive Chest CT CT – Basilar fibrosis parellel densities pleural plaques peripheral honeycombing
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Grade IV Asbestosis Lots of peripheral damage
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Asbestosis Course Latency 20-30 years Progressive DOE
Possible Respiratory Failure Possible Malignancy
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Asbestosis Management
Smoking Cessation Prevention of Further Exposure O2 PRN Prompt Tx of Respiratory Infections Immunizations
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Silicosis Pneumconiosis Secondary to Inhlation of Crystalline Silica Dust
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Types of Crystalline Silica
Quartz (most common) Granite (30% silica) Slate (40% silica) Sandstone (virtually pure silica) Cristobalite (quite toxic) Tridymite
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Silicosis Types Chronic –slow onset Accelerated Acute Silicosis
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Pathology - Chronic Silica Surface Interacts to Produce Radicals
Macrophage Injury Cytokines Generated Inflammation Fibrosis CXR with Simple Silicosis Least pathological
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Chronic Silicosis Small Round Pulmonary Nodules Upper Lung Zones
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Accelerated Silicosis
Increased exposure Shorter latency ( 10 years) More likely to develop PMF
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PMF Larger Opacities (>10 mm diameter) Mid-Upper Zones
Hilar Adenopathy Progressive massive fibrosis Look like big tumors, big well demarcated – accelerated silicosis developed into PMF
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Presentation - Chronic/Accelerated
10-30 Year Latency - Chronic Sx Within 10 Yrs Exposure - Accelerated DOE Cough Variable Adventitious Breath Sounds
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Acute Silicosis Rare Proteinaceous Alveolar Filling
Interstitial Thickening Minimal Pulmonary Fibrosis More Lower Zone Association
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Silicoproteinosis Acute Silicosis No hylar lymphadenopathy
Silicoproteinosis is the radiographic hallmark of acute silicosis
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Presentation - Acute Sx in Weeks to Years. DOE Dry Cough
Pleuritic Pain – only one that has it so far Appetite Fatigue Rapid Progression May really look like pneumonia, but they don’t respond to AB, and their hx suggests some exposure
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Evaluation History and PE CXR Lack of Other Likely Etiology
? Role of Chest CT PFTs FEV1, FEV1/FVC Ratio, DLCO Lung Bx
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Treatment - Symptomatic Only
Bronchodilators – b/c of obstruction (from PFT) O2 PRN Infection Control Immunizations PPD/TB Awareness –inc risk +/- Steroids Lung Transplant Prevention
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Hypersensitivity Pneumonitis A.K.A. Extrinsic Allergic Alveolitis
Types: Acute Subacute Chronic
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Hypersensitivity Pneumonitis Extrinsic Allergic Alveolitis
Lung Inflammation Secondary to Exposure to an Allergen Not an immune response this time
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HP Epidemiology Farmers Bird Fanciers Veterinarians Textile workers
Manufacturers Other (many) From organic dusts, from animals etc
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Prevalence Widely Variable Farmer’s Lung Bird Fancier’s
9% Farmers in Humid Zones 2% in Drier Zones Bird Fancier’s 6-21% per Year Risk in Cigarette Smokers – dec immune response and allergic response of lungs
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HP Etiology Inflammation Many inciting agents
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Acute HP - Presentation
Follows 4-6 hours after heavy exposure Abrupt Fever/Chills Malaise Cough Chest Tightness Dyspnea Rales on Exam Similar to pneumonia
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Acute HP Labs, Little Help Poss. ESR, Ig’s, RF, CRP, LDH
Bronchoalveolar lavage (BAL)- Lymphocytosis Mild Hypoxemia PFT’s - Mixed If you don’t have a WBC or Eos not likely infection Check for inflammation
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Acute HP - Cont. CXR - Undependable
Normal ML/LL Interstitial Pattern CT - Possible Ground Glass Appearance
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Acute HP Course Sx Hours to Days Xray Resolution Weeks
Fast on fast off
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Subacute HP Gradual Onset Cough Fatigue Wt. Loss Anorexia
Pneumonia, cancer, among other things
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Subacute HP - Presentation
S/A Acute Frequent DLCO More hypoxic
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Subacute HP - Course Slower Improvement Improved With Steroids
Weeks to Months Improved With Steroids
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Chronic Progressive HP
Insidious Onset S/A Above Possible Digital Clubbing Irreversible Pulmonary Fibrosis Occurs very slowly Changes in lungs that don’t go away
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Chronic Progressive HP Work Up
Labs S/A Above Except Poss BAL PMNs or Eosinophils PFTs Restriction and Obstruction DLCO Xray Upper Lobe Fibrotic Changes Lung Volume Dx Via Lung Bx BAL – Bronchial alveolar levage Neutrophils and/or eosinophils
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Chronic Progressive HP - Tx
S/A Acute, subacute Steroids
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HP - Overall Prevention/Care
Environmental Hygiene Protective Devices Removal From Exposure Steroid Therapy
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Smoke Inhalation The Inhalation of Gases and Aerosolized Particles Liberated by the Burning of Fuel. Particles put up into the air
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Smoke Inhalation Prevalence 5000 Fire Deaths/Year in U.S.
Most d/t Smoke Inhalation Mortality a/w Burns 77% of Deaths from Combined Inhalation and Cutaneous Injuries Caused or Directly Impacted by Pulmonary Complications.
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Smoke Production Oxidation – burning of the fuel
Pyrolysis – boiling of the particles. The changing of a material from a solid to a gas by virtue of extreme heat
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Injury Mechanisms Thermal Hypoxic Gas Inhalation
24 Hr Onset Hypoxic Gas Inhalation immediate Onset - hypoxia Bronchopulmonary Toxins – toxins that affect lungs and tissues 12-36 Hr Onset Systemic Toxins
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Thermal Injury Assessment
Stridor – can hear air movement in lg airways. Can have them breath really fast to assess risk Accessory Muscle Use Hypoxia/Hypercapnia Deep Face/Neck Burns Oropharyngeal Blistering/Edema Possibly Normal CXR
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Bronchopulmonary Toxins
pH Incompatability – can be irritating Free Radicals Soot – particles stick to airways and send contents - Adds to systemic delivery
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Systemic Toxins Carbon Monoxide Hydrogen Cyanide
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Carbon Monoxide Odorless Tasteless Colorless Nonirritating
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Carbon Monoxide - Presentation
Variable HA Nausea Malaise Dyspnea Siezures Arrhythmia CHF Coma Angina
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Carbon Monoxide - Diagnosis
ABG - Measured Avoid Reliance on SaO2 Monitor – gives false readings
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Hydrogen Cyanide Formed by Pyrolysis
Interrupts Aerobic Metabolism – we can’t live anaerobicly very well.
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Cyanide - Presentation
Rapid Coma Apnea Arrhythmia Severe Lactic Acidosis Difficult to Diagnose Thisulfate – donor for rhodanese – enzume which detoxifies cyanide
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Smoke Inhalation - Treatment
Mechanical – adress injuries Toxicological – address poisons
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Treatment - Cont. High Flow O2 Possibly Hyperbaric O2
Intubation – PEEP – keeps pressure on pt even when pt has pushed out all air –positive end expiratory pressure COPD Patients Upper Airway Edema – protects airways Bronchodilators
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Cyanide Treatment Amyl Nitrate Thiosulfate
Oxidizes Hemoglobin to Methemoglobin May Worsen Hypoxemia – contraindicated if CO poisoning also present Thiosulfate Converts Cyanide to Thiocyanide Hydoxocobalamin (approved in U.S. in ’06) Converts Cyanide to Cyanobalamin – best one for use
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Later Issues Tracheobronchial Sloughing in 3-4 Days – irritation of airway – cough up tissue Pneumonia ARDS Pulmonary Edema Hypermetabolism Generally Full Recovery in Surviving Patients
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