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OccupationalLung

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

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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 DiseaseA.K.A.-Interstitial Pulmonary Fibrosis

• Multitude of Parenchymal lung diseases– Coal worker’s pneumoconiosis– Silicosis– Asbestosis– Hypersensitivity pneumonitis– Other exposures– Granulomatous disorders– Idiopathic…

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Interstitial Lung Disease

– Similar• Clinical presentation

• Chest Xray findings

• Progression

• Pathology

– Involve• Alveolar changes

• Airway changes

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ILD - Epidemiology

• Inorganic Dust Exposure– Silicates

• Silica• Asbestos

– Carbon• Coal• Graphite

• Organic Dusts– Hypersensitivity Pneumonitis

• Chemical Exposure• Auto Immune• Unknown

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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

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ILD - Evaluation

• Initial:– Complete History & Physical Exam

– Routine Labs

– CXR

• Secondary– Serologies

– PFTs

– ABG

– High Resolution Chest CT

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History

• Age

• Gender

• Smoking Hx– Pt and spouse /family

• Duration of Sx

• Prior Med Usage– R.E. – Autoimmune, CTD, Idiopathic

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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.”

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CWP

• Types:

– Simple (SCWP)

– Complicated (CCWP) or Progressive Massive

Fibrosis (PMF)

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CWP Epidemiology

• Location - Coal Country– 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

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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

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CWP Pathology

• Anthracosis

– Coal Workers

– City Dwellers

– Smokers

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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

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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

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CWP Presentation

• SCWP - Asymptomatic

• CCWP

– Cough

– Dyspnea

– Decreased Lung Function

– RV Failure Late

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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

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ILD - CT

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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

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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

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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

• DOE

• Progressive DOE

• Rare:– Cough– Sputum– Wheeze

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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

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Grade IV Asbestosis

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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

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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

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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

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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

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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 PneumonitisA.K.A.

Extrinsic Allergic Alveolitis

• Types:

– Acute

– Subacute

– Chronic

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Hypersensitivity PneumonitisExtrinsic Allergic Alveolitis

• Lung Inflammation Secondary to Exposure

to an Allergen

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HP Epidemiology

• Farmers

• Bird Fanciers

• Veterinarians

• Textile workers

• Manufacturers

• Other (many)

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Prevalence

• Widely Variable• Farmer’s Lung

– 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

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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

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• CXR - Undependable

– Normal

– ML/LL Interstitial Pattern

• CT - Possible Ground Glass Appearance

Acute HP - Cont.

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Acute HP Course

• Sx Hours to Days

• Xray Resolution Weeks

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Subacute HP

• Gradual Onset

– Cough

– Fatigue

– Wt. Loss

– Anorexia

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• S/A Acute

• Frequent DLCO

Subacute HP - Presentation

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• Slower Improvement

– Weeks to Months

• Improved With Steroids

Subacute HP - Course

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• Insidious Onset

• S/A Above

• Possible Digital Clubbing

• Irreversible Pulmonary Fibrosis

Chronic Progressive HP

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• 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

Chronic Progressive HP Work Up

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• S/A Acute, subacute

• Steroids

Chronic Progressive HP - Tx

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• Environmental Hygiene

• Protective Devices

• Removal From Exposure

• Steroid Therapy

HP - Overall Prevention/Care

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• The Inhalation of Gases and Aerosolized

Particles Liberated by the Burning of Fuel.

Smoke Inhalation

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• 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.

Smoke Inhalation

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• 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

Smoke Production

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• Thermal– 24 Hr Onset

• Hypoxic Gas Inhalation– immediate Onset - hypoxia

• Bronchopulmonary Toxins – toxins that affect lungs and tissues– 12-36 Hr Onset

• Systemic Toxins

Injury Mechanisms

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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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• pH Incompatability – can be irritating

• Free Radicals

• Soot – particles stick to airways and send

contents -

– Adds to systemic delivery

Bronchopulmonary Toxins

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• Carbon Monoxide

• Hydrogen Cyanide

Systemic Toxins

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• Odorless

• Tasteless

• Colorless

• Nonirritating

Carbon Monoxide

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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

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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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• Amyl Nitrate– 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

Cyanide Treatment

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• Tracheobronchial Sloughing in 3-4 Days – irritation of airway – cough up tissue

• Pneumonia• ARDS• Pulmonary Edema• Hypermetabolism• Generally Full Recovery in Surviving

Patients

Later Issues

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Reference: (1) Schwarz, MI, King, TE Jr. Approach to the evaluation and diagnosis of interstitial lung disease. In: Interstitial Lung Disease, 4th ed, King, TE Jr, Schwarz, MI (Eds), B.C. Decker, Hamilton, ON, Canada. 2003. p.1. (2)King, T. E. Approach to the Adult with Interstitial Lung Disease. In UpToDate, Rose, BD (Ed), UpToDate, Waltham, MA, 2006 (3) Drug-induced and iatrogenic infiltrative lung disease. Camus P; Bonniaud P; Fanton A; Camus C; Baudaun N; Foucher P. Clin Chest Med 2004 Sep;25(3):479-519, vi. (4) Morgan WK, Seaton A: Occupational Lung Diseases. WB Saunders Co; 1975:149-210. (5) Richards, J.E. (2005) Coal Worker’s Pneumoconiosis. Retrieved September 6, 7 2006, from Emedicine. Web site: http://www.emedicine.com/med/topic398.htm (6) Coalfields Photograph Album. Retrieved September 7, 2006, from UKY Appalachian Center Web site: http://www.uky.edu/RGS/AppalCenter/new_jpgs/goode14.jpg (7) King, T.E. Asbestosis. In UpToDate, Rose, BD (Ed), UpToDate, Waltham, MA, 2006 (8) Weissman, DN, Wagner, GR. Silicosis. In UpToDate, Rose, BD (Ed), UpToDate, Waltham, MA, 2006 (9) Talmadge, E.K. Epidemiology and Causes of Hypersensitivity Pneumonitis. In UpToDate, Rose, BD (Ed), UpToDate, Waltham, MA, 2006 (10) Mandel, J. Hales, C.A. Smoke Inhalation. In UpToDate, Rose, BD (Ed), UpToDate, Waltham, MA, 2006 (11) King, T.E. Approach to the Adult With Interstitial Lung Disease. In UpToDate, Rose, BD (Ed), UpToDate, Waltham, MA, 2008