Download Occupational Lung Disease

Occupational
Lung
Disease
• By John J. Beneck MSPA, PA-C
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Occupational Lung Disease
• Interstitial Lung Disease
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Coal Worker’s Pneumoconiosis (black lung)
Silicosis
Asbestosis
Hyersensitivity Pneumonitis (allergic rxn)
• Smoke Inhalation
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Abbreviations
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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
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LDH-Lactate dehydrogenase
LL-lower lobe
ML-Middle lobe
OLD-Occupational lung diseasePFTsPulmonary 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
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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
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Coal worker’s pneumoconiosis
Silicosis
Asbestosis
Hypersensitivity pneumonitis
Other exposures
Granulomatous disorders
Idiopathic…
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Interstitial Lung Disease
– Similar
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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
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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
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↑ 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:
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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
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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
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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
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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
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? 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
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HP Epidemiology
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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
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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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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
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Subacute HP
• Gradual Onset
– Cough
– Fatigue
– Wt. Loss
– Anorexia
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Subacute HP - Presentation
• S/A Acute
• Frequent  DLCO
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Subacute HP - Course
• Slower Improvement
– Weeks to Months
• Improved With Steroids
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Chronic Progressive HP
• Insidious Onset
• S/A Above
• Possible Digital Clubbing
• Irreversible Pulmonary Fibrosis
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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
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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.
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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
– 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
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HA
Nausea
Malaise
Dyspnea
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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
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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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Cyanide Treatment
• 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
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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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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; 1975:149210.
(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
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