Occupational asthma and lung diseases - CCOHS: Occupational Health
Occupational lung diseases radiology
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Transcript of Occupational lung diseases radiology
OCCUPATIONAL LUNG DISEASES
Dust Deposition and Lymphatic Clearance:
deposition of particles 1–5 µm in diameter in and around the respiratory bronchioles- centrilobular location
Perilymphatic disease subpleural,peribronchovascular or along lobular septae.
Posterosuperior segment predilection of dust retention.
PNEUMOCONIOSIS CLASSIFICATION ACCORDING TO ILO (INTERNATIONAL LABOUR OFFICE) TYPE OF OPACITIES
Silicosis, coal worker's pneumoconiosis
nodular opacities:p = <1.5 mmq = 1.5-3 mmr = 3-10 mm
Asbestosis linear opacities:
s = fine t = medium u = coarse/blotchy
PROFUSION/SEVERITY 0 = normal 1 = slight 2 = moderate 3 = advanced
Induction PeriodsShort:
AsthmaInfections Allergic alveolitisToxic poisonings
Long:PneumoconiosesNeoplasms
acute reactions chronic reactions
inflammation and edema fibrosis or granuloma
1.Upper Respiratory Tract Irritation
Occupational Rhinitis2.Airway Disorders
Occupational AsthmaReactive Airways Dysfunction
(Byssinosis)3.Inhalation injury
Hypersensitivity Pneumonitis4.Pleural Disease
Pleural effusions and pleuritis (Asbestos)
1.Interstitial Fibrosing Diseases
Asbestosis (non-malignant pulmonary disease)
SilicosisCoal
Workers’PneumoconiosesBerylliosisChronic Bronchitis and
Chronic Airways Disease2.Malignancies
Malignant MesotheliomaLung CancerLaryngeal CancerSinonasal Cancer
CLASSIFIED
fibrotic ( focal nodular ,diffuse
fibrosis)
nonfibrotic (particle-laden macrophages,no fibrosis )1.silicosis -Nodular fibrosis
2.coal worker pneumoconiosis-Macule formation with focal emphysema 3.asbestosis --Diffuse fibrosis4.berylliosis- Granulomatous reaction5.talcosis
1.siderosis 2.stannosis 3.baritosis
Silicosis
principal sources- free silica in mining, quarrying, and tunneling.
fine crystalline silicon dioxide Inhalation
Silica particles- breakdown of macrophage releases enzymes –progressive fibrogenic response even after cessation of dust exposure.
Silicosissmall, well-circumscribed nodules that are 2–5
mm in dia, mainly inv upper & posterior lung zones.
GGO20% calcify centrallyLymphadenopathy is commonEggshell calcification of hilar nodes (5%) DDx: Sarcoidosis
SILICOSIS
2 clinical forms: Acute silicosis (alveolar silicoproteinosis) classic silicosis (chr interstitial reticulonodular disease)
simple complicated
OBSTRUCTIVE LUNG DISEASE LUNG CANCER
Silicotuberculosis
Acute Silicosis
Rare heavy exposure to free
silica-in closed spaces for 6–8 months.
rapidly progressive, with death caused by respiratory failure.
HRCT - "crazy paving" pattern
No silicotic nodules.DD-Alveolar proteinosis
(silicoproteinosis)
bilateral consolidation , GGO in perihilar region“central bat-wing consolidation .”
CHRONIC SIMPLE SILICOSIS
10--20 years of dust exposureRt upper lobes--posterior lung zones
nodules are in perilymphatic distributioncentered along the bronchovascular
bundles, centriacinar portion of the lobule, & in the subpleural lung, where the nodules form these pseudoplaques.
1-10mm well defined rounded opacities centrilobular & peribronchial;
nodules surrounded by focal emphysema (focal dust emphysema)
calcify
hilar + mediastinal lymphadenopathy, may calcify in 5% (eggshell pattern)
Simple silicosispseudoplaques
diffuse nodular opacities with relative sparing of the basal lung zones
HRCT shows numerous small nodules
Complicated Silicosis (PROGRESSIVE MASSIVE FIBROSIS)
large opacities >1 cm in diametermid zone /periphery of upper lung migrating toward hila
Relatively bilateral symmetric + nonsegmental
conglomerate sausage-shaped masses with ill-defined margins (in advanced stages)
compensatory emphysema in unaffected portion between mass + pleura
slow change over yearsmay calcify + cavitate (ischemic necrosis/TB)
CXR-large b/l opacities in the upper zones of the lung, as well as upward elevation of both hila.
CT-shows bilateral conglomerate masses with calcifications, findings that represent PMF in the upper zone of both lungs.
OBSTRUCTIVE LUNG DISEASE AND LUNG CANCER
chronic bronchitis, & Emphysema.
Tobacco smoking may cause an additive effect.
Silicotuberculosissynergistic relationship between silicosis + tuberculosis
Coal miners are exposed to dusts that contain a mixture of coal, mica and silica in varying proportions.
COAL WORKER PNEUMOCONIOSIS
CWP
Simple CWP- asymptomatic & is often a radiographic diagnosis.
Progressive massive fibrosis (PMF) can occur more frequently with exposure to silica.
CXR- small nodules predominantly in upper & posterior zone. Hilar lymph node enlargement is not uncommon
eggshell calcification does not generally occur. usually bilateral, progressive, and may cavitate or
become calcified. DD--tumors, tuberculosis scars, or Caplan’s
nodules
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CAPLANS SYNDROME
coal workers with rheumatoid disease may develop nodules even after relatively low exposures to dust.
The lesions are typically subpleural.The lesions may grow rapidly,appear in
crops(in contrast to silicotic/CWP nodules that appears over a period of time)cavitate and produce a pneumothorax
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Differentiate PMF from lung cancerClinically and radiologically importantbilateral occurrence : DDx with tumors or
tuberculosis Unilateral masses occur : DDx is difficult
Chest PA Shape of mass Calcification Satellite Nodules Course of PMF
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Differentiate from lung cancer
Shape of mass typically in periphery of lung smooth, sharp, elongated lateral border parallel rib
cage projected 1~3 cm from lateral costal margin medial border : ill-defined vs. lateral : sharp tends to be thin, carcinomas tend to be spherical
Calcification thick eggshells -> exclude primary lung cancer central dot calcification, Linear calcifications ; not in cancer
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Differentiate from lung cancerSatellite Nodules multiple small nodules near a lung mass in
pneumoconiosis or infection rare in carcinoma
Course of PMF mass formed by coalescence of nodule, rather
than by growth of a single nodule mass has decreased in size
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Differentiate from lung cancer
# MR imaging : useful
★ lung cancer vs PMFHigh SI on T2WI vs low SI T1WI, T2WI Low SI on T2WI MR images -> PMF
# PET Intensive uptake of FDG in PMF Observation of resultant mass enhancement on
images -> confusion of PMF with lung cancer
Histopathologic analysis should be performed
Progressive massive fibrosis
(a)HRCT scans --irregularly marginated 20–30mm nodules accompanied by smaller satellite nodules and surrounding reticulation in the upper lobe of both lungs. (b) T1-w image - slightly hyperintense lesions in both upper lobes.(c) T2-w image -absence of signal at the lesion sites and a small pleural effusion in the rt lung. (d) PET-CT scan -increased uptake of FDG in both nodules and in a right paratracheal LN.
Lung cancer and coal worker pneumoconiosis
(a) HRCT- welldefined 2-cm-diameter nodule in an upper segment of the lower lobe of the left lung, a finding that represents a combined neuroendocrine large cell carcinoma and adenocarcinoma, as well as multiple smaller nodules(b) T2-weighted -high-signal-intensity nodule in the lower lobe.(c) (PET)-CT scan - a high uptake of FDG in the nodule, suggestive of malignancy. (d) gross specimen- left lower lobectomy shows the cancer (arrow) and multiple black-pigmented nodules (arrowheads)In the lung parechyma and pleural surface
refers to pulmonary fibrosis secondary to asbestos exp.
Risk factors: Longer (approx. 20 years) exposure to the amphibole fiber type.
not associated with smokingTwo large groups: serpentines (Chrysotile)and
amphiboles(crocidolite).
Asbestosis
2 major sources of asbestos dust:(a) the primary occupations in asbestos mining.(b) secondary occupations --insulation manufacturing,
textile manufacturing, construction, shipbuilding, and the manufacture and repair of gaskets and brake linings.
Asymptomatic until 20 years after initial exposure.Long asbestos fiber (up to 100 µm in length),
penetrates deeply into the lung and pleura, and has a fibrogenic effect on respiratory bronchioles, alveoli, and pleura.
Asbestos-related diseases
Benign
Pleural diseases 1.plaques2.diffuse pleural thickening 3.effusion4.calcification
Parenchymal diseases 1.Asbestosis [parenchymal
fibrosis caused by asbestos inhalation]2.Rounded atelectasis 3.Benign fibrotic masses4.Transpulmonary bands
Malignancy 1.Malignant mesothelioma 2.Bronchogenic carcinoma
FOCAL PLEURAL PLAQUES (65%):
Incidence: most common manifestation of exposure
Location: bilateral + multifocal; following rib contours;
Site: parietal pleura (visceral pleura typically spared)
Plaques are often holly leafed shaped
Apices + costophrenic angles typically spared.
DIFFUSE PLEURAL THICKENING : smooth uninterrupted diffuse thickening
of parietal pleura extending over at least 1/4 of chest wall (visceral pleura involved in 90%, but difficult to demonstrate)
smooth; difficult to assess when viewed en face
Usually involves the costophrenic angles May be associated with rounded
atelectasis
DDx: pleural thickening from parapneumonic effusion, hemothorax, connective tissue disease
pleural plaques right side∕ rounded atelectasis
diffuse pleural thickening
Diaphragmatic pleural plaques
visceral pleural plaque in the right major fissure & curvilinear bands of hyperattenuation in the posterior subpleural area.
calcified pleural plaques hallmark of asbestos exposure.
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PLEURAL CALCIFICATION:HALLMARK of asbestos exposure!
detected by radiography in 25%, by CT in 60%Histo: calcification starts in parietal pleura;
calcium deposits may form within center of plaques
Dense lines paralleling the chest wall, mediastinum, pericardium, diaphragm
Bilateral diaphragmatic calcifications with clear costophrenic angles are PATHOGNOMONIC
advanced calcifications are leaflike with thick-rolled edges
DDx: talc exposure, hemothorax, empyema, therapeutic pneumothorax for TB (often unilateral, extensive sheet like on visceral pleura)
Pleural effusionearliest manifestation -within 10 years of
exposure, usually transient but requires close follow-up .
AsbestosisParenchymal fibrosis begins in and around the respiratory
bronchioles in the lower lobes adjacent to the visceral pleura
progress to diffuse interstitial fibrosis and "honeycombing," with complete destruction of the alveolar architecture.
Asbestos bodies- observed microscopically in bronchoalveolar lavage fluid or tissue section .
It may remain static or progress over time.
Radiologic changes consist of
small, irregular opacities or linear hyperattenuating areas
fine reticulations
coarse linear pattern with honeycombing.
most severe in the posterior subpleural lower lungs.
RETICULAR INFILTRATES
HONEYCOMB LUNG
Prone HRCT scan –b/l subpleural reticular hyperattenuating areas, small cysts, traction bronchiectasis, & GGO.
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ASBESTOSIS VS IPF
FAVORS ASBESTOSISPleural plaquesSubpleural branching opacitiesSubpleural curvilinear linesParenchymal bandsHomogeneous subpleural opacities
o Pleural plaqueso Sub pleural curvilinear
lineso Parenchymal bands
Traction bronchectasis
Bronchiloectasishoneycombing
ASBESTOSIS IPF
ATELECTATIC ASBESTOS PSEUDOTUMOR/ ROUND ATELECTASIS/ FOLDED LUNG
In folding of redundant pleura + segmental/subsegmental atelectasis
b/l posterobasal, 2.5-8 cm focal subpleural mass abutting a region of thickened pleura
CT: rounded/lentiform shaped peripheral mass abutting pleura pleural thickening ± calcification curving of pulmonary vessels and bronchioles into
edge of lesion (vacuum cleaner/comet tail sign )volume loss of affected lobe
crow's feet = linear bands radiating from mass into lung
Comet tail sign
PARENCHYMAL BAND “CROWS FEET”
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LUNG CANCER In those with asbestosis, the cancer is more likely to arise in the lower lobes in contrast to general smokers. Associations with lung cancer and mesothelioma
Asbestos-related lung cancer is usually either squamous cell or adenocarcinoma
Bronchogenic carcinoma is almost always associated with cigarette smoking Mesotheliomas are not related to cigarette smoking Mesotheliomas most often due to crocidolite particles
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MesotheliomaMesothelioma is a rare pleural malignancy seen
with asbestos exposure. The majority have no plaques. Long thin fibers are
more likely to induce mesothelioma, thus crocidolite is more neoplastic than chrysotile.
The hemithorax is usually small, pleural effusion is nearly universal.
Prognosis is poor, 12 month median survival.
MesotheliomaRare.majority have no plaques.
crocidolite is more neoplastic than chrysotile.
small, pleural effusionpoor Prognosis.
Malignant mesothelioma
• both parietal and visceral pleura mass.Local invasion is common
•CXR -Ipsilateral effusion to the pleural disease & contralateral pleural plaques •diagnosed by Open biopsy .
Mesothelioma indicated by the central pleural effusion
Byssinosis in a 56-year-old woman who had had frequent episodes of “Monday fever” and dyspnea while working in a cotton factory over a 7-year period. (a) Chest radiograph shows diffuse, ill-defined haziness, predominantly in the lower lung zones. (b) High-resolution CT scan shows numerous ill-defined small nodules with ground-glass attenuation in both lungs.
Mercury vapor poisoning in a 34-year-old woman worked for a mercurythermometer manufacturer for 30 months. presented with headache and dyspnea and suffered from chronicgingivitis.Chestxray showed perivascular haziness and fine reticular opacities in the parahilar area of both lungs. CT scan shows areas of ground-glass attenuation, poorly defined centrilobular nodules (arrows), and bronchial wall thickening. Note the relative sparing of the periphery of both lungs.
Occupational Lung CancersAsbestosArsenicBischloromethyl
etherCoke oven fumesInsoluble Hexavalent
chromium cmpds
Soluble nickelMustard gasRadon daughters
asbestosis lower lobes cancer is more likely-squamous cell or adenocarcinoma Bronchogenic carcinoma is almost always associated with cigarette smoking
SIDEROSIS
inert iron oxide/metallic iron depositsdiffuse fine reticulonodular opacities (may disappear
after exposure discontinued)small round opacities (indistinguishable from
silica/coal)
NO secondary fibrosis + NO hilar adenopathy
HRCT:--widespread poorly defined centrilobular micronodulesbranching linear structuresextensive ground-glass attenuation without zonal
predominance
BERYLLIUM-INDUCED LUNG DISEASE
extremely light metal Beryllium with a high modulus of elasticity (stiffness).
chronic beryllium disease (CBD or berylliosis)- delayed-type hypersensitivity reaction -granulomatous
lung disease similar to sarcoidosis. Lung primarily affected. Other sites -extrapulmonary lymph nodes, skin,
salivary glands, liver, spleen, kidney, bone, myocardium, and skeletal muscle.
usually nonspecific Symptoms – later--Dyspnea -mc symptom.
XRAY chest -50% patients normal.
Abnormal findings -hilar adenopathy,increased interstitial markings.
HRCT:GGO,parenchymal nodules,septal lines.
The diagnosis of CBD is based on the presence of: History of beryllium exposure positive blood or bronchoalveolar lavage beryllium-specific lymphocyte proliferation test presence of non-necrotizing granuloma on lung
bx 25% may show negative results
CONCLUSIONSILICOSIS--multiple small rounded opacities in upper lobes5% Eggshell calcification of hilar nodes.
Asbestosis--Pleural without parenchymal disease.B/l Parietal pleural plaques in the mid lung –mc.50% Pleural calcification.
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