slide1 l.
Download
Skip this Video
Loading SlideShow in 5 Seconds..
Mohammad Tohidi M.D. Professor of Internal Medicine Department of Pulmonary Medicine Ghaem Hospital MUMS Mashh PowerPoint Presentation
Download Presentation
Mohammad Tohidi M.D. Professor of Internal Medicine Department of Pulmonary Medicine Ghaem Hospital MUMS Mashh

Loading in 2 Seconds...

play fullscreen
1 / 86

Mohammad Tohidi M.D. Professor of Internal Medicine Department of Pulmonary Medicine Ghaem Hospital MUMS Mashh - PowerPoint PPT Presentation


  • 209 Views
  • Uploaded on

Mohammad Tohidi M.D. Professor of Internal Medicine Department of Pulmonary Medicine Ghaem Hospital MUMS Mashhad IRAN. Silicosis. Case Scenario(1).

loader
I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
capcha
Download Presentation

PowerPoint Slideshow about 'Mohammad Tohidi M.D. Professor of Internal Medicine Department of Pulmonary Medicine Ghaem Hospital MUMS Mashh' - maura


An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
slide1

Mohammad Tohidi M.D.

Professor of Internal Medicine

Department of Pulmonary Medicine

Ghaem Hospital MUMS Mashhad IRAN

case scenario 1
Case Scenario(1)
  • 57 year old retired non-smoker man referred with the cc of dry cough for 1year.In addition he has had mild ED but no other complaint. Past Hx & system review were negative.His VS,general PE &

chest exam were normal.Chest X ray showed diffuse reticulonodular pattern There were no hilar enlargement & calcification.

case scenario 2
Case Scenario(2)
  • HRCT scan of the lung revealed small rounded opacities & thickening of alveolar septa

no ground glass pattern,hilar adenopathy

& pleural effusion.He had >30 years Hx of stone cutting & grinding.With this Hx & immaging studies, in the absence of another causes,diagnosis of simple silicosis was apparent.

definition
DEFINITION
  • Silicosis is a fibrotic lung disease attributable to the inhalation of crystalline silica, usually in the form of quartz and, less commonly, as cristobalite and tridymite
  • Amorphous silica is relatively nontoxic
introduction
Introduction
  • Silicosis (also known as Grinder's disease and Potter's rot) is a form of occupational lung disease caused by inhalation of crystalline silica dust, and is marked by inflammation and scarring in forms of nodular lesions in the upper lobes of the lungs.
where s it come from
Where’s it come from?

Crystalline forms of silica (Silicon Dioxide or SiO2) include quartz, cristobalite, and tridymite. Quartz is the most common type, and is a major component of rocks including granite, slate, and sandstone.

silica
Silica
  • Silica is the second most common mineral on earth. It is found in sand, many rocks such as granite, sandstone, flint and slate, and in some coal and metallic ores.
silica14
Silica
  • The cutting, breaking, crushing, drilling, grinding, or abrasive blasting of these materials may produce fine silica dust.
silicosis history
Silicosis – history
  • This respiratory disease was first recognized in 1705 by Ramazzini who noticed sand-like substances in the lungs of stonecutters
silicosis history16
Silicosis – history

Full description by Bernardino Ramazzini (1633-1714) in early 18th century. “...when the bodies of such workers are dissected, they have been found to be stuffed with small stones.”Diseases of Workers (De Morbis Artificum Diatriba, 1713).

silicosis history17
Silicosis – history
  • The name silicosis (from the Latin silex or flint) was attributed to Visconti in 1870
silicosis history18
Silicosis - history
  • First U.S. description in 19th century.
  • Term silicosis introduced in 1870, from Latin silex, or flint.
  • Prevalence increased markedly with introduction of mechanized mining.
  • Came to national attention 1930-1931 with construction of Hawk’s Nest Tunnel in Gauley Bridge, West Virginia. Called “the worst industrial accident in U.S. history.” At least 764 tunnel workers died from silicosis. Hawk’s Nest disaster led to Congressional hearings in 1936, and new laws protecting workers in many states.
  • Prevalence of silicosis has greatly declined in recent decades because of effective industrial hygiene measures.
silicosis history19
Silicosis - history
  • The full name for this disease when caused by the specific exposure to fine silica dust found in volcanoes is pneumonoultramicroscopicsilicovolcanoconiosis, and at 45 letters it is the longest word in any of the major English dictionaries.
silicosis history20
Silicosis - history
  • The prevalence of silicosis led some men to grow what is called a miner's mustache, in an attempt to intercept as much dust as possible.
diseases associated with exposure to silica dust 1
Diseases Associated with Exposure to Silica Dust(1)
  • Silicosis Chronic silicosis Accelerated silicosis Acute silicosis (silicoproteinosis)(fine dust, intense exposure , high silica)

Progressive massive fibrosis

  • Chronic Obstructive Pulmonary Disease Emphysema Chronic bronchitis Mineral dust-induced small airway disease
diseases associated with exposure to silica dust 2
Diseases Associated with Exposure to Silica Dust(2)

Lung CancerMycobacterial InfectionMycobacterium tuberculosis Nontuberculous Mycobacteria Immune-Related DiseasesProgressive systemic sclerosis Rheumatoid arthritis Chronic renal disease Systemic lupus erythematosus

pulmonary toxicology
Pulmonary Toxicology

• Particle size is critical.

• Peak dust inhalation

occurs with particles

having a diameter of 0.5 to

3 microns (μm).

• RCS is invisible to the

human eye.

• Pulmonary clearance

mechanisms:

macrophages & the

mucociliary escalator

slide24
The induction period between initial silica exposure and development of radiographically detectable nodular silicosis is usually 10 years. Shorter induction periods are associated with heavy exposures, and acute silicosis may develop within 6 months to 2 years following massive silica exposure.
slide25
Silicosis is an occupational hazard to mining, sandblasting, quarry, ceramics and foundry workers, as well as grinders, stonecutters and those continually exposed to silica dust.
variety of occupations
Variety of occupations
  • Construction, and surface and underground rock drilling
  • Foundries are also a main source of silica dust
  • workers involved with the repair, rehabilitation, or demolition of concrete structures
variety of occupations27
Variety of occupations
  • New types of pneumoconiosis often turn out to be silicosis in an industry not previously thought to be at risk or a mixed-dust pneumoconiosis in which silica is implicated with other dusts
  • Silicosis is often the result of exposure in the remote past and not in the current workplace
pathology 1
Pathology(1)
  • When small silica dust particles are inhaled, they can embed themselves deeply into the tiny alveolar sacs and ducts in the lungs, where oxygen and carbon dioxide gases are exchanged. There, the lungs cannot clear out the dust by mucous or coughing
pathology 2
Pathology(2)
  • Characteristic lung tissue pathology in nodular silicosis consists of fibrotic nodules with concentric "onion-skinned" arrangement of collagenfibers, central hyalinization, and a cellular peripheral zone, with lightly birefringent particles seen under polarized light
pathology 3
Pathology(3)
  • In acute silicosis, microscopic pathology shows a periodic acid-Schiff positive alveolar exudate (alveolar lipoproteinosis) and a cellular infiltrate of the alveolar walls
pathogenesis 1
PATHOGENESIS(1)
  • There is agreement that freshly fractured silica, such as that generated during sandblasting, is more toxic to the alveolar macrophages than is "aged" silica
  • clay components, may adhere to the surfaces of silica particles, producing "coated" silica, which is less toxic than uncoated silica dust
  • the incidence of silicosis is decreased by concomitant exposure to other dusts
pathogenesis 2
PATHOGENESIS(2)

4 The intensity of the exposure determines the nature of the lung injury. Low-intensity exposure generally produces aggregates of fibrosis with relative sparing of the lung architecture, whereas high-intensity exposure causes widespread pulmonary inflammation and collagen deposition

5 Individual susceptibility to the disease may play a role

slide35
Particles engulfed by macrophages:

transported upward and removed from lungs retained in the lung “Frustrated Phagocytosis”

cascade of toxic effects

inflammatory process

pneumoconiosis

fibrosis in the lung tissue

pathogenesis 3
Pathogenesis(3)
  • When fine particles of silica dust are deposited in the lungs, macrophages that ingest the dust particles will set off an inflammation response by releasing tumor necrosis factors, interleukin-1, leukotriene B4 and other cytokines. In turn, these stimulate fibroblasts to proliferate and produce collagen around the silica particle, thus resulting in fibrosis and the formation of the nodular lesions
pathogenesis 4
Pathogenesis(4)
  • Furthermore, the surface of silicon dust can generate silicon-based radicals that lead to the production of hydroxyl and oxygen radicals, as well as hydrogen peroxide, which can inflict damage to the surrounding cells
slide38
Silicosis
  • MC chronic occupational disease in the world
  • caused by inhalation of crystalline silicon dioxide (silica).
  • Acute silicosis -accumulation of a lipoproteinaceous material within alveoli
  • Chronic silicosis - slowly progressing, nodular, Fibrosing pneumoconiosis
  • Pathogenesis
  • crystalline forms -more fibrogenic (quartz –worst)
  • silica particles lung macrophages ingest them  activation and release of mediators  IL-1, TNF, oxygen-derived free radicals
  • Anti-TNF monoclonal antibodies can block lung collagen accumulation in mice
  • Morphology.
    • Early stages –tiny nodules in the upper zones
    • disease progresses–nodules coalesce into hard, collagenous scarscentral softening and cavitation (due to superimposed tuberculosis or to ischemia)
    • X-ray–egg shell calcification in the lymph nodes
    • Advanced stage - PMF
  • Histology
  • Nodular lesions -concentric layers of hyalinized collagen surrounded by a dense capsule
  • Birefringent silica particles in polarized microscopy
epidemiology
EPIDEMIOLOGY
  • The prevalence of silicosis is difficult to estimate
  • the reported cases have been estimated to represent only one third of the total cases of silicosis
  • In calculating an individual's risk for silicosis, duration and intensity of exposure are of primary interest but peak exposure also may be important.
epidemiology cont d
EPIDEMIOLOGY(cont’d)
  • In the United States, NIOSH has estimated that at least 1.7 million workers are exposed to silica, of whom between 1500 and 2360 will develop silicosis each year
prevalence
Prevalence
  • Silicosis is the most common occupational lung disease worldwide, it occurs everywhere but is especially common in developing countries
clinical features 1
CLINICAL FEATURES(1)
  • The main symptom is breathlessness, first noted during exertion and later at rest as the large working reserve of the lung is diminished. In chronic silicosis, in the absence of other respiratory disease, even this symptom may be absent
  • a patient with chronic silicosis may present without symptoms for assessment of an abnormal chest radiograph
clinical features 2
CLINICAL FEATURES(2)
  • The appearance of breathlessness may mark the development of a complication such as progressive massive fibrosis or tuberculosis, or may reflect associated airway disease
  • Cough and sputum production are common symptoms and usually relate to chronic bronchitis, but may reflect the development of tuberculosis or lung cancer
clinical features 3
CLINICAL FEATURES(3)
  • Chest pain is not a feature of silicosis, nor are systemic symptoms such as fever and weight loss, which should be attributed to tuberculosis or lung cancer until proven otherwise.
  • Clubbing is also not a feature of silicosis
clinical features 4
CLINICAL FEATURES(4)
  • In accelerated and acute silicosis, the time scale of symptom evolution is in years or months rather than decades. In acute silicosis, breathlessness may become disabling within months, followed by impaired gas exchange Cyanosis

Cor pulmonale

Respiratory insufficiency

slide47
Patients with silicosis are particularly susceptible to tuberculosis (TB) infection - known as silicotuberculosis. The reason for the increased risk - 10-30 fold increased incidence - is not well understood. It is thought that silica damages pulmonary macrophages, inhibiting their ability to kill mycobacteria
types of silicosis
Types of Silicosis

(1) Chronic silicosis

Occurs after 15-20 years of exposure to moderate to low levels of silica dust. Chronic silicosis itself is further subdivided into:

simple

complicated silicosis(PMF)

chronic silicosis
Chronic silicosis
  • This is the most common type of silicosis. Patients with this type of silicosis may not have obvious symptoms, so a chest X-ray is necessary to determine if there is lung damage.
slide50
(2) Asymptomatic silicosis

Early cases of the disease do not present any symptoms

slide51
(3) Accelerated silicosis

Silicosis that develops 5-10 years after high exposure to silica dust. Symptoms include severe shortness of breath, weakness, and weight loss

slide52
(4) Acute silicosis

Silicosis that develops a few months to 2 years after exposure to very high concentrations of silica dust.

diagnosis of silicosis
Diagnosis of Silicosis
  • In general, three key elements play a role in the diagnosis of silicosis:
  • A history of silica exposure sufficient to cause the degree of illness and the appropriate latency from the time of first exposure
  • Chest imaging (usually a conventional chest radiograph) that shows opacities consistent with silicosis
  • Absence of another diagnosis more likely to be responsible for the observed abnormalities
diagnosis of silicosis54
Diagnosis of Silicosis
  • Abnormal chest X-ray (or chest CT scan) consistent with silicosis
  • History of significant exposure to silica dust
  • Medical evaluation to exclude other possible causes of abnormal chest x-ray
  • Pulmonary function tests are helpful to gauge severity of impairment, but NOT for diagnosis.
  • Lung biopsy rarely indicated (since no effective treatment, biopsy is done only when other diagnoses are being considered)
silicosis can be misdiagnosed
Silicosis can be misdiagnosed
  • Silicosis can mimic:
    • Sarcoidosis (benign inflammation of unknown cause)
    • Idiopathic pulmonary fibrosis (lung scarring of unknown cause)
    • Lung cancer
    • Several other lung conditions (chronic infection, collagen-vascular disease, etc.)

Can usually make right diagnosis with detailed history (occupational & medical) or, rarely, a lung biopsy.

lung function
LUNG FUNCTION
  • The lung function profile is determined by the extent of silicosis as well as associated or concomitant airway and vascular changes
  • In chronic silicosis, spirometric tests (FEV1, FEV1/FVC, and maximal midexpiratory flow) usually reflect airflow limitation.
lung function57
LUNG FUNCTION
  • In the accelerated and acute forms, functional changes are more marked and progression is more rapid. In acute silicosis, lung function shows a restrictive defect and impairment of gas exchange, which leads to respiratory failure and eventually to death from intractable hypoxemia
lung function58
LUNG FUNCTION
  • Reduction in diffusing capacity is generally apparent in more advanced chronic silicosis and probably reflects associated emphysema.
  • It is possible that most of the lung function changes associated with chronic silicosis can be attributed to the associated emphysema.
chest imaging
Chest imaging
  • The three main radiographic presentations of silicosis are:

simple silicosis progressive massive fibrosis

silicoproteinosis

simple silicosis
Simple silicosis 
  • Simple silicosis refers to a profusion of small (less than 10 mm in diameter) nodular opacities (nodules). The nodules are generally rounded but can be irregular, and are distributed predominantly in the upper lung zones
progressive massive fibrosis
Progressive massive fibrosis 
  • Progressive massive fibrosis (PMF, or conglomerate silicosis) occurs when these small opacities gradually enlarge and coalesce to form larger, upper- or mid-zone opacities more than 10 mm in diameter
slide62
PMF
  • The hila are retracted upward in association with upper lobe fibrosis and lower lobe hyperinflation
  • Hilar adenopathy with prominent calcification is often present. The opacities of PMF can be asymmetrical, and may mimic a neoplastic process. Cavitation may also be present in advanced disease, or in the setting of mycobacterial superinfection
silicoproteinosis
Silicoproteinosis
  • Silicoproteinosis occurs following overwhelming exposure to respirable crystalline silica over a short time, and is the radiographic hallmark of acute silicosis The chest radiograph demonstrates a characteristic basilar alveolar filling pattern, without rounded opacities or lymph node calcifications.
slide64
HRCT
  • There is general agreement that CT/HRCT is superior to conventional chest radiography for documentation of PMF lesions and emphysematous changes associated with silicosis
slide65
pleural effusions are unusual,but pleural thickening appears to be common, especially among patients with more severe disease. In a series of 110 patients with biopsy proven silicosis followed for a mean of 14 years, pleural effusions were noted in 12 patients (11 percent), but pleural thickening was present in 64 patients (58 percent)
normal simple silicosis
Normal Simple silicosis

noal chest x-ray

radiographic features 2
RADIOGRAPHIC FEATURES(2)
  • Silicotic nodules are usually, although not invariably, symmetrically distributed and tend to occur first in the upper zones .later, although not invariably, other zones are involved. Occasionally the nodules are calcified, resembling microlithiasis
radiographic features 3
RADIOGRAPHIC FEATURES(3)
  • Enlargement of the hilar nodes may precede the development of the parenchymal lesions. "Eggshell" calcification, when present, is strongly suggestive although not pathognomonic, of silicosis
  • Pleural plaques may occur but are not a common feature.
radiographic features 4
RADIOGRAPHIC FEATURES(4)
  • Progressive massive fibrosis is characterized by the coalescence of small rounded opacities to form larger lesions they are graded on the ILO scale according to size and extent (categories A to C).
radiographic features 5
RADIOGRAPHIC FEATURES(5)
  • CT assessment is superior to the chest radiograph not only in assessing the presence and extent of silicotic nodulation, but also in revealing early conglomeration.
  • With time, the mass lesions tend to contract, usually to the upper lobes, leaving hypertranslucent zones at their margins and often at the lung bases. In this process, small rounded opacities, previously evident, may disappear, resulting in a picture that needs to be distinguished from tuberculosis
radiographic features 6
RADIOGRAPHIC FEATURES(6)
  • The rapid development of several large lesions suggests rheumatoid silicosis, but new lesions, especially if cavitated, should be regarded as evidence of mycobacterial disease
  • Acute silicosis is characterized radiologically by diffuse changes that usually display an air space and interstitial pattern rather than the usual nodularity
diagnosis serology
Diagnosis: Serology
  • Hypergammaglobulinemia
  • RF
  • ANF
  • S-ACE
  • Increased incidence of systemic sclerosis

described in SA gold miners

treatment
Treatment
  • Silicosis is an irreversible condition with no cure. Treatment options currently focus on alleviating the symptoms and preventing complications
treatment77
Treatment
  • The disease will generally progress even without further exposure,but the rate of deterioration is probably reduced
treatment78
Treatment
  • There is currently interest in the use of lung lavage to remove silica from the lung, but a favorable impact on progression of acute or chronic silicosis has not been demonstrated.
treatment79
Treatment
  • Treatment of all forms of silicosis should be directed toward control of mycobacterial disease. This is especially true for acute and accelerated silicosis and silicosis in workers with human immunodeficiency virus infection
  • All patients with silicosis should have a tuberculin skin test and, if it is positive, be offered treatment for latent tuberculosis infection
treatment80
Treatment
  • Interventions to interrupt the inflammatory process that leads to chronic silicosis including the inhalation of aluminum or polyvinylpyridine-N-oxide and oral tetrandine have not been shown to be successful
treatment81
Treatment
  • The interaction between silica exposure and smoking in the development of COPD makes it particularly important to implement smoking cessation programs in the workplace
treatment82
Treatment
  • Because acute and accelerated silicosis carry such a poor prognosis and tend to occur in younger persons, consideration should be given to lung transplantation in such cases
prevention
Prevention
  • The best way to prevent silicosis is to identify work-place activities that produce crystalline silica dust and then to eliminate or control the dust. Water spray is often used where dust emanates. Dust can also be controlled through dry air filtering
prevention84
Prevention
  • The most important aspect of the management of silicosis relates to its prevention
  • a sustained effort must be made to increase awareness of silicosis. Recent deaths from silicosis in younger individuals in the United States have occurred after exposure in the construction and manufacturing sectors, with none from mining
slide85
Silicosis
  • MC chronic occupational disease in the world
  • caused by inhalation of crystalline silicon dioxide (silica).
  • Acute silicosis -accumulation of a lipoproteinaceous material within alveoli
  • Chronic silicosis - slowly progressing, nodular, Fibrosing pneumoconiosis
  • Pathogenesis
  • crystalline forms -more fibrogenic (quartz –worst)
  • silica particles lung macrophages ingest them  activation and release of mediators  IL-1, TNF, oxygen-derived free radicals
  • Anti-TNF monoclonal antibodies can block lung collagen accumulation in mice
  • Morphology.
    • Early stages –tiny nodules in the upper zones
    • disease progresses–nodules coalesce into hard, collagenous scarscentral softening and cavitation (due to superimposed tuberculosis or to ischemia)
    • X-ray–egg shell calcification in the lymph nodes
    • Advanced stage - PMF
  • Histology
  • Nodular lesions -concentric layers of hyalinized collagen surrounded by a dense capsule
  • Birefringent silica particles in polarized microscopy