Silicosis: Difference between revisions
Esther Lee (talk | contribs) (Undo revision 753268 by Esther Lee (talk)) |
No edit summary |
||
| Line 56: | Line 56: | ||
Characteristic lung tissue pathology in nodular silicosis consists of fibrotic nodules with concentric "onion-skinned" arrangement of [[collagen]] fibers, central hyalinization, and a cellular peripheral zone, with lightly birefringent particles seen under polarized light. In acute silicosis, microscopic pathology shows a periodic acid-Schiff positive alveolar exudate (alveolar lipoproteinosis) and a cellular infiltrate of the alveolar walls. | Characteristic lung tissue pathology in nodular silicosis consists of fibrotic nodules with concentric "onion-skinned" arrangement of [[collagen]] fibers, central hyalinization, and a cellular peripheral zone, with lightly birefringent particles seen under polarized light. In acute silicosis, microscopic pathology shows a periodic acid-Schiff positive alveolar exudate (alveolar lipoproteinosis) and a cellular infiltrate of the alveolar walls. | ||
==Symptoms== | ==Symptoms== | ||
Revision as of 17:52, 24 September 2012
Template:DiseaseDisorder infobox
|
Silicosis Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Silicosis On the Web |
|
American Roentgen Ray Society Images of Silicosis |
For patient information click here
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Silicosis from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
Diagnostic Criteria | History and Symptoms | Physical Examination | Laboratory Findings | EKG | Chest X ray | CT | MRI | Echocardiography or Ultrasound | Other Imaging Findings | Other Diagnostic Studies
Treatment
Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies
Case Studies
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. The cutting, breaking, crushing, drilling, grinding, or abrasive blasting of these materials may produce fine silica dust. It can also be in soil, mortar, plaster, and shingles. Silicosis is due to deposition of fine dust (less than 1 micrometre in diameter) containing crystalline silicon dioxide in the form of alpha-quartz, cristobalite, or tridymite.
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.
Pathology
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.
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.
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.
Characteristic lung tissue pathology in nodular silicosis consists of fibrotic nodules with concentric "onion-skinned" arrangement of collagen fibers, central hyalinization, and a cellular peripheral zone, with lightly birefringent particles seen under polarized light. In acute silicosis, microscopic pathology shows a periodic acid-Schiff positive alveolar exudate (alveolar lipoproteinosis) and a cellular infiltrate of the alveolar walls.
Symptoms
Because silicosis is progressive, signs of it may not appear until years after exposure.[1] Symptoms include:
- Tachypnea or shortness of breath after physical exertion
- Dry or severe cough, often persistent and accompanied by hoarseness of the throat
- Fatigue or tiredness
- Changes in breathing pattern (rapid breathing or shallow breathing)
- Loss of appetite
- Chest pain
- Fever
- Gradual dark shallow rifts in nails eventually leading to cracks
In advanced cases, the following may also occur:
- Cyanosis
- Cor pulmonale
- Respiratory insufficiency
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
Classification of silicosis is made according to the disease's severity, onset, and rapidity of progression. These include:
- 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 and complicated silicoses. 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.
- Asymptomatic silicosis
Early cases of the disease do not present any symptoms
- Accelerated silicosis
Silicosis that develops 5-10 years after high exposure to silica dust. Symptoms include severe shortness of breath, weakness, and weight loss.
- Acute silicosis
Silicosis that develops a few months to 2 years after exposure to very high concentrations of silica dust. Symptoms of acute silicosis include severe disabling shortness of breath, weakness, and weight loss, often leading to death.
Diagnosis
Patient history should reveal exposure to silica dust due to occupation. Physical check up will reveal decreased chest expansion and abnormal breath sounds. Pulmonary function test will reveal reduced lung capacity.
Chest x-ray will confirm the presence of nodules in the lungs, especially in the upper lobes. Typically, it will also reveal eggshell calcification of the hilar lymph nodes. In rare cases, pulmonary nodules may also be calcified. In advanced cases of silicosis, coalescence of nodules may show up as large masses.
A computed tomography or CT scan can also provide a mode detailed analyses of the nodules, and can reveal cavitation due to concomitant mycobacterial infection.
Treatment
Silicosis is an irreversible condition with no cure. Treatment options currently focus on alleviating the symptoms and preventing complications. These include:
- Stopping further exposure to silica and other lung irritants, including tobacco smoking.
- Cough suppressants.
- Antibiotics and antitubercular agents to prevent tuberculosis. These include isoniazid, rifampin, and pyrazinamide.
- Chest physiotherapy to help the bronchial drainage of mucus.
- Oxygen administration to avoid hypoxemia.
- Bronchodilators to facilitate breathing.
- Lung transplantation to replace the damaged lung tissue is the most effective treatment, but is associated with severe risks of its own.
Experimental treatments include:
- Whole-lung lavage (see Bronchoalveolar lavage)
- Inhalation of powdered aluminium, d-penicillamine and polyvinyl pyridine-N-oxide.
- Corticosteroid therapy.
- The herbal extract tetrandine may slow progression of silicosis.[2]
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.
See also
External links
Notes
Template:Respiratory pathology
bg:Силикоза de:Silikose it:Silicosi nl:Silicose simple:Silicosis sl:Silikoza uk:Силікоз