Homepage | Imprint
Lumrix Logo
 
 
Lumrix Wiki Logo
[ICD 10 Search]



Back
[ICD 10 Search]

 

 

Silicosis

{{{Name|Silicosis}}}
[[Image:{{{Image}}}|190px|center|]]
{{{Caption|}}}
ICD-10 J62
ICD-O: {{{ICDO}}}
ICD-9 502
OMIM }}}
MedlinePlus }}}
eMedicine }}}
DiseasesDB }}}

Silicosis (also known as Grinder's disease) is a form of pneumoconiosiscaused by inhalation of crystalline silicadust, and is marked by inflammationand scarring in forms of nodular lesions in the upper lobes of the lungs.

Silicosis (especially the acute form) is characterized by shortness of breath, fever, and cyanosis (bluish skin). It may often be misdiagnosed as pulmonary edema(fluid in the lungs), pneumonia, or tuberculosis.

This respiratory disease was first recognized in 1705 by Ramazzini who noticed sand-like substances in the lungs of stonecutters. The name silicosis (from the latin silex or flint) was attributed to Visconti in 1870.

Inhaltsverzeichnis

  • 1 Silica
  • 2 Pathology
  • 3 Prevalence
  • 4 Symptoms
  • 5 Types of Silicosis
  • 6 Diagnosis
  • 7 Treatment
  • 8 Prevention
  • 9 See also
  • 10 External links

Silica

Silica is the second most common mineralon earth. It is found in concrete, masonry, sandstone, rock, paint, and other abrasives. 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?m in diameter) containing crystalline alpha-quartz silica or silicon dioxide.

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 the small silica dust particles are breathed into the lungs, they can embed themselves deeply into the tiny alveolar sacs and ducts 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, macrophagesthat ingest the dust particles will set off an inflammationresponse by releasing tumor necrosis factor, interleukin-1, leukotriene B4and other cytokines. In turn, these stimulate fibroblaststo proliferate and produce collagen around the silica particle, thus resulting in fibrosisand the formation of the nodular lesions.

Furthermore, the surface of silicon dust can generate silicon-based radicals that lead to the production of hydroxyland 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 collagenfibers, 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.

Prevalence

Although silicosis has been known for centuries, the industrialization of mining has lead to an increase in silicosis cases. In the United States, a 1930 epidemic of silicosisdue to the construction of the Hawk's Nest Tunnel near Gauley Bridge, West Virginiacaused the death of more than 400 workers.

Also, the mining establishment of Delamar Ghost Town, Nevada was ruined a dry-mining process that produced a silicosis-causing dust. After hundreds of deaths from silicosis, the town was nicknamed The Widowmaker.

Indeed, silicosis is an occupational hazard to mining, sandblasting, quarry and foundryworkers, as well as grinders, stonecutters and those continually exposed to silica dust.

Due to protective measures, such as using respirators, death rates of silicosis in Western countries have been steadily declining.

Symptoms

The symptoms of silicosis include:

  • Tachypneaor 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

In advanced cases, the following may also occur:

  • Cyanosis
  • Cor pulmonale
  • Respiratory insufficiency

Patients with silicosis are particularly susceptible to tuberculosis(TB) infection.

Types of Silicosis

Classification of silicosis is made according to the disease's severity, onset, and rapidity of progression. These include:

  • Chronic silicosis

A form of the disease that develop after 20 years or longer of exposure 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.

  • Asymptomatic silicosis

Early cases of the disease do not present any symptoms

  • Acute silicosis

Silicosis that develops after 1 to 3 years of exposure to very high concentration of silica dust.

  • Accelerated silicosis

Silicosis that develops after an average of 10 years of exposure to high concentration of silica dust.

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 calcificationof 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 scancan also provide a mode detailed analyses of the nodules, and can reveal cavitation due to concomittant 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.
  • Antibioticsand antitubercular agents to prevent tuberculosis. These include isoniazid, rifampin, and pyrazinamide.
  • Chest physiotherapyto help the bronchial drainage of mucus.
  • Oxygenadministration to avoid hypoxemia.
  • Bronchodilatorsto facilitate breathing.

Experimental treatments include:

  • Whole-lung lavage
  • Aluminum inhalation
  • Corticosteroid

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.

See also

  • Pneumoconiosis
  • Asbestosis

External links

  • Silicosis- eMedicine
  • Silicosis- Health in Plain English (with pictures)bg:????????

de:Silikose es:Silicosis simple:Silicosis

Retrieved from "http://en.wikipedia.org/Silicosis"



This article is licensed under the GNU Free Documentation License.
It uses material from the http://en.wikipedia.org/wiki/Silicosis Wikipedia article Silicosis.

 
  All text is available under the terms of the GNU Free Documentation License