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{{Silicosis}}
{{Silicosis}}
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{{CMG}} {{AE}} {{AV}}


==Overview==
==Overview==
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.
*Silicosis is caused by inhalation of one of the forms of crystalline silica, most commonly [[quartz]]. Silicosis is seen among [[sandblasters]], underground miners, [[foundry]] and [[quarry workers]], and in other dust-exposed trades.
 
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.
 
 
==Overview==
'''Shigellosis''' is a common [[foodborne]] or [[waterborne]] infectious illness caused by ''Shigella'' species, a [[gram-negative]], [[non-motile]], [[facultatively anaerobic]], non-[[spore]]-forming rod. ''Shigella'' was first discovered by Dr. Kiyoshi Shiga following a bacillary dysentery outbreak in Japan in 1896. It is commonly spread by the fecal-oral route in regions of poor sanitation. Although individuals of all age groups may acquire shigellosis, high risk patients include young children, elderly patients, and immunocompromised patients. Clinical manifestations typically include diffuse, colicky [[abdominal pain]], [[fever]], and mucoid/bloody [[diarrhea]] that develop as early as 12 hours to 3 days following ingestion of ''Shigella'' and typically self-resolve within 5 to 7 days of symptom onset. If left untreated, the majority of patients recover spontaneously, but intestinal and systemic complications, such as [[post-infectious arthritis]] ([[Reiter's syndrome]]) or [[hemolytic uremic syndrome]] (HUS), may develop in a few individuals. Individuals with suspected infection should undergo blood and stool work-up for appropriate diagnosis and choice of antimicrobial agents. The cornerstones of the treatment of shigellosis are fluid and salt replacement and antibiotic therapy. Antibiotic therapy is recommended among all patients and usually consists of a 3 day course of [[trimethoprim/sulfamethoxazole]] or [[ciprofloxacin]] in patients with a documented resistant strain. Although there is currently no vaccine for shigellosis, primary prevention consists of proper hand hygiene, as well as safe food and water practices.


==Historical Perspective==
==Historical Perspective==
Shigella was first discovered by Dr. Kiyoshi Shiga following a bacillary dysentery outbreak in Japan in 1896. Since then, several outbreaks have occurred.
*The term silicosis was first introduced by [[Visconti]] 1870, derived from the Latin word silex, or flint.
*[[Mining]], [[tunneling]], [[sand stone industry]], stone quarrying and [[dressing]], [[iron]] and [[steel foundries]] and [[flint crushing]] are the occupations most closely related to the hazards of silica exposure


==Pathophysiology==
==Pathophysiology==
A small inoculum of ''Shigella'' (10 to 200 organisms) is sufficient to cause shigellosis. ''Shigella'' is commonly spread by the [[fecal-oral route]] in regions of poor sanitation ([[foodborne]] or [[waterborne]] transmission). ''Shigella'' first invades the epithelial cells of the large intestine by using [[M cell]]s as entry ports for [[transcytosis]]. ''Shigella'' then invades [[macrophage]]s and induces cellular [[apoptosis]], which results in [[inflammation]], generation of [[proinflammatory cytokine]]s, and recruitment of [[polymorphonuclear neutrophil]]s (PMNs). Following transcytosis and macrophage apoptosis, ''Shigella'' avoids extracellular exposure and spreads intercellularly using [[actin polymerization]] processes (rocket propulsion). As PMNs invade the site of active inflammation, the integrity of the intestinal epithelial barrier is lost, and adsorption of fluids and nutrients is impaired, resulting in clinical manifestations of shigellosis (e.g. diarrhea). On gross pathology, [[hyperemia]] with development of [[ulcer]]s and [[edema]] are typical findings. On microscopic pathology, infiltration of PMNs and inflammatory [[pseudomembrane]]s are characteristic features.
*When small [[silica]] dust particles are inhaled, they can embed themselves deeply into the tiny [[alveolar sac|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 [[fibrosis|fibrotic nodules]] with concentric "onion-skinned" arrangement of [[collagen]] fibers, [[hyalinization|central hyalinization]], and a cellular peripheral zone, with lightly [[birefringence|birefringent particles]] seen under [[polarized light]]. In acute silicosis, microscopic pathology shows a [[Periodic acid schiff|periodic acid-Schiff positive]] alveolar exudate (alveolar [[lipoproteinosis]]) and a cellular infiltrate of the alveolar walls.


==Classification==
==Classification==
Shigella species are classified into four serogroups: ''Shigella dysenteriae'', ''Shigella flexneri'', ''Shigella boydii'', and ''Shigella sonnei''.
Silicosis is classified into five categories: ''Simple chronic'', ''Complicated chronic'', ''Interstitial Pulmonary Fibrosis'', ''Acclerated silicosis'', and ''Acute silicosis''.


==Causes==
==Causes==
Shigellosis is usually a foodborne or waterborne illness caused by an infection with ''Shigella'' species. ''Shigella'' is a [[gram-negative]], [[non-motile]], [[facultatively anaerobic]], non-[[spore]]-forming [[rod]].
*Silicosis is caused by the inhalation of [[crystalline silica]], including [[quartz]], [[cristobalite]], and [[trimidite]].
*Of all three, [[quartz]] is most abundant and is frequently associated with the development of silicosis upon prolonged exposure and/or exposure at extremely high concentrations


==Differential Diagnosis==
==Differential Diagnosis==
Shigellosis must be differentiated from other diseases that cause [[fever]], [[bloody diarrhea]], [[dehydration]], [[tachycardia]] and [[low blood pressure]], such as Enterohemorrhagic ''E.coli'' (EHEC) infection, [[Ebola]], [[Typhoid fever]], [[Malaria]], and [[Lassa fever]].
Silicosis must be differentiated from other diseases that cause [[cough]], [[dyspnea]], [[pulmonary nodules]] and [[fibrosis]] seen on [[chest x-ray]] such as [[asbestosis]], [[tuberculosis]], [[aspergillosis]] and pulmonary malignancy.


==Epidemiology and Demographics==
==Epidemiology and Demographics==
Although individuals of all age groups may acquire shigellosis, the majority of affected individuals are children between the age of 2 to 5. There is no gender or racial predominance of shigellosis. More than 160 million cases are reported annually, of which more than 95% are reported in the developing countries. Shigella sonnei accounts for the majority of shigellosis cases in the developed (industrialized) countries, while Shigella flexneri accounts for the majority of shigellosis cases in the developing countries.
*Protective measures such as [[respirators]] have brought a steady decline in death rates due to silicosis in Western countries. Unfortunately, this is not true of less developed countries where work conditions are poor and [[respiratory equipment]] is seldom used.


==Risk Factors==
==Risk Factors==
All individuals are at risk of developing shigellosis. Individuals at high risk of developing shigellosis or complications of shigellosis are young children between the age of 2 to 5, elderly individuals, and individuals who engage in anal sexual intercourse, HIV-positive individuals, and travelers to developing countries in regions of poor sanitation.
*All the occupations dealing with the siliceous rock are at risk for silicosis. Occupations include, excavations in mines, tunnels, quarries, underground galleries, dry cutting, grinding, sieving and manipulation of minerals and [[rock]], manufacturing of [[silicon carbide]], [[glass]], [[porcelain]], [[earthenware]] and other ceramic products, manufacturing and maintenance of abrasives and detergent powders, [[foundry work]], [[milling work]], [[sandblasting]] and [[grinding]], [[pottery]] [[industry]], handling quartz conglomerates and ornamental stone, [[dental prostheses]].


==Natural History, Complications and Prognosis==
==Natural History, Complications and Prognosis==
Clinical manifestations of shigellosis typically develop 12 hours to 3 days following ingestion of ''Shigella''. Patients often first develop colicky, diffuse [[abdominal pain]] and [[fever]], followed by [[diarrhea]] and [[tenesmus]]. If left untreated, shigellosis typically self-resolves within 5 to 7 days of onset of clinical manifestations in the majority of patients. High risk patient populations (young children, elderly, or immunocompromised patients) are at increased risk of developing complications, which may be intestinal or extra-intestinal. Classical complications include [[post-infectious arthritis]] ([[Reiter's syndrome]]) and [[hemolytic uremic syndrome]] (HUS). Prognosis is generally excellent for immunocompetent individuals. Factors that are associated with poorer prognosis include prolonged duration of disease, development of complications, and infection of high risk patients.
*Silicosis develops very slowly in most cases. Often decades elapse in progression to clinical disease from the beginning. Usually starts as simple silicosis and progress further after not less than 10 years of exposure to silica. Accelerated silicosis is a variant of silicosis occurred due to intense exposure to silica for 5-10years. All forms of silicosis can progress in the absence of continued exposure.  
*[[Tuberculosis]], [[mycosis]] , [[pneumothorax]] are some of the complications of silicosis.


==Diagnosis==
==Diagnosis==
===History and Symptoms===
===History and Symptoms===
Symptoms may range from mild abdominal discomfort to severe colicky, diffuse [[abdominal pain]]. Patients may initially have small volume watery [[diarrhea]] that precedes [[dysentery]]. The majority of patients report [[mucoid diarrhea]], and up to 50% of patients report [[bloody diarrhea]]. Other common symptoms include [[fever]], [[nausea]] and [[vomiting]], and [[tenesmus]].
*Symptoms include [[dyspnea]], [[cough]], [[fatigue]] or [[tiredness]], [[loss of appetite]], [[chest pain]] and[[fever]]
*In advanced cases, [[cyanosis]], [[cor pulmonale]] and [[respiratory insufficiency]] can occur


===Physical Examination===
===Physical Examination===
Patients with shigellosis usually appear lethargic. Physical examination of patients with shigellosis is usually remarkable for diffuse [[abdominal tenderness]] in more than 70% of cases and [[fever]] in approximately 25% to 40% of cases. Less commonly, physical examination is remarkable for signs of [[dehydration]], such as [[hypotension]], [[tachycardia]], and dry mucous membranes.
*Physical examination of the chest in silicosis is often unremarkable, although a variety of [[abnormal breath sounds]], including [[crackles]], [[rhonchi]], or [[wheezes]], occur as the disease progress.


===Laboratory Findings===
===Laboratory Findings===
The majority of patients with shigellosis have no significant derangements in either blood or stool work-up. Common findings include [[leukocytosis]] with [[left shift]] on blood examination, and blood and/or mucus in stools on stool examination. Multiple blood and stool cultures are needed to rule out [[bacteremia]] and to obtain [[antibiotic susceptibility]] testing, but the majority of cases yield negative cultures. Hematology, renal, and liver function testing may be required in some cases to rule out the development of any complications associated with shigellosis, such as severe [[dehydration]], [[cholestatic liver disease]], or [[hemolytic uremic syndrome]] (HUS).
*There are no specific laboratory tests for the diagnosis of silicosis, except a careful occupational history.  
*A [[complete blood count]] with differential, [[GM-CSF|granulocyte macrophage-colony stimulating factor]] (GM-CSF) antibodies, [[Blood culture|blood]] and [[sputum cultures]] and [[BNP|natriuretic peptide]], are helpful in excluding other causes.
*Assessment of [[oxygenation]] is important, either with [[Pulse oximetry|pulse oxygen saturation]] or [[arterial blood gas]], to determine the severity of respiratory impairment and whether the patient will be able to tolerate diagnostic procedures.


===Other Diagnostic Studies===
===Other Diagnostic Studies===
Other diagnostic studies, such as [[enzyme-linked immunoassay]] (ELISA), [[polymerase chain reaction]] (PCR), or colon/rectal biopsies, are not always necessary but may be required for the diagnosis of shigellosis in the minority of patients, such as high risk patients who are hospitalized and in need of urgent management).
*Other diagnostic studies, such as [[Pulmonary function tests]], [[spirometry]], [[bronchoscopy]] and [[lung biopsy]], are not always necessary but may be required for the diagnosis of silicosis in the minority of patients, with no significant history of exposure and to differntiate silicosis from other diseases.


==Treatment==
==Treatment==
===Medical Therapy===
===Medical Therapy===
The cornerstones of the treatment of [[Shigellosis]] are fluid and [[salt]] replacement and [[antibiotic]] therapy. For the majority of patients, oral fluid replacement is adequate and should consist of [[water]], [[glucose]], and [[electrolytes]] such as [[sodium]], [[chloride]], [[potassium]] and [[bicarbonate]]. IV fluids should be reserved for patients with severe disease who cannot tolerate oral therapy, and should be tailored to their lab findings. Antimotility agents should be avoided as they prolong the duration of the infection. Antibiotic therapy is recommended among all patients and usually consists of a 3 day course of either [[trimethoprim/sulfamethoxazole]] or [[ciprofloxacin]] in patients with a documented resistant strain.
*Generally, management of silicosis aims to manage other respiratory comorbidities (e.g. [[COPD]] or [[tuberculosis]]) and to treat silicosis-associated complications
*Supportive therapy include [[smoking cessation]], [[oxygen|supplemental oxygen]] is administered to prevent complications of chronic [[hypoxemia]] and treatment with [[bronchodilators]] to facilitate breathing if airflow limitation is present on [[spirometry]].


===Primary Prevention===
===Primary Prevention===
There is no vaccine to prevent shigellosis. Primary prevention consists of proper hand hygiene, as well as safe food and water practices. Special care should be taken when handling diapers as they may be an important source for the spread of ''Shigella''.
*Prevention of silicosis is by identification of work-place activities with high concentrations of [[silica|crystalline silica]] dust and elimination or control of the exposure. Early intervention with the control or cessation of adverse exposures may result in reversal of symptoms and airflow limitation.
 


==References==
==References==

Latest revision as of 13:32, 24 June 2015

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aparna Vuppala, M.B.B.S. [2]

Overview

  • Silicosis is caused by inhalation of one of the forms of crystalline silica, most commonly quartz. Silicosis is seen among sandblasters, underground miners, foundry and quarry workers, and in other dust-exposed trades.

Historical Perspective

Pathophysiology

Classification

Silicosis is classified into five categories: Simple chronic, Complicated chronic, Interstitial Pulmonary Fibrosis, Acclerated silicosis, and Acute silicosis.

Causes

  • Silicosis is caused by the inhalation of crystalline silica, including quartz, cristobalite, and trimidite.
  • Of all three, quartz is most abundant and is frequently associated with the development of silicosis upon prolonged exposure and/or exposure at extremely high concentrations

Differential Diagnosis

Silicosis must be differentiated from other diseases that cause cough, dyspnea, pulmonary nodules and fibrosis seen on chest x-ray such as asbestosis, tuberculosis, aspergillosis and pulmonary malignancy.

Epidemiology and Demographics

  • Protective measures such as respirators have brought a steady decline in death rates due to silicosis in Western countries. Unfortunately, this is not true of less developed countries where work conditions are poor and respiratory equipment is seldom used.

Risk Factors

Natural History, Complications and Prognosis

  • Silicosis develops very slowly in most cases. Often decades elapse in progression to clinical disease from the beginning. Usually starts as simple silicosis and progress further after not less than 10 years of exposure to silica. Accelerated silicosis is a variant of silicosis occurred due to intense exposure to silica for 5-10years. All forms of silicosis can progress in the absence of continued exposure.
  • Tuberculosis, mycosis , pneumothorax are some of the complications of silicosis.

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Other Diagnostic Studies

  • Other diagnostic studies, such as Pulmonary function tests, spirometry, bronchoscopy and lung biopsy, are not always necessary but may be required for the diagnosis of silicosis in the minority of patients, with no significant history of exposure and to differntiate silicosis from other diseases.

Treatment

Medical Therapy

Primary Prevention

  • Prevention of silicosis is by identification of work-place activities with high concentrations of crystalline silica dust and elimination or control of the exposure. Early intervention with the control or cessation of adverse exposures may result in reversal of symptoms and airflow limitation.

References

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