Discussion
Silicosis is a fibro nodular lung disease caused by inhalation of dust containing crystalline silica (alpha-quartz or silicon dioxide), which is distributed widely, or its polymorphs (tridymite or
cristobalite), which are distributes less widely. Silicosis has been a human scourge since antiquity. In 1705, Ramazzini cited Diembrock´s description of the lungs of stonecutters “in
whom he found heaps of sand that in running the knife through the pulmonary vesicles he thought he was cutting through some sandy body. In 1870, Visconti introduced the term silicosis, derived from
the Latin silex, or flint. It has been known by many other names, such as miner`s phthisis, stonecutter`s disease, potter`s asthma, and grinder`s rot. The principal sources of industrial exposure to
silica are free silica in mining, quarrying, and tunnelling, stonecutting, polishing, and cleaning monumental masonry, sandblasting, and glass manufacturing, and in foundry work, pottery, and
porcelain manufacturing, brick lining, boiler scaling, and vitrous enamelling. Patients with chronic disease may be asymptomatic with an abnormal chest radiograph or have dyspnoea. In some cases, the
onset of dyspnoea means a complication, such as progressive massive fibrosis, tuberculosis, or airway disease. Cough may accompany the disease or mean chronic bronchitis, tuberculosis, or lung
cancer. In chronic silicosis, lung function may be normal, or there may be an obstructive, restrictive, or a mixed obstructive/restrictive pattern. Impairment of function is faster in accelerated
disease. In acute disease, impairment of gas exchange is a prominent feature. The characteristic radiologic abnormality seen in patients with silicosis consists of small, well-circumscribed nodules
that are usually 2-5mm in diameter but range from 1 to 10mm, mainly involving the upper and posterior lung zones. The appearance of large opacities or hyperattenuating areas over 1cm in diameter
(progressive massive fibrosis) indicates the presence of complicated silicosis. These masses tend to develop in the midzone or periphery of the upper lung and migrate toward the hila, leaving over
inflated emphysematous spaces between the conglomerate mass and the pleura. They are often bilateral, symmetric, can demonstrate calcification, and, more rarely, cavitation. The borders of these
masses tend to be more irregular than truly ill-defined. The irregularities are the result of strand of fibrotic reaction around the conglomerate masses. The opacities tend to be homogeneous since
they represent large masses of fibrotic reaction. A heterogeneous appearance should be the result of no normal intervening alveoli, and there is no evidence of air bronchogram effects. Comparison
with old films is essential to eliminate the possibility of a new superimposed process. Egg-shell calcifications in hilar and mediastinal lymph nodes are occasionally seen. CT features are similar to
those seen on standard radiographs, but coalescence of nodules and the development of conglomerate masses can often be detected at an earlier stage. Conglomerate masses of complicated silicosis can
be associated with disruption of normal vessels and bulla formation. CT is also better at revealing gross disruption of pulmonary parenchyma in the upper lung zones in complicated disease.