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Silicosis

Silicosis is the most common form of pneumoconiosis. It's a progressive disease characterized by nodular lesions, which frequently progress to fibrosis. It's classified according to the severity of the pulmonary disease and the rapidity of its onset and progression, although it usually occurs as a simple asymptomatic illness.

Causes

Those who work around silica dust, such as foundry workers, boiler scalers, and stone cutters, have the highest incidence of the disease. Silica in its pure form occurs in the manufacture of ceramics (flint) and building materials (sandstone). It occurs in mixed form in the production of construction materials (cement). It's also found in powder form (silica flour) in paints, porcelain, scouring soaps, and wood fillers and in the mining of gold, lead, zinc, and iron.

Sand blasters, tunnel workers, and others exposed to high concentrations of respirable silica may develop acute silicosis after 1 to 3 years. Those exposed to lower concentrations of free silica can develop accelerated silicosis, usually after about 10 years of exposure.

The prognosis is good unless the disease progresses to the complicated fibrotic brain.

Signs and Symptoms

  • chronic cough
  • shortness of breath with exercise, usually in patients who have progressive massive fibrosis

Additional symptoms that may be associated with this disease, especially in acute silicosis:

  • fever
  • cough
  • weight loss
  • severe breathing difficulty

Diagnostic tests

Chest X-rays in simple silicosis show small, discrete, nodular lesions distributed throughout both lung fields, although they typically concentrate in the upper lung zones. The lung nodes may appear enlarged and show eggshell calcification. In complicated silicosis, X-rays show one or more conglomerate masses of dense tissue.

Pulmonary function tests demonstrate reduced forced vital capacity (FVC)in complicated silicosis. If the patient has obstructive disease (emphysematous silicosis areas), forced expiratory volume in 1 second (FEV1) is reduced. A patient with complicated silicosis also has reduced FEV1 but has a normal or high ratio of FEV1 to FYC. When fibrosis destroys alveolar walls and obliterates pulmonary capillaries or when it thickens the alveolocapillary membrane, the diffusing capacity for carbon monoxide falls below normal. Both restrictive and obstructive disease reduce maximal voluntary ventilation.

Arterial blood gas analysis reveals a normal partial pressure of arterial oxygen in simple silicosis, but it may drop significantly below normal in late stages or complicated disease. The patient has normal partial pressure of arterial carbon dioxide (Paco2) in the early stages of the disease, but hyperventilation may cause it to drop below normal. If restrictive lung disease develops - particularly if the patient is hypoxic and has severe alveolar ventilatory impairment­Paco2 may increase above normal.

Treatment

The goal is to relieve respiratory symptoms, manage hypoxia and cor pulmonale, and prevent respiratorytract infections and irritations. Treatment includes careful observation for the development of tuberculosis.

Daily bronchodilation aerosols and increased fluid intake (at least 3 L [3.2 qt] daily) relieve respiratory signs and symptoms. Steam inhalation and chest physiotherapy (such as controlled coughing and segmental bronchial drainage) with chest percussion and vibration help clear secretions.

In severe cases, the patient may need oxygen by cannula, mask, or mechanical ventilation (if he can't maintain arterial oxygenation). Respiratory tract infection warrants prompt antibiotic administration.

Prevention

If you work in a high-risk occupation or have a high-risk hobby, wear dust masks and do not smoke. Other protection prescribed by OSHA, such as a respirator, may be indicated.



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