Berylliosis - a type of pneumoconiosis - is a systemic granulomatous disease that mainly affects the lungs. It occurs in two forms: acute nonspecific pneumonitis and chronic noncaseating granulomatous disease with interstitial fibrosis, which may cause death from respiratory failure and cor pulmonale. In about 10% of patients with acute berylliosis, chronic disease develops 10 to 15 years after exposure.
Most patients with chronic interstitial disease have only slight to moderate disability from impaired lung function and other symptoms. With each acute exacerbation, though, the prognosis worsens.
This occupational disease can affect workers in beryllium alloy, ceramics, foundry, grinder, cathode ray tube, gas mantle, missile, and nuclear reactor industries. It's associated with the milling and use of beryllium but not with beryl are mining.
Berylliosis - also known as beryllium poisoning or beryllium disease - may also affect beryllium workers' families (from beryllium dust shaken off clothing) and others who live near beryllium alloy sites.
CausesInhaling beryllium dust, fumes, and mists causes berylliosis; the pattern of disease depends on the amount inhaled. Beryllium may also be absorbed through the skin. How the element exerts its toxic effect isn't known.
Signs and Symptoms
Symptoms of acute berylliosis come on suddenly and rapidly. The main symptoms are due to severe lung inflammation. These symptoms include:
Symptoms of chronic berylliosis develop slowly. Sometimes, symptoms may not appear until many years after exposure to beryllium. Chronic berylliosis produces two main pathologic changes:
In severe cases, berylliosis may lead to heart failure.
Chest X-rays in acute berylliosis suggest pulmonary edema, demonstrating an acute miliary process or a patchy acinous filling and diffuse infiltrates with prominent peribronchial markings. Findings in chronic berylliosis include reticulonodular infiltrates, hilar adenopathy, and large coalescent infiltrates in both lungs.
Pulmonary function studies demonstrate decreased vital capacity, forced vital capacity, residual volume to total lung capacity ratio, diffusing capacity for carbon monoxide, and compliance. These decreased values occur as fibrosis stiffens the lungs.
Arterial blood gas analysis indicates diminished partial pressure of arterial oxygen (Pao2) and partial pressure of arterial carbon dioxide.
In vitro lymphocyte transformation test, if positive, confirms the diagnosis. The test is also used to monitor workers' occupational exposure to beryllium.
Beryllium patch test, if positive, establishes a patient's hypersensitivity to beryllium but doesn't confirm the disease.
Tissue biopsy and spectrographic analysis, if positive, support but don't confirm the diagnosis.
Urinalysis may identify beryllium excreted in urine, indicating exposure to the metal. Differential diagnosis must rule out sarcoidosis and granulomatous in fections.
A beryllium ulcer requires excision or curettage. Acute berylliosis requires prompt corticosteroid therapy. If the patient has hypoxia, he may need oxygen delivered by nasal cannula or mask (usually 1 to 2 L/minute). If he has severe respiratory failure, he may need mechanical ventilation if the Pao2 falls below 40 mm Hg.
The patient with chronic berylliosis usually receives corticosteroid therapy to attempt to alter the disease's progression; maintenance therapy may be lifelong.
Respiratory symptoms may respond to bronchodilators, increased fluid intake (at least 3 L [3.2 qt] daily), and chest physiotherapy. Diuretic agents, digitalis preparations, and sodium restriction may help the patient with cor pulmonale.
Avoiding or limiting exposure to beryllium is the best way to prevent berylliosis. To do so, do the following:
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