Published online 2021 Oct 9

Silicosis, an occupational menace is an irreversible lung disease caused by inhalation of tiny particles of crystalline silica.

With heavy exposure, silica may pass into the bloodstream and be deposited elsewhere. Extrathoracic silicosis is less documented in the literature and is always associated with pulmonary silicosis. These calcifications can be seen in splenic hilum, liver, lymph node and paravertebral regions.

Silicosis with splenic involvement is believed to be secondary and is often regarded as ‘metastatic’. Both hematogenous and retrograde lymphatic spread is possible.

Hematogenous spread occurs as a result of direct spread from bloodborne embolic lesions following the rupture of dust-laden hilar node into a pulmonary vein.

Lymphatic spread maybe anterograde or retrograde. Three mechanisms have been described. Firstly, silica may enter pulmonary lymphatics, that drain into the thoracic duct and then to the bloodstream.

Secondly, it may drain from the diaphragmatic surfaces of the inferior lobes through vessels situated in the ligamentum pulmonale into abdominal pre-aortic nodes.

Finally, retrograde lymph flow from posterior mediastinal nodes into peripancreatic nodes, and the spleen has been implied.

Splenic silicosis should be considered in the differentials of splenic calcifications, especially when there is a history of occupational exposure to silica.  The typical calcification can be found in the liver, spleen, abdominal, axillary, and cervical lymph nodes of silicotic patients, and is always accompanied by similar intrathoracic nodal calcification.