Presentation
Persistent dyspnea for the last three years. Orthopnoiec dyspnea, increasing fatigue, and subfebrile fever for a week. In the anamnesis – working on a foundry factory for more than 40 years. Non-smoker.
Patient Data
CT was done a year ago outside our hospital.
There is a soft tissue mass with some gas foci in its structure in the right hilar region, predominantly located in S1-3,6. It has slightly irregular margins, compresses the right main bronchus, totally obturates B1, and almost obturates BB2-3.
There are multiple nodules bilaterally, predominantly in the central regions. The nodules preferentially have centrilobular distribution, but subpleural nodules can also be seen. Their sporadic calcification can be seen.
Moderate centrilobular emphysema with upper-lobe predominance and several foci of paraseptal emphysema, mainly in S8-10 of the left lung, can be seen.
Pleura is mildly thickened with upper predominance with small foci of calcium on the left.
There is a significant mediastinal lymphadenopathy with prominent amorphous calcifications in the lower and upper paratracheal, subcarinal, and left and right hilar lymph nodes.
These findings may correspond with chronic nodular silicosis associated with pulmonary tuberculosis or lung cancer.
The patient denied from the biopsy, and pulmonary tuberculosis was excluded.
CT was done at the admission to our hospital. CT was done without breath synchronization due to the incapability of the patient.
There is a decrease in the size of the right lung with a mediastinal shift to the right.
Previously detected soft tissue mass has significantly enlarged, developed a cavity with irregular inner margins and air-fluid level. There are several tiny calcifications in its structure.
There is an increased compression of the right main bronchus and all other bronchial branches. Lumens of aerated bronchi are widened and deformed.
There is also a focus of subpleural consolidation in S8-10 of the right lung with air bronchogram in its structure.
Inhomogeneous increase of the left lung attenuation can be seen with mild thickening of the interlobular interstitium. Multiple nodules with central zone predominance are preserved unchanged.
Mild pleural effusion on the left can be seen. Pleural bilateral thickening, mediastinal lymphadenopathy with prominent calcifications is preserved without changes.
The findings may correspond with chronic silicosis complicated by lung cancer development.
Case Discussion
The patient died of multiorgan failure in the intensive care unit a few days after CT.
On the autopsy diagnosis of silicosis was confirmed. The histologic investigation of the mass revealed non-keratinized squamous cell carcinoma G2 with necrotic foci and neutrophil infiltration. Mediastinal lymph nodes were invaded by tumor cells. No metastases into the left lung or distant metastases were found.
Silicosis is an occupational pulmonary interstitial disease caused by the continual inhalation of crystalline silica (SiO2) 1. Briefly speaking, a central point in the pathogenesis is an excess local inflammatory response to inhalation of small silica particles. Three different mechanisms can provoke this exuberant inflammation. Firstly, the inability of alveolar macrophages to eliminate ingested silica particles leads to cell death and further aggravation of the inflammatory process. Secondly, in a more acute condition, silica exposure induces type II pneumocyte hyperplasia and secretion of proteinaceous material and surfactant into alveoli, which also leads to local inflammation. Finally, silica particles provoke inadequate inflammatory response by themselves because they contribute synthesis of oxygen-free radicals 2,3.
Inflammation is considered as a significant mechanism of carcinogenicity in silicosis 4,5. The IARC (International Agency of Research on Cancer) included silica exposure in a group of factors that are definitely carcinogenic to humans 6. The association between silicosis and lung cancer was also verified in other studies 4.
In this patient, silicosis manifested in the form of simple silicotic nodules (macrophages’ aggregates circled by collagen 7) with perilymphatic distribution. Taking into account other typical for silicosis radiological findings 8,9 (bronchial wall thickening, pleural thickening, presence of emphysema, and lymph nodes calcification), the diagnosis can be easily suggested. The mass in the right lung obviously did not look like a nodular conglomerate, so a differentiation between pulmonary tuberculosis and lung tumor was reasonable.
In this case, silicosis did not evolve into progressive massive fibrosis, developing a lung tumor instead. Chronisation features and differences are not fully understood and are probably connected with individual variations in immune responses 2,3,7.