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  Table of Contents 
CASE REPORT
Year : 2021  |  Volume : 25  |  Issue : 3  |  Page : 185-187
 

Splenic silicosis: Arare cause of splenic calcifications


Department of Pulmonary Medicine, Jawaharlal Institute of Postgraduate Medical Education and Research(JIPMER), Puducherry, India

Date of Submission29-Aug-2020
Date of Acceptance23-Mar-2021
Date of Web Publication9-Oct-2021

Correspondence Address:
Dr. Dharm P Dwivedi
Department of Pulmonary Medicine, Jawaharlal Institute of Postgraduate Medical Education and Research(JIPMER), Puducherry-605006
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijoem.ijoem_340_20

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  Abstract 


Silicosis, an occupational menace is an irreversible lung disease caused by inhalation of tiny particles of crystalline silica. It is an occupational hazard both in industrialized as well as developing nations. Thoracic involvement is commonly described following exposure to silica, but extrathoracic involvement is a rare occurrence and often an incidental finding. It can manifest as calcifications in the liver, spleen, abdominal, axillary and cervical lymph nodes in addition to intrathoracic involvement. Silicosis as a cause of splenic calcifications often gets buried under the common differentials like tuberculosis, acquired immunodeficiency syndromes, amyloidosis, and Gamna-Gandy bodies. We herein describe a case of chronic complicated silicosis with splenic calcifications which appear similar to intrathoracic calcifications.


Keywords: Occupational lung disease, silica, silicosis, spleen, splenic calcification


How to cite this article:
Bai M, Dwivedi DP, Babu VM, Warrier LS, Chauhan AS. Splenic silicosis: Arare cause of splenic calcifications. Indian J Occup Environ Med 2021;25:185-7

How to cite this URL:
Bai M, Dwivedi DP, Babu VM, Warrier LS, Chauhan AS. Splenic silicosis: Arare cause of splenic calcifications. Indian J Occup Environ Med [serial online] 2021 [cited 2021 Nov 28];25:185-7. Available from: https://www.ijoem.com/text.asp?2021/25/3/185/327918





  Introduction Top


Silicosis, an extremely studied pneumoconiosis is a fibrosing disease of the lungs caused by the inhalation, retention, and pulmonary reaction to crystalline silica. Although the occurrence of calcified silicotic nodules in the lungs and eggshell calcification of hilar lymph nodes is well known, silicosis affecting extrathoracic structures is rarely seen. We herein describe a case of pulmonary silicosis with splenic involvement and briefly review the literature on splenic silicosis.


  Case Details Top


A 50-year-old man was admitted at the hospital for complaints of acute onset breathlessness associated with wheezing. He did not give a history of recurrent respiratory infections. There was no previous history of pulmonary tuberculosis and he denied prior ATT intake. He was a borewell digger by occupation for more than 20 years. He was a smoker (35 pack-years). At the time of presentation, he was dyspneic at rest with a room air saturation of 84%. Breathlessness improved with supplemental oxygen and non-invasive bi-level positive airway pressure mode of ventilation, which was commenced in view of type 2 respiratory failure.

CT thorax and abdomen showed multiple eggshell calcifications in the mediastinal and hilar lymph nodes, areas of scattered calcifications in the lung parenchyma, areas of progressive massive fibrosis in the left upper lobe, diffuse fibrobronchiectatic, emphysematous changes and irregular coarse calcifications in the spleen [Figure 1]. Routine blood investigations and complete blood count were within normal limits. Sputum for acid-fast bacilli, GeneXpert, and mycobacterial culture were negative for Mycobacterium tuberculosis (MTB). Tuberculin skin test was negative. Sputum pyogenic culture was reported as normal oropharyngeal flora. Although histopathologically not proven, the typical occupational history, clinical manifestations, CT findings support the diagnosis of pulmonary silicosis with splenic involvement.
Figure 1: Computed Tomography Images Showing(a and b) Multiple Enlarged Calcified Mediastinal and Hilar Lymph Nodes. Calcifications Are Also Seen Within Areas of Progressive Massive Fibrosis.(c) Irregular Coarse Calcified Lesion is Noted in the Mid Pole of the Spleen.(d) Fibrobronchiectatic Changes and Areas of Progressive Massive Fibrosis Are Seen in Bilateral Upper Lobes

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  Discussion Top


Silicosis is defined as a disease resulting from chronic occupational exposure to silica dust. Silica is carried by macrophages to pulmonary hilar lymph nodes and gets concentrated there. With heavy exposure, silica may pass into the bloodstream and be deposited elsewhere.[1] 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.[2]

Routes of spread

Silicosis with splenic involvement is believed to be secondary and is often regarded as 'metastatic'.[4] 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.[5] 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.

Radiological appearance

Splenic silicosis is often characterised by several small rounded calcified opacities measuring up to 2 mm, commonly described as punctuate splenic calcifications. The radiological appearance of calcifications is usually similar to those seen in the lung. In our case, the calcifications were polymorphous in shape and size. Jacobson et al.[3] in 1967 laid down the criteria for the radiological entity called eggshell calcification. They are as follows: (1) Shell-like calcifications measuring up to 2 mm in thickness must be present in the peripheral zone of at least two nodes. (2) The calcifications may be solid or broken. (3) In at least one of the lymph nodes, the ring-like shadow must be complete. (4) The central portion of the lymph node may show additional calcifications. (5) One of the affected lymph nodes must be at least 1 cm in its greatest diameter.

Role of tuberculosis

Tuberculosis (TB) has been implicated in the induction of calcification of silicotic nodules.[5] Though the role of tuberculosis is uncertain, many authors believe that in nearly 40 to 60% of the cases, the lesions are due to superadded tuberculosis infection.[1] The detection of tuberculosis is often difficult, even at autopsy, since ischemia and fibrosis prevent the formation of typical TB granulomas with areas of caseous necrosis.[1] Also, it may be unfeasible to prove an active infection even histologically unless acid-fast bacilli are detected. The culture of the lesions of massive fibrosis is the 'go-to' method to confirm or rule out active TB infection.[1] Despite the possible role of TB in the induction of calcification in silicotic nodules and lymph nodes, it is now believed that calcification can occur without a superimposed infection. Our case is unique as there is no history of tuberculosis and MTB was not isolated.


  Conclusion Top


Splenic silicosis should be considered in the differentials of splenic calcifications, especially when there is a history of occupational exposure to silica. The differential diagnosis of punctuate splenic calcifications include tuberculosis, acquired immunodeficiency syndromes, histoplasmosis, healed pneumocystis carinii infection, collagen vascular disease, amyloidosis, and Gamna-Gandy bodies.[6] 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.

Acknowledgement

We thank Dr Praveen B and Dr Sivaselvi for their exceptional service and support that enabled appropriate management of the patient.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Langlois SL, Sterrett GF, Henderson DW. Hepatosplenic silicosis. Australas Radiol 1977;21:143-9.  Back to cited text no. 1
    
2.
Slavin RE, Swedo JL, Brandes D, Gonzaales- Vitale JC, Osornio-Vargas A. Extrapulmonary silicosis. A clinical, morphologic, and ultrastructural study. Hum Pathol 1985;16:393-412.  Back to cited text no. 2
    
3.
Belt TH. Silicosis of the spleen: A study of the silicotic nodule. J Pathol Bact 1939;49:39-44.  Back to cited text no. 3
    
4.
Belt TH. Silicosis of the spleen: A study of the silicotic nodule. J Pathol Bact 1939;49:39.  Back to cited text no. 4
    
5.
Polachek AA, Pijanowski WJ. Extrathoracic egg-shell calcifications in silicosis. Am Rev Respir Dis 1960;82:714.  Back to cited text no. 5
    
6.
Vanhoenacker FM, Van den Brande P, De Schepper AM. Hepatosplenic antracosilicosis: A rare cause of splenic calcifications. Eur Radiol 2001;11:1184-6.  Back to cited text no. 6
    


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