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CHEST RADIOLOGY Table of Contents   
Year : 2002  |  Volume : 12  |  Issue : 3  |  Page : 341-342
Calcified superior vena cava thombosis; An unusual cause of mediastinal calcification


Dept of Radiology & Nephrology, CMC, Vellore, India

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Keywords: SVC thrombosis, calcification, CT

How to cite this article:
Shyamkumar N K, John B, John G T, Cherian R, Thomas P P, Korah I P. Calcified superior vena cava thombosis; An unusual cause of mediastinal calcification. Indian J Radiol Imaging 2002;12:341-2

How to cite this URL:
Shyamkumar N K, John B, John G T, Cherian R, Thomas P P, Korah I P. Calcified superior vena cava thombosis; An unusual cause of mediastinal calcification. Indian J Radiol Imaging [serial online] 2002 [cited 2020 Aug 8];12:341-2. Available from: http://www.ijri.org/text.asp?2002/12/3/341/30506

   Introduction Top


Superior vena cava (SVC) thrombosis is known to occur secondary to many conditions such as malignancy, catheterization, granulomatous disease, retrosternal goiter and aortic aneurysm [1]. Spontaneous SVC thrombosis is also known to occur [2]. The clinical manifestations are swelling of the upper limbs and face [3] Radiological assessment includes plain radiography, CT, transesophageal ultrasound, MRI, angiograms and isotope scan.

We report a case of calcified SVC thrombosis in a child with chronic renal failure on haemodialysis. The clinical and radiological presentations were unusual for SVC thrombosis


   Case Report Top


An 11 year old boy with nephrotic syndrome secondary to focal and segmental glomerulosclerosis presented with severe chronic renal failure. Haemodialysis was started, the vascular access being a double lumen catheter inserted into the right internal jugular vein.

The chest radiograph obtained at presentation was normal. The frontal chest radiograph taken 2 years later showed a well-defined calcified lesion, measuring 7 x 1.5cms in the right side of the mediastinum. There was no mediastinal widening. The lateral radiograph showed the lesion to be lying in the middle mediastinum. On both views, the calcification was vertically oriented, with its lower end overlapping the right atrial shadow. This finding had developed since the film taken 20 months before, at the time of admission.

Computed tomography was performed and showed this well defined lesion to be intraluminal ie in the SVC and right atrium, with partial obliteration of the SVC. The density measured more than 800HU. Collateral formation was not seen. Treatment was not considered necessary in view of the absence of symptoms.

The patient received a renal transplant. Within 5 months, the graft failed due to recurrence of focal and segmental sclerosis. Hemodialysis was restarted with access through the femoral vein and subsequently switched to continuous ambulatory peritoneal dialysis.


   Discussion Top


The usual clinical features of SVC thrombosis are upper limb edema and prominent dilated superficial veins [3]. Asymptomatic cases have also been reported [4]. It is thought that partial obstruction of SVC occurring slowly may allow collateral circulation to develop, preventing the development of clinical features of SVC obstruction [1]. In the case we report, the patient did not have any clinical features of SVC thrombosis or CT evidence of collaterals.

Brown et al observed features of SVC thrombosis in 9 patients among 783 cases who underwent Hickman catheter insertion [3]. It has been noted that implantation of subcutaneously tunneled central venous catheter for hemodilaysis is associated with risk of thrombosis [5]. SVC thrombosis is known to occur in patients with renal failure. Nephrotic syndrome being a hypercoagulable state, may be complication by venous thrombosis [2]. Our patient had two predisposing factors for the development of thrombosis, i.e. catheter insertion and nephrotic syndrome.

The commonest plain radiographic sign of SVC thrombosis is mediastinal widening. Another radiographic sign described is displacement of jugular catheter by the thrombus[3]. In this case, mediastinal calcification was seen which has been described before as a plain radiographic sign of SVC thrombosis. Mediastinal widening was absent.

Thrombosis may evolve as propagation, embolisation and removal by fibrinolytic activity or organization with recanalization [6]. Dystrophic calcification may take place in long standing dead and dying tissue [7].

n conclusion, the patient did not have any clinical or the usual radiological features of SVC thrombosis or obstruction. Though it is known that long standing venous thrombi can undergo dystrophic calcification, calcified SVC thrombus on a plain radiograph has not been previously reported.

 
   References Top

1.Yedlicka JW, Schwltz K, MoncadaR, Flisak M.CT finindings in SVC obstruction. Seminars in Roentgenology 1989;24(2) 84-90.   Back to cited text no. 1    
2.Hanna J Truemper E, Bastib E,SVC thrombosis and chylothorax: relationship in Paediatric nephritic syndrome. Paediatr-Nephrol 1997;1(1)20-2.   Back to cited text no. 2    
3.Brown G, Husband JE. Mediastinal Widening A valuable Radiographic sign of superior vena cava thrombosis. Clinical Radiology 1993 1993;47:45-420.   Back to cited text no. 3    
4.Wanscher M, Frifelt JJ, Smith-Sivertsen C anderson APD, Rasmusen AD, Garcia RS, Kohler F. Thrombosis caused by poly urethane double-lumen subclavian SVC catheter and haemodialysis. Crit.Care Med.1988;16:624-628.   Back to cited text no. 4    
5.Banalagay E, Perlmutter J, Palevsley P. Central venous hemodialusis catheter related SVC syndrome. Clin. Nephrol. 1993; 40:59-60.   Back to cited text no. 5    
6.Robbins SL, Kumar V fluid and hemodynamic derangements. In: Robins SL, Kumar V, eds. Basic Patholgoy 4th edition Philadephia W B Saunders 1987;3-27.   Back to cited text no. 6    
7.Ramzi S C. Cell injury and adaptation. In: Robins SL, Kumar V, eds. Basic pathology 4th edition Philadelphia W B Saunders 1987;3-27  Back to cited text no. 7    

Top
Correspondence Address:
N K Shyamkumar
Dept of Radiology & Nephrology, CMC, Vellore
India
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Source of Support: None, Conflict of Interest: None


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[Figure - 1], [Figure - 2], [Figure - 3]



 

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    Introduction
    Case Report
    Discussion
    References
    Article Figures

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