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Unnithan and Roy: Superior vena cava obstruction in a 65-year-old man

Introduction

Superior vena cava obstruction (SVCO) is characterized by an array of symptoms due to impairment of blood flow through the superior vena cava (SVC) into the right atrium, and the causes may be intrinsic or extrinsic. Symptoms that prompt suspicion of this syndrome include dyspnoea, coughing, and swelling of the face, neck, upper trunk and extremities.1 In rare cases, patients may complain of hoarseness, chest pain, dysphagia and haemoptysis. Physical signs that may be noted on presentation are neck and thoracic vein distension, oedema of the face or upper extremities, plethora and tachypnoea. Rare symptoms include cyanosis, Horner’s syndrome and paralysed vocal cords.2

Case report

A 65-year-old man presented with facial swelling and hoarseness of 15 days’ duration, as well as a cough with whitish scanty frothy expectoration along with low-grade intermittent fever for a period of 8 months. There was no history of chest pain, no obvious shortness of breath or pedal swelling and he had no history of abdominal distension or icterus.

He was not an alcoholic but had been a heavy smoker for the last 30 years (60 pack-years) and had been addicted to opium for the last 20 years. He had not attended any health care facility in the last 8 months and this article reports the presentation of the patient for the first time after he developed facial swelling.

On examination, the patient was conscious, alert and co-operative, but his face was puffy and he was experiencing congestion. There was no cyanosis, pallor, clubbing or oedema; however, his jugular venous pressure was raised and the external neck veins were dilated and non-pulsatile (Figure 1). Lymph nodes were not palpable but the upper chest wall showed dilated veins that were also present in the upper abdominal wall and the veins were filling downwards (Figure 2).

FIGURE 1

Dilated non-pulsatile neck veins.

7-2-10-fig1.jpg
FIGURE 2

Dilated veins on chest and abdominal wall.

7-2-10-fig2.jpg

The patient’s routine blood and urine investigations were normal. Sputum was negative for acid-fast bacilli (AFB) and chest radiography showed right upper zone fibrosis with mediastinal widening (Figure 3). Contrast-enhanced high-resolution computed tomography (CT) of the thorax showed an enlarged mediastinal lymph node with ring enhancement [lower paratracheal, right paratracheal station number 4 (4R)] (Figure 4).

FIGURE 3

Right upper zone fibrosis with mediastinal widening.

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FIGURE 4

Contrast-enhanced high-resolution CT of the thorax: enlarged mediastinal lymph node with ring enhancement (lower paratracheal, 4R).

7-2-10-fig4.jpg

Fibre-optic bronchoscopy showed that the patient had normal vocal cords and no endobronchial growth, but there were frothy secretions coming from the right upper lobe bronchus and bulging was seen in the right lower paratracheal region.

Transbronchial needle aspirate was taken from paratracheal R4, where bulging was seen, and this revealed the presence of AFB. Bronchial aspirate was taken from the right upper lobe bronchus but it showed no evidence of AFB or any other micro-organism or of malignant cells. Testing the transbronchial needle aspirate after 6 weeks for tuberculosis (TB) using Battle Area Clearance, Training, Equipment and Consultancy (BACTEC™) showed growth of mycobacteria but the results of bronchial lavage showed no growth.

Meanwhile, the patient was prescribed daily rifampicin, isoniazide, ethambutol and pyrazinamide (Zinamide®, Genus). He was also given 100 mg intravenous hydrocortisone three times a day for 3 days until his acute condition improved, followed by 16 mg oral methylprednisolone (Solu-Medrone, Pfizer) that was gradually tapered off over 4 weeks.

The patient was discharged after 6 weeks with definite symptomatic and clinical improvement. A 3-month follow-up for the antitubercular treatment was satisfactory and repeat CT showed that the lymphadenopathy had resolved.

Discussion

Superior vena cava syndrome is usually associated with malignancy in the form of bronchogenic carcinoma, which is the most common cause, followed by thymoma, lymphoma and germ cell tumours, among other causes. Currently, an associated malignancy is the cause of SVC syndrome in more than 90% of patients.2,3 This contrasts with studies in the early 1950s in which a large proportion of cases were non-malignant.4 Infectious causes (e.g. syphilis, tuberculosis) have decreased because of improvements in antibiotic therapy; however, in developing countries, non-malignant infectious causes continue to account for a significant proportion of cases of SVC syndrome.3

Interestingly, thrombosis from central venous instrumentation (catheter, pacemaker, guidewire) is a recognized complication of central venous access, but these procedures are quite commonly carried out, especially for haemodialysis or cardiac catheterization and, therefore, this is increasingly becoming a common non-malignant cause of SVC syndrome.5

In 1996, a case of SVCO due to tubercular mediastinal abscess was reported from the All India Institute of Medical Sciences, New Delhi.6 The authors reported that, up to that point, only two cases had been reported from India – one due to pulmonary TB and the other due to mediastinal lymphadenopathy.7 Mediastinal lymphadenitis with or without concomitant pulmonary TB is a relatively better known cause of benign SVCO, as is evident from a few case reports. One case of suppurative mediastinal lymphadenitis was reported from the Mayo Clinic, MN, USA, in 1998,8 and a case of tubercular lymphadenitis invading the SVC was reported in 2008.9 An interesting case was reported in 2000 in a patient with type 1 human immunodeficiency virus (HIV) with pulmonary TB who developed a paradoxical reaction to anti-TB treatment that resulted in SVCO due to inflammatory mediastinal lymphadenitis.10

This unusual case of TB mediastinal lymphadenopathy highlights the fact that TB must be kept in mind as a differential diagnosis in patients presenting with acute-onset SVCO, especially in developing countries in the setting of TB endemics with or without a high prevalence of HIV. A timely diagnosis, high index of suspicion and appropriate treatment lead to immediate relief of the vascular obstruction and often a complete cure.

References

1. 

Parker R, Thomas C, Bennett L. Emergencies in Respiratory Medicine. Oxford: Oxford University Press; 2007. http://dx.doi.org/10.1093/med/9780199202447.001.0001

2. 

Beeson MS. Superior Vena Cava Syndrome in Emergency Medicine. URL: Emedicine.medscape.com/article/760301-overview (accessed 12 November 2012).

3. 

Wilson LD, Detterbeck FC, Yahalom J. Superior vena cava syndrome with malignant causes. N Engl J Med 2007; 356:1862–9. http://dx.doi.org/10.1056/NEJMcp067190

4. 

Schechter MM. The superior vena cava syndrome. Am J Med Sci 1954; 227:46–56. http://dx.doi.org/10.1097/00000441-195401000-00007

5. 

Gopaluni S, Warwicker P. Superior vena cava obstruction presenting with epistaxis, haemoptysis and gastro-intestinal haemorrhage in two men receiving haemodialysis with central venous catheters: two case reports. J Med Case Rep 2009; 3:6180. http://dx.doi.org/10.1186/1752-1947-3-6180

6. 

Kumar A, Khilnani GC, Kumar S, Sharma SK. Acute superior vena cava obstruction due to tubercular mediastinal abscess. Indian J Chest Dis Allied Sci 2007; 49:165–7.

7. 

Bandopadhyay SK, Sarkar N, Ghosh S, Dasgupta S. Tubercular mediastinal lymphadenopathy presenting as superior vena cava syndrome. J Assoc Phys India 2002; 50:1194–5.

8. 

Roy D, Thompson KC, Price JP. Benign superior vena cava syndrome due to suppurative mediastinal lymphadenitis: anterior mediastinoscopic management. Mayo Clin Proc 1998; 73:1185–7. http://dx.doi.org/10.4065/73.12.1185

9. 

Lee N, Lui G, Wong KT, Lam R, Cockram CS. Reversible superior vena cava obstruction caused by tuberculous lymphadenitis. Q J Med 2008; 101:987. http://dx.doi.org/10.1093/qjmed/hcn105

10. 

Mínguez C, Roca B, González-Miño C, Simón E. Superior vena cava syndrome during the treatment of pulmonary tuberculosis in an HIV-1 infected patient. J Infect 2000; 40:187–9. http://dx.doi.org/10.1016/S0163-4453(00)80015-8





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