Clinical History
A 55 year old male patient was evaluated at our department for a painless neck swelling. The patient underwent neck ultrasound, chest X-Ray and CT examination.
Imaging Findings
A 55 year old male patient was evaluated at our department for a painless neck swelling. The patient also described backache under analgesic treatment for several months.
Ultrasound neck examination revealed at supine position echogenic material within the right internal jugular vein. The shape of the echogenic material changed according to transducer pressure intensity (Fig. 1a-c), the controlateral internal jugular vein was normal (Fig. 2). At erect position (Fig. 3). The echogenic material was completely dissolved. At supine position (Fig. 4) after several minutes the echogenic material was seen again. The findings were indicative of slow flow within the internal jugular vein due to external compression or internal stenosis.
A chest radiography was ordered in order to exclude an external compression. Indeed the chest radiography was performed and an upper lobe mass was demonstrated (Fig. 3). A CT examination was also performed for lung cancer staging (Fig. 4) and showed a multilobular upper lobe mass extended and infiltrate the adjacent rib and vertebra.
Discussion
The superior vena cava syndrome (SVCS) is characterised by gradual compression or obstruction of the superior vena cava.
Its presentation is often associated with a gradual increase in the symptoms and can be life threatening. Early in the clinical course of (SVCS) few, if any, signs or symptoms may be observed. Typically, symptoms accelerate as the underlying malignancy increases in size and/or invasiveness. Dyspnoea is the most common symptom, followed by trunk or extremity swelling. Other symptoms include facial swelling, cough, orthopnoea, headache, nasal stuffiness, and light-headedness. None of these symptoms were present in our case.
Physical examination often reveals facial or upper extremity oedema. The degree of facial oedema has been described as facial engorgement. The degree of jugular venous distention varies. Other markers of lung malignancy, such as Horner syndrome, paralysis of the vocal cords, and paralysis of the phrenic nerve, are rarely present. None of these symptoms were present in our case.
Extrinsic compression of the superior vena cava is possible because it has a thin wall with a low intravascular pressure. It is relatively easy to compress. The low intravascular pressure also allows for the possibility of thrombus formation. The subsequent obstruction to flow causes an increased venous pressure, which results in interstitial oedema and retrograde collateral flow.
Superior vena cava syndrome is chiefly associated with malignancy. Currently, more than 90% of patients with superior vena cava syndrome have an associated malignancy as the cause. In the early 1950s a large proportion of cases were non-malignant. Of the non-malignant causes of superior vena cava syndrome, thrombosis from central venous instrumentation (catheter, pacemaker, guidewire) is an increasingly common event, especially as these procedures become more common.
In our case the superior vena cava syndrome (SVCS) produced by external compression of the superior vena cava from the large apical mass (lung cancer-pancoast) and this compression depicted as slow flow in superior vena cava and subsequent in the controlateral internal jugular vein is a prodromal phase of jugular vein thrombosis.
Differential Diagnosis List
Pancoast tumor producing compression SVCS
Final Diagnosis
Pancoast tumor producing compression SVCS
