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Superior Vena Cava Syndrome Imaging

Practice Essentials

Superior vena cava (SVC) syndrome (SVCS) is a constellation of symptoms that result from obstruction of the SVC (see the images from a single case, below). The superior vena cava (SVC) is formed in the upper middle part of the mediastinum by the junction of the brachiocephalic veins. It is 6-8 cm long and drains into the right atrium at approximately the level of the right mainstem bronchus. The azygous vein loops over the right mainstem bronchus and connects to the posterolateral wall of the SVC. The SVC lies in a relatively confined space and is surrounded by several lymph node groups that predispose it to compression, invasion, or involvement in inflammatory conditions.

A CT scan of the chest is the initial test of choice to determine whether an obstruction is being caused by external compression or a thrombosis. Diagnosis of SVC thrombosis by CT includes lack of SVC enhancement; intraluminal filling defects or narrowing; and visualization of the collateral vessels. The modality of choice for SVCS is contrast-enhanced CT with multiple phase imaging. The SVC can be studied during routine contrast-enhanced chest CT.

SVCS is caused by compression, invasion, and/or thrombosis of the superior vena cava and/or the brachiocephalic veins.
 Obstruction of blood flow in the SVC can be characterized by facial, neck, and upper extremity swelling; facial plethora; distended chest and neck veins; and cyanosis.

Although some cases of SVCS are caused by nonmalignant conditions, such as thrombosis and fibrosing mediastinitis, thoracic malignancies have been reported to be responsible for 60-85% of cases.
 The most frequent malignancies are bronchogenic carcinoma (in order of decreasing frequency: small cell carcinoma, squamous cell carcinoma, adenocarcinoma, large cell carcinoma), followed by non-Hodgkin lymphoma. Many other malignancies have been reported; essentially, any mediastinal mass may compress or invade the SVC.

Benign causes include central venous catheters (increasing in frequency), pacemaker wires, fibrosing mediastinitis, thoracic aortic aneurysms, and a multitude of unusual conditions.

Superior vena cava syndrome (case 1). The patient

Superior vena cava syndrome (case 1). The patient was a 35-year-old man with a 3-year history of progressive upper-extremity and fascial swelling. The patient had undergone treatment for histoplasmosis in the past. CT scan shows a narrowed superior vena cava with adjacent calcified lymph nodes and posterior soft tissue thickening.

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Superior vena cava syndrome (case 1, cont'd). Sono

Superior vena cava syndrome (case 1, cont’d). Sonogram shows markedly damped venous waveform with complete loss of normal venous pulsatility and minimal respiratory variation.

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Superior vena cava syndrome (case 1, cont'd). Veno

Superior vena cava syndrome (case 1, cont’d). Venogram shows almost complete occlusion of the superior vena cava with dramatic collateral drainage through the left superior intercostal vein.

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Superior vena cava syndrome (case 1, cont'd). A Pa

Superior vena cava syndrome (case 1, cont’d). A Palmaz P308 stent mounted on a 12-mm balloon was deployed in the superior vena cava after it was predilated to 8 mm. The stent was subsequently dilated to 14 mm.

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Superior vena cava syndrome (case 1, cont'd). Veno

Superior vena cava syndrome (case 1, cont’d). Venogram obtained after stenting shows a widely patent superior vena cava with no collateral drainage. Pressure measurements after stenting showed a 1- to 2-mm residual gradient.

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Superior vena cava syndrome (case 1, cont'd). Sono

Superior vena cava syndrome (case 1, cont’d). Sonogram obtained 1 year after stenting shows near-normal venous pulsatility and respiratory phasicity. The patient experienced a complete resolution of symptoms.

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