Clinical Presentation

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Superior Vena Cava Syndrome

Mita Sanghavi Goel, M.D. July 17, 2002

Clinical Presentation


  • May be mild if obstruction is proximal to the azygous vein

  • Usually neck, upper extremity, and/or facial swelling, especially around the eyes.

  • Dyspnea, cough

  • Hoarseness, tongue swelling, headaches, nasal congestion, epistaxis, hempoptysis, dysphagia, pain, epistaxis, dizziness, syncope, and lethargy

  • Symptoms exacerbated by lying down or leaning forward

Physical signs

  • Dilated neck veins

  • Cyanosis

  • Increased collateral blood vessels of the anterior chest wall

  • Edema of the face, arms and chest

  • Non pitting edema of the neck “Stoke’s Collar”

  • Severe cases include glossal and laryngeal edema, proptosis, and obtundation

  • Stridor

  • Pleural and pericardial effusion


Anything causing substantial reduction of venous return from the head, neck, or upper extremities. Can result from either intrinsic (10%) or extrinsic (90%) compression of the superior vena cava.

Malignant Causes

  • Malignant tumors cause >90% of all cases of SVC syndrome

  • Lung cancer, particularly small cell and squamous cell lung cancer, cause 85% of all malignancy-associated SVC syndrome, usually bronchogenic carcinoma (70%)

  • Lymphoma is the second most common malignant cause

  • Metastatic tumors to the mediastinum, including testicular and breast cancers.

Benign Causes

  • Aortic aneurysm

  • Enlarged thyroid

  • Thrombosis

  • Fibrosing mediastinitis from prior irradiation, methysergide ingestion, or infection (Histoplasmosis, M. tuberculosis)


Largely clinical diagnosis

  • CXR may show mass, widening of the mediastinum (generally right- sided), or pleural effusion (present in 25% of patients with SVC syndrome and are generally right-sided)

  • CT Scan provides the most reliable definition of mediastinal anatomy. Will show diminished or absent opacification of central venous structures and prominent collateral venous circulation

  • MRI offers no advantage over CT scan

  • Upper extremity venography complements CT or MRI with defining level if obstruction


  • Emergent therapy indicated if:

    • Tracheal obstruction

    • CNS abnormalities such as stupor or seizures are present because may indicate increased intracranial pressure

  • If otherwise stable, treatment depends on the cause of SVC syndrome

    • XRT– primary treatment for SVC caused by non-small cell lung cancer and other metastatic tumors; however important to have tissue diagnosis before beginning XRT because XRT will obfuscate histology

    • Chemotherapy – effective when underlying tumor is chemosensitive, such as small cell lung cancer or lymphoma

    • Intravascular stents – effective palliative treatment. Often reserved for recurrent SVC syndrome (which is 10-30% of patients)

    • Surgery – immediate relief if SVC syndrome from a benign cause

    • Removal of foreign body and anticoagulation – if etiology is thrombus secondary to central venous catheter placement. Anticoagulation helps prevent embolization. If detected early enough, fibrinolytic therapy without catheter removal may be sufficient. Additionally low-dose coumadin (1-2 mg/day) reduces thrombus incidence

    • Steroids – decreases cerebral or pharyngeal edema

    • Diuretics– may provide temporary relief if respiratory symptoms present

Natural history

Most (75-90%) improve symptomatically within one week of initiating treatment.

Mortality depends on underlying etiology of SVC syndrome


Chen JC, Bongard F, Klein SR. A contemporary perspective on superior vena cava syndrome. Am J Surg 1990; 160:207-211.

Cecil Textbook of Medicine. Last accessed via July 15, 2002.

Harrison’s Online. Last accessed July 13, 2002.

Markman M. Diagnosis and management of superior vena cava syndrome. Clev Clin J Med 1999; 66:59-61.

Roberts JR, Bueno R, Sugarbaker DJ. Multimodality treatment of malignant superior vena caval syndrome. Chest 1999; 116:835-837.

Beth Israel Deaconess Medical Center Residents’ Report

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