syphilis, and pyogenic infections. In addition, the
increased current use of invasive monitoring devices,
such as central lines, cardiac pacemakers, catheters for
total parenteral nutrition, and Swan-Ganz monitoring
devices, is associated with increasing reports of throm-
bosis of the superior vena cava. Finally, aneurysms of
the aorta and aortic branches are occasionally responsi-
ble for causing SVCS.
2 – 9
CLINICAL PRESENTATION
The typical symptoms of SVCS are most obvious
when obstructive disease is almost complete. Patients
with SVCS most often present with complaints of facial
edema and erythema, swelling of the neck and/or
arms, and visible dilatation of the veins in the upper
extremity. Patients with SVCS may also complain of dys-
pnea, persistent cough, and orthopnea. As the disease
progresses, the symptoms may include hoarseness, peri-
orbital edema, dysphagia, headaches, dizziness, syn-
cope, lethargy, and chest pain. Other findings may
include confusion and laryngeal and/or glossal edema.
In some cases, the nerves that cross the superior
mediastinum (ie, vagus and phrenic nerves) are affect-
ed by SVCS. This nerve involvement can lead to
hoarseness and paralysis of the diaphragm. These
symptoms may be worsened by positional changes such
as bending forward, stooping, or lying down. Patients
with SVCS and vagus or phrenic nerve involvement
find significant symptom relief when they are in an
upright position, and many of these patients sleep in a
chair to avoid dyspnea.
The venous hypertension associated with SVCS can
sometimes produce cerebral vessel thrombosis and
hemorrhage with dire results. Of all the symptoms of
SVCS, the most life-threatening complications are cere-
bral or laryngeal edema.
2 –10
DIAGNOSIS
The diagnosis of SVCS can be made simply on physi-
cal examination. In cases in which the extent of disease
B h i m j i : S u p e r i o r V e n a C a v a S y n d r o m e : p p . 4 2 – 4 6 , 6 3
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