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Superior Vena Cava Syndrome: A Systematic Review

Article  in  The Journal of the Egyptian Medical Association · January 2009

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 Superior Vena Cava Syndrome: A Systematic Review
Alaa M. MSc., El mezaien M. MD., and Amin M. MD.
Cardiothoracic Surgery Department, Faculty of Medicine, Suez Canal University, Ismailia, Egypt.

Abstract
The aim of the study is to review the different surgical modalities in the treatment of
superior vena cava syndrome in a trial to put guidelines for different surgical techniques.
Surgical treatment of benign SVC syndrome is effective over the long term, with secondary
endovascular interventions to maintain graft patency. Straight spiral saphenous vein graft
remains the conduit of choice for surgical reconstruction, with results superior to those with
other types of grafts. Endovascular treatment is effective over the short term, with frequent
need for repeat interventions. It does not adversely affect future open surgical
reconstruction and may prove to be a reasonable primary intervention in selected patients.
Patients who are not suitable for or who fail endovascular intervention merit open surgical
reconstruction. ©2009 Journal of Egyptian Society of Cardiothoracic Surgery

Keywords : “Superior vena cava syndrome”, “Treatment of superior vena cava syndrome”,
“Surgical management of SVC syndrome”, “Saphenous vein graft, SVC syndrome”, “femoral
vein graft, SVC syndrome”, “autologous venous conduits, SVC syndrome”, “allografts and
pericardial conduits, SVC syndrome”, “ SVC syndrome, stenting” and “Endovascular therapy,
SVC syndrome”.

Definition: Historical Note:

Acquired disease of the systemic veins is
obstruction, partial or complete, of the
major veins of the thorax. The veins that
are of surgical importance are the
superior and inferior venae cavae (SVC
and IVC). Left and right innominate
(brachiocephalic) veins, including the
jugular-subclavian vein confluence, are
major tributaries of the SVC and may be
considered collectively with conditions of
the SVC. Congenital anomalies of the
venae cavae and axillary vein conditions,
such as effort thrombosis, are not
considered.
SVC obstruction is acquired by extrinsic
compression, direct invasion by disease
processes, or thrombosis. Obstruction
may be partial or complete. SVC
syndrome is the result of venous
hypertension in the head, neck, and arms
caused by impeded blood flow by SVC
obstruction.
William Hunter described the first
recorded case of SVC syndrome in 1757 in
a patient with syphilitic aneurysm of the
aorta.H6 SVC obstruction was due to
compression by the aneurysm. William
Osler described SVC compression in his
classis text of 1892: “Along the convex
border of the ascending part of the aorta,
aneurism frequently develops, and may
grow to a large size… In this situation the
sac is liable indeed to compress the
superior vena cava, causing engorgement
of the vessels of the head and the arm.O1
William Stokes’ text of 1853 described
SVC obstruction and noted the more
frequent occurrence with cancer: “AS an
indication of intrathoracic tumor, an
extensively varicose state of the superficial
veins of the neck and thorax is probably
less frequent in aneurismal than in
cancerous disease… The superior cava
may be adherent to the tumour, and
become narrowed, not only by pressure,
but by adhesion of its internal surfaces.S21

Corresponding Author Tel.: +201141463162, +20663352127

Email: mohamedalaa_2000@yahoo.com
 M. Alaa et al./ Journal of Egyptian Society of Cardiothoracic Surgery 34 (2009)
Symptoms and signs of SVC obstruction
have since become recognized as an
unmistakable syndrome. Gomes and
Hufnagel reviewed cases of SVC
obstruction reported before 1975.G3 Data
from more than 90 publications, including
1980 cases reported in the literature since
1934, were reviewed by Nieto and Doty in
1986.N3 The first successful bypass
operation for SVC obstruction were
performed using autologous femoral vein
grafts by Klassen and colleagues in 1951
and by Bricker and McAfee in 1952.B4, K5
In 1965, Hanlon and Danis also tried using
other large veins to replace or bypass the
SVC, employing variously the femoral,
subclavian, and jugular veins.H2
In 1962, Benvenuto and colleagues
constructed a composite panel graft
pieces of saphenous vein for replacing the
SVC.B2 The operative approach to relieve
venous obstruction up to 1970 was
reviewed by Haimovici and colleagues.H1
They concluded that autologous veins are
preferable for venous replacement. All
reported experimental and clinical
experience with vena cava replacement or
bypass up to 1974 was reviewed by
Scherck and colleagues.S2
A number of conduits had been tried,
including autologous, homologous T3, and
heterologous vein and aorta as well as
various synthetic materials. These authors
concluded that autologous vein grafts of
nearly the same size as the SVC were most
likely to remain patent. To obtain such a
large vein from elsewhere in the body,
with resultant venous drainage problem,
or constructing a composite graft from a
smaller vein.
Synthetic grafts were attractive because
of their convenience and availability and
because of the variety of sizes available. In
1973, Effeney and colleagues reported
successful bypass of the SVC using
polyester graft.E1
In 1977, Avasthi and Moghissi used a
polyester graft interposed between
innominate vein on the left side and right
atrial appendage to bypass the obstructed
SVC.A5 Thrombosis of polyester grafts
limited success of the procedure.
Expanded polytetrafluoroethylene (PTFE)
was used successfully as a venous
replacement conduit in experimental
venous operations in dogs.F2, H4, S9 Hiratzka
and colleagues showed that PTFE and
polyester were equally poor venous
substitute conduits in the experimental
setting and that they did not approach the
effective patency of autologous vein
grafts.H5 Reichle and colleagues suggested
that this is probably due to the fact that
autologous vein grafts have a living
endothelial surface even after initial
endothelial desquamation, whereas
prosthetic graft surfaces are composed of
collagen matrix.R1 Nevertheless, success
using PTFE grafts has been reported.
Antiplatelet-adhesive drugs may be of
benefit in maintaining patency of PTFE
grafts.H3 Dartevelle and colleagues
demonstrated 12 of 13 PTFE grafts used
to replace the SVC were patent an
average of 24 months after operation.D1
Composite vein grafts constructed from
saphenous or external jugular veins, in
paneled or longitudinal fashion, have
been used clinically for SVC bypass or
replacement.A2, S4
In 1974, Chiu and colleagues reported
constructing a composite vein graft from
external jugular vein, which was matched
to the size of the SVC.C3 The donor vein,
was opened longitudinally and wrapped in
spiral fashion around tubular stent of
approximately the same size as the SVC.
Vein edges were then sutured together to
form the conduit. The graft occluded in
the initial three experiments in dogs; after
that however, 10 consecutive grafts
remained patent for up to 15 months. This
 M. Alaa et al./ Journal of Egyptian Society of Cardiothoracic Surgery 34 (2009)
report prompted successful application in
humans by Doty and Baker in 1976.D3
Successful percutaneous balloon
dilatation of the SVC in a child was
reported by Rocchini and colleagues
subsequently reported successful
dilatation of an SVC stricture in an adult
caused by pacemaker electrode.S6
In 1987, Rosch and colleagues used an
expandable wire stent to treat SVC
obstruction cause by malignant disease
that recurred after maximum radiation
therapy.
Morphology and Pathogenesis:
Morphology
Superior Vena Cava; It measures about 6
to 8 cm. in length, and is formed by the
junction of the two innominate veins. It
begins immediately below the cartilage of
the right first rib close to the sternum,
and, descending vertically behind the first
and second intercostal spaces, ends in the
upper part of the right atrium opposite
the upper border of the third right costal
cartilage: the lower half of the vessel is
within the pericardium. In its course it
describes a slight curve, the convexity of
which is to the right side. Relations; In
front are the anterior margins of the right
lung and pleura with the pericardium
intervening below; these separate it from
the first and second intercostal spaces and
from the second and third right costal
cartilages; behind it are the root of the
right lung and the right vagus nerve. On its
right side are the phrenic nerve and right
pleura; on its left side, the
commencement of the innominate artery
and the ascending aorta, the latter
overlapping it. Just before it pierces the
pericardium, it receives the azygos vein
and several small veins from the
pericardium and other contents of the
mediastinal cavity. The portion contained
within the pericardium is covered, in front
and laterally, by the serous layer of the
membrane. The superior vena cava has no
valves.
Collateral Circulation
SVC obstruction stimulates formation of
extensive venous collateral circulation.
The azygos vein is the only major venous
channel that enters the SVC and is the
most important collateral pathway. It
begins opposite the first or second lumbar
vertebra, by a branch, the ascending
lumbar vein; sometimes by a branch from
the right renal vein, or from the inferior
vena cava. It enters the thorax through
the aortic hiatus in the diaphragm, and
passes along the right side of the vertebral
column to the fourth thoracic vertebra,
where it arches forward over the root of
the right lung, and ends in the superior
vena cava, just before that vessel pierces
the pericardium. In the aortic hiatus, it lies
with the thoracic duct on the right side of
the aorta; in the thorax it lies upon the
intercostal arteries, on the right side of
the aorta and thoracic duct, and is partly
covered by pleura.
Tributaries; It receives the right subcostal
and intercostal veins, the upper three or
four of these latter opening by a common
stem, the highest superior intercostal
vein. It receives the hemiazygos veins,
several oesophageal, mediastinal, and
pericardial veins, and, near its
termination, the right bronchial vein. A
few imperfect valves are found in the
azygos vein; but its tributaries are
provided with complete valves.
When SVC obstruction is located to a
patent azygos vein, there is retrograde
flow through the azygos and hemiazygos
veins to the lumbar veins below the
diaphragm and to the IVC. When
obstruction is proximal to the patent
azygos vein, collateral veins in the neck
 M. Alaa et al./ Journal of Egyptian Society of Cardiothoracic Surgery 34 (2009)
allow blood flow to enter the azygos
system and continue directly into the
distal SVC below the obstruction. When
connection of the azygos vein to the SVC
is included in the obstruction, more
complex and varied pathway must
develop to drain the upper compartment.
One prominent system consists of the
internal thoracic veins, which connect to
superior and inferior epigastric veins and
subsequently to the IVC by way of the
external iliac veins. Lateral thoracic veins
drain to thoracoepigastric veins;
eventually, blood flow may enter the
femoral veins. Paraspinous veins form a
collateral network that connects to the
IVC via lumbar veins. The esophageal
venous network also can decompress the
thorax via the left gastric vein to the
portal system. This pathway is not very
important unless esophageal varicose
veins develop, and only rarely are
associated with bleeding into the
gastrointestinal tract. Subcutaneous veins
are a particularly important means of
bringing blood flow from the upper
compartment below the diaphragm to the
IVC. Despite extensive collateral
circulation that may develop, venous
pressure in SVC obstruction as high as 200
to 500 cm of water has been recorded.
Cerebral venous decompression may be
provided through a single internal jugular
vein, because the veins of the right and
left sides of the brain are in continuity
through midline venous sinuses.L6
Superior and inferior sagittal sinuses drain
the cerebral hemispheres to the
confluence of sinuses that communicate
through transverse and sigmoid sinuses to
either internal jugular vein. The cavernous
venous sinuses also connect both sides of
the brain to either internal jugular vein.
Cerebral venous drainage, therefore, may
by adequate through either of the internal
jugular veins to the right atrium.
Pathogenesis
SVC obstruction may be caused by a
spectrum of malignant and benign
diseases. Disease in any adjacent
structure may contribute to SVC
syndrome. The common causes of SVC
obstruction have changed over the past
50 years. In 1949, the most common were
thoracic malignancy (33%), aortic
aneurysm (30%), and chronic
granulomatous mediastinitis (19%).M5 In
1962 and 1979, that proportion fell to
3%.L6 Today, malignant etiologies account
for more than 90% of cases, but iatrogenic
causes such as indwelling catheters are
becoming more frequent, and an
increasing number of infectious causes
have been reported in immunosupressed
patients.E2
Benign Causes
Reviews from Mayo Clinic and Cleveland
Clinic reported mediastinal
granulomatous disease resulting in
fibrosing mediastinitis as a prominent
cause of benign SVC obstruction.M1, P1
The most common etiologic agent is
histoplasmosis, which causes a caseating
granulomatous process in mediastinal
lymph nodes that compresses, fibroses,
and contracts around the SVC and may
result in secondary thrombosis. Fibrosing
mediastinitis resulting from radiation
therapy can be progressive and involve
the SVC years after radiation treatment
has been completed.
Iatrogenic causes have been increasing in
importance because increased use of
invasive intravenous procedures, such as
cardiac pacemaker electrodes, central
venous-pulmonary artery catheters,
hyperalimenation and chemotherapy
catheters, and extracorporeal membrane
oxygenation (ECMO).
 M. Alaa et al./ Journal of Egyptian Society of Cardiothoracic Surgery 34 (2009)

Mazzetti and colleagues reviewed

pacemaker electrodes as a cause and
found 4 cases of SVC obstruction among
2600 patients followed in pacemaker
clinic.M4 They also reviewed 37 cases
reported in the literature and concluded
that prevalence of this complication is
likely lower than 1 in 1000.
Williard and colleagues reported the
Memorial Sloan-Kettering Cancer Center
experience with thrombosis of long-term
vascular access.W1 Occurrence of
thrombosis of access catheters placed
through the SVC was 7%, versus 19% for
catheters placed in the IVC. About half the
thromboses involved just the catheter;
the other half involved the blood vessel
through which the catheter was
introduced. Substantial morbidity is
associated with chronic central venous
access catheters, with IVC occlusion
occurring in 4.5% and SVC occlusion in
11% of 510 infants having 756 central
venous catheters for parenteral
nutrition. S22 Head and neck swelling
developed in all with SVC occlusion,
pleural effusions developed in 50%, and 2
infants died. Thrombosis of the SVC
around these catheters is especially
troublesome when they are required for
permanent life support and cannot be
conveniently removed. In addition,
thrombosis frequently follows the entire
intravascular course of the catheter and cardiac and pulmonary diseases, and
thus is extensive, involving the major SVC mediastinal hematomas.
venous tributaries.
SVC thrombosis can be an important Malignant Causes
complication after extracorporeal Intrathoracic malignancy now accounts
membrane oxygenation. Zreik and for more than 90% of SVC obstructions,
colleagues reported 7 of 60 neonates with bronchogenic carcinoma responsible
(12%; CL 7% - 18%) had either complete or for 67% to 82%.N3 SVC syndrome develops
partial SVC obstruction.Z1 in 3% to 15% of patients with
Other benign causes include benign bronchogenic carcinoma.
tumors, vascular aneurysm, a variety of
 M. Alaa et al./ Journal of Egyptian Society of Cardiothoracic Surgery 34 (2009)
Bronchogenic carcinoma cell type
associated with SVC obstruction appears
to be somewhat variable, which may in
part be related to difference in tumor
classification schemes used by different
investigators. Squamous (epidermoid)
carcinoma accounts for 22% to 27% of
cases and appears to be relatively
consistent across reports. Small-cell
carcinoma is the most variable (18% to
46%), although its etiologic role appears
to increasing.
Lymphoma is the second most frequent
cause of SVC obstruction, accounting for
5% to 15% of cases. These malignancies
are located in the anterior mediastinum
and produce obstruction by external
compression from the front. Thoracic
metastasis from extrathoracic
malignancies, particularly breast and
testicle, accounts for a small number of
SVC obstructions.
Malignancy is also the most common
cause of SVC obstruction in children. In
contrast in adults, however, non-Hodgkin
lymphoma is the leading etiology.I1
Clinical Features and Diagnostic Criteria
Superior Vena Cava Syndrome
Because extrinsic compression usually
produces obstruction gradually, collateral
circulation develops, so obstruction is
usually well tolerated and the patient has
few, if any, signs and symptoms. If
obstruction develops rapidly, as in
malignant tumor invasion and in infants
and children with central venous
catheters, collateral circulation may not
have time to develop and adequately
decompress the upper compartment
veins; then, SVC syndrome is more
obvious. The most severe syndrome
develops in cases of SVC thrombosis in
which obstruction is sudden and collateral
venous channels have no time to develop.
Thrombosis may involve major caval
tributaries and thus eliminate major
collateral pathways. Thrombosis is often
associated with SVC obstruction from any
cause and compounds the problem
because: (1) subsequent fibrotic
organization of the clot results in
permanent SVC closure, and (2)
thrombosis does not respond to
treatment directed at the primary disease
process that caused the SVC obstruction.
 M. Alaa et al./ Journal of Egyptian Society of Cardiothoracic Surgery 34 (2009)

Thoracic lymphatic ducts drain to the

subclavian veins and are affected by
venous hypertension associated with SVC
obstruction; pulmonary lymphatics may
also be secondarily affected, leading to
increased lung water and dyspnea.
Respiratory insufficiency is frequently
associated with acute SVC obstruction and
may be difficult to manage. Chylous
pleural effusion may be associated with
thoracic lymphatic obstruction.

Symptoms
Patients with SVC obstruction usually
present with a well-established syndrome
that is easily recognized and
unmistakable. Only rarely does complete
SVC obstruction occur without noticeable
signs or symptoms. The typical syndrome
consists of swelling of face, neck, and
arms; shortness of breath; orthopnea; and
cough. Patients may notice tightness of a
shirt collar and that their face is flushed
and swollen, especially around eyes.
Other symptoms include hoarseness,
stridor, tongue swelling, nasal congestion,
epistaxis, dysphagia, headache, dizziness,
syncope, lethargy, and chest pain.
Symptoms are aggravated by bending
forward, stooping, or lying down. Many
patients become dyspenic when
recumbent and must sleep in a chair.
Signs
The most common signs are dilatation and
tortuosity of upper body veins, plethora
or cyanosis of the face, and swelling of
face, neck, or arm. Other signs include
proptosis, glossal edema, rhinorrhea,
laryngeal edema, mentation changes,
elevated venous and cerebrospinal fluid
pressures, and Chylous pleural effusions.
Signs and symptoms suggesting cerebral
or laryngeal edema were shown to be of
prognostic importance by Lochridge and
colleagues.L6 Headache, vertigo, visual
disturbances, decreased mentation,
stupor, somnolence, and convulsion
indicating cerebral edema.K2, L6;
hoarseness and stridor suggest laryngeal
edema.
Diagnosis
Clinical diagnosis is usually obvious.
Location, degree, and causes of SVC
obstruction should be characterized in
every case. There is some controversy
about how specific this characterization
should be, because more than 90% of
cases are due to malignancy. Some think
that palliating the intrathoracic
malignancy should proceed without delay.
Others argue that SVC syndrome is
seldom a medical emergency and should
be characterized as completely as
possible, in an orderly fashion, so that
treatment can be specific. Although tissue
diagnosis can usually be obtained, in some
cases it may be difficult and even
hazardous to do so. Patients seek relief of
symptoms of SVC and seldom complain of
 M. Alaa et al./ Journal of Egyptian Society of Cardiothoracic Surgery 34 (2009)
symptoms related to the etiologic cause
of the obstruction. Treatment of SVC
syndrome should be accompanied by
diagnostic measures and therapy directed
at the causative primary disease.
Chest Radiography
Chest radiography is helpful but not
specific in diagnosing SVC obstruction.
Because bronchogenic carcinoma is the
most common cause of SVC syndrome,
the chest radiograph often shows a right-
sided hilar mass suggests lymphoma.
Venography
The most useful diagnostic procedure is
bilateral arm contrast venography.D6, S20 It
establishes:
 Location of SVC obstruction.
 Degree of obstruction.
 Degree of involvement of caval
tributaries.
 Extent of collateral venous
pathways.
 Extrinsic compression versus
intrinsic SVC obstruction.
Identifying retrograde propagation of
thrombosis that involves caval tributaries
may indicate that caval obstructive
symptoms are not likely to respond to
non-operative therapy. Using venography
in 36 patients, Stanford and Doty defined
four patterns of venous circulation useful
in planning therapy:
 Type I: Partial obstruction (up to
90% stenosis) of the SVC with
patency of the azygos-right atrial
pathway.
 Type II: Near complete to
complete obstruction (90% to
100%) of the SVC with patency and
antegrade flow in the azygos-right
atrial pathway.
 Type III: Near complete to
complete obstruction (90% to
100%) of the SVC with reversal of
azygos blood flow.
 Type IV: Complete obstruction of
the SVC and one or more of the
major caval tributaries, including
the azygos systems.
Digital Contrast Angiography, Venous
Phase
Digital contrast angiography in the venous
phase is also helpful in assessing collateral
circulation.
Two-Dimensional Echocardiography
Masses in the SVC are imaged with great
clarity by two-dimensional
echocardiography. The image is dynamic,
so movement of obstructing lesions may
be detected. It is useful in evaluating clot
formation on central venous catheters
and other foreign devices.
Computed Tomography
Computed tomography (CT) provides an
effective, non-invasive means of analyzing
the SVC and its tributaries that has
increasing importance in the workup of
SVC syndrome and masses in the right
atrium and IVC. Its advantages are
outlined by Moncada and colleagues M8:
 M. Alaa et al./ Journal of Egyptian Society of Cardiothoracic Surgery 34 (2009)

 Caval anatomy can be related to avoided in favor of direct approach in

surrounding mediastinal which SVC obstruction is treated along
structures. with establishing an etiologic diagnosis.
 Mediastinal masses or lymph
node pathology relative to the
SVC can be located.
 It aids directed needle biopsy of
mediastinal masses.
 Patency of the internal jugular
veins in the neck can be assessed
despite extensive occlusion of
tributaries of the SVC.

Magnetic Resonance Imaging

Magnetic resonance imaging (MRI) is
useful in assessing graft patency after
operation for SVC obstruction. L3

Other Diagnostic Methods

Other diagnostic imaging, including
cytology, isotope venography,
bronchoscopy, lymph node biopsy,
mediastinal biopsy, mediastinotomy with
biopsy, and exploratory thoracotomy, are
indicated for individual cases.A1, J1
However, risks of intervention – patient
discomfort, bleeding, and interruption of
venous collaterals – should be weighed
against the chance of a successful
diagnosis. More invasive diagnostic tests
may worsen SVC syndrome and should be
 M. Alaa et al./ Journal of Egyptian Society of Cardiothoracic Surgery 34 (2009)
Natural History:
The natural history of SVC obstruction and
accompanying SVC syndrome is variable
and depends on etiology of the
obstruction, rapidity of onset, extent of
the obstructive process, and extent of
collateral venous circulation. Collateral
venous circulation usually develops
rapidly in response to SVC obstruction and
is often sufficient to relieve SVC
syndrome. The relationship of SVC
obstruction to location and patency of the
azygos vein has an important effect on
natural history.S20
When the azygos vein is closed, central
thoracic collateral circulation is eliminated
and SVC syndrome is worse because
venous drainage from the upper
compartment is dependent on smaller,
less reliable venous channels in the chest
wall and skin.
Malignant diseases resulting in acute SVC
obstruction and thrombosis may not
resolve with thrombolytic and radiation
therapy. Acute SVC obstruction associated
with signs of cerebral and laryngeal
edema results in death within 6 weeks,
apparently related to SVC syndrome
rather than the primary etiology of the
caval obstruction.L6 The malignant process
responds to tumor therapy in a variable
manner, depending in part to cell type,
ultimately determining the patient’s fate.
Surgical intervention may be beneficial if
the SVC syndrome is life threatening and
allows treatment of the malignancy to
proceed in an orderly fashion with the
patient comfortable. Minimal tumor
invasion of the SVC or compression by
benign tumor may stimulate formation
and propagation of blood clot within the
vena cava.
Fibrosis associated with clot resolution
and late clot propagation may be
accompanied by worsening of symptoms
and signs of SVC syndrome, despite
adequate venous collateralization. Thus,
SVC obstruction may persist even though
there appears to be good response of the
tumor to treatment. Some benign causes
of SVC obstruction lead to severe and
relentless inflammation and fibrosis,
resulting in recurrent and extending
obstruction. Clot propagation within the
venous system proximal to the primary
site of SVC obstruction may lead to
progression of SVC syndrome in patients
with benign etiology. Clot formation
around indwelling catheters is especially
prone to extensive thrombosis of the SVC
and major thoracic and cervical venous
tributaries. Some patients with SVC
obstruction may never develop adequate
collateral circulation even though the
causative process is stabilized or arrested.
Technique of operation
Reconstructing thoracic venous drainage
usually requires bypassing obstructed
native venous channels using, ideally,
autologous tissue conduits to provide
optimum long-term outcome. Venous
conduits include spiral saphenous vein,
femoral vein, straight saphenous vein, and
composite autologous vein grafts.D5 In
unusual situations, alternative venous
conduits such as azygos vein – IVC or
jugular vein – femoral vein grafts, can be
used. In the absence of availability of
autologous venous tissue, aortic allograft,
venous allograft, and pericardial tube
construction can serve as a conduit.
Prosthetic graft materials are generally
inferior to autologous tissue grafts.
Successful bypass grafting depends on (1)
Adequate size of the conduit and (2)
Proper orientation. Graft diameter should
closely match that of native inflow vein to
prevent residual obstructive flow
gradients. Graft length should be
measured so that it is not redundant, to
prevent graft kinking and obstruction.
Both graft inflow and outflow should be
free of intraluminal obstructions, such as
 M. Alaa et al./ Journal of Egyptian Society of Cardiothoracic Surgery 34 (2009)
atrial trabeculations, adherent venous
thrombus, or abnormal vascular intima.
Spiral Saphenous Vein Graft
The most extensive experience has been
with the spiral saphenous vein graft
conduit, a concept developed
experimentally by Chiu and colleagues
and applied clinically by Doty and Baker.
C3, D3
Operation is performed through a median
sternotomy or, more recently, via a
minimal incision using a partial upper half
sternotomy. A simultaneous incision is
made in the thigh over the course of
saphenous vein. The left innominate vein
is mobilized to the left internal jugular –
left subclavian vein junction. When the
innominate vein and subclavian-jugular
confluence are thrombosed, it is
necessary to mobilize either the left or
right internal jugular vein as the outflow
point from the upper venous
compartment and the inflow to the graft.
In this situation the midline incision may
be extended to the left or right and the
strap muscles divided to provide an
unrestricted passageway for the bypass
conduit. The largest jugular vein may also
be exposed and mobilized through a
secondary cervical incision. The two
incisions are joined in a tunnel beneath
the sternocleidomastoid muscle. Biopsy
samples of abnormal tissue surrounding
the SVC are obtained.
Diameter of the inflow vein (usually left
innominate or jugular) and distance from
vein to right atrial appendage are
measured. After mobilizing the saphenous
vein, its average diameter is measured.
Length of saphenous vein to be removed
is determined from (1) the ratio of the
desired graft diameter to the average
diameter of the saphenous vein (SV) and
distance to right atrial (RA) appendage
according to the following formula:
𝑺𝑽 𝒍𝒆𝒏𝒈𝒕𝒉 𝒕𝒐 𝒓𝒆𝒎𝒐𝒗𝒆 (𝒄𝒎) =
𝑰𝒏𝒇𝒍𝒐𝒘 𝒗𝒆𝒊𝒏 𝒅𝒊𝒂𝒎𝒆𝒕𝒆𝒓 (𝒎𝒎)
×
𝑺𝑽 𝒅𝒊𝒂𝒎𝒆𝒕𝒆𝒓 (𝒂𝒗𝒆𝒓𝒂𝒈𝒆)
𝑰𝒏𝒇𝒍𝒐𝒘 𝒗𝒆𝒊𝒏 𝒕𝒐 𝑹𝑨 𝒂𝒑𝒑𝒆𝒏𝒅𝒂𝒈𝒆 𝒍𝒆𝒏𝒈𝒕𝒉 (𝒄𝒎)
For example, if the innominate vein
diameter is 12 mm, saphenous vein
diameter is 4 mm, and distance to right
atrial appendage is 10 cm, then 30 cm of
saphenous vein is required (12/4 x 10 = 30
cm).
The required length of saphenous vein is
removed and its side branches ligated.
The vein is incised longitudinally through
the entire length. A thoracostomy tube of
the same diameter as the innominate or
jugular vein is selected as a stent. The
opened vein graft is flattened and
wrapped around the stent in spiral
fashion, with the endothelial surface of
the vein against the stent. Continuous
stitches of No. 7-0 polypropylene suture
are used to join the edges of the graft,
forming a large conduit with the same
internal diameter as the stent. There is no
advantage of a larger or smaller conduit. A
smaller conduit could, in theory, have a
hemodynamic advantage by increasing
flow velocity in the graft. However,
because the graft diameter is always
smaller than that of the SVC, flow through
the graft is always torrential, obviating
need to reduce graft diameter to less than
that of the inflow vein, which could
produce stasis.
 M. Alaa et al./ Journal of Egyptian Society of Cardiothoracic Surgery 34 (2009)
After administering heparin (100 units/kg)
intravenously, the innominate vein is
ligated as closely as possible to the SVC. A
soft jaw vascular clamp is applied at the
internal jugular – subclavian vein junction
and the innominate vein divided, retaining
as much length as possible. Distal end of
innominate vein is oversewn for secure
closure. The vein is cut back until all
thrombus or any abnormality of the
intima or vessel wall is removed. The graft
is pushed slightly off the end of the stent
to allow construction of an end-to-end
anastomosis to the innominate vein using
continuous No. 7-0 polypropylene suture.
If the internal jugular vein is selected as
the site for anastmosis, a partial occlusion
clamp is applied at the intended outflow
point and an end-to-side anastomosis
performed. The stent is then removed
from the graft. When the graft must cross
the thoracic inlet coming from the jugular
vein anastomosis, an external stent is
employed to prevent compression of the
graft. A short segment of an externally
reinforced PTFE graft somewhat larger
than the spiral vein graft as it crosses the
thoracic inlet.
A curved vascular clamp is placed across
the right atrial appendage, and the tip is
excised. The opening in the appendage is
cleared of trabeculae to ensure
unrestricted blood flow. The graft is
anastomosed to the appendage, using
continuous No. 5-0 polypropylene suture.
The completed bypass graft must be
oriented correctly and be the right length.
Extra length serves no advantage and runs
a risk of kinking the graft or impending
blood flow.
Direct Operation on Superior (or Inferior)
Vena Cava
Direct operations on the SVC or IVC are
performed when there is tumor or blood
clot partially obstructing the lumen.
Operations are usually performed for
renal cell carcinoma where there is a long
non-adherent tumor in the IVC or the
right atrium extending from the renal
primary, which cannot be safely removed
from the IVC below the liver. Blood clot
may form around intraluminal catheters
such as those used for parenteral feeding,
 M. Alaa et al./ Journal of Egyptian Society of Cardiothoracic Surgery 34 (2009)
chemotherapy, or cardiac pacing. In these
cases, the clot may adhere to the foreign
body or vascular intima, making non-
operative removal of organized clot
hazardous or impossible. There may be
infection associated with the foreign body
or invading the clot.
A median sternotomy is made. Strategy
for inserting the venous uptake cannulae
is based on location of the clot or tumor
to be removed. If the mass is located
completely within the SVC, a two-stage
venous uptake cannula is inserted through
the right atrium only, or it may be
supplemented with another catheter in
the femoral vein or right jugular vein if
there is in adequate venous uptake.
Masses in the right atrium require
peripheral cannulation of the femoral or
internal jugular vein.
Operative Steps
A right thoracotomy in the 4th or 5th
intercostal space is the standard approach
for upper lobe tumours invading the SVC.
Complete median sternotomy is
recommended for tumours of the anterior
mediastinum. Both approaches allow
optimal exposure of the operatory field;
through the right thoracotomy we have
easy access to the lung parenchyma, the
SVC, the trachea, the pulmonary hilum
and right atrium; however, through this
approach it is more difficult to control the
left brachiocephalic vein. Median
sternotomy allows a wide exposure of the
mediastinum and the dissection can be
easily extended into the neck. This
approach can be turned into a “trap door
incision” if a more comfortable exposure
of the right lung and subclavian vessels is
required.
Intra-operative management: Resection
and reconstruction of the SVC is
considered a major technical challenge
due to the potential detrimental effects of
clamping a patent vessel. Partial caval
clamping or clamping a chronically
obstructed SVC is generally well tolerated;
on the other hand, occlusion of a patent
SVC may produce intracranial bleeding,
brain edema and damage, and a
potentially lethal reduction of cardiac
output. These complications can be
avoided by careful patient selection and
intraoperative monitoring and
management.
A double lumen endobronchial tube is
placed to achieve one–lung ventilation. A
radial arterial line and a venous line in the
internal jugular vein are inserted routinely
to obtain continuous pressure
monitoring. Two additional venous lines
are placed in the lower limbs to achieve
volume expansion during venous
clamping.
A Foley catheter is inserted to monitor
urine output. ECG monitoring is obviously
mandatory. Transesophageal
echocardiography (TEE) is optional as well
as nasogastric tube placement; the latter
may be of help as an anatomical marker
during dissection for lung cancer
extensively involving the mediastinum.
Closure of up to 50% of the SVC
circumference can be performed without
any hemodynamic imbalance. In patients
with tight or complete obstruction of the
vessel venous clamping does not
significantly modify cerebral circulation
and cardiac output. In both cases the
duration of venous clamping is not a
limiting factor and the operation can be
safely performed without feeling stressed
by the potential length of the
reconstructive step. During complete
clamping of the unobstructed SVC, there
is a clear hemodynamic derangement with
an increase of the mean venous pressure
 M. Alaa et al./ Journal of Egyptian Society of Cardiothoracic Surgery 34 (2009)

in the cephalic districts and a decrease in plasma should be used.

mean arterial pressure with a consequent Vasoconstrictive agents are
reduced brain arterial–venous gradient. indicated to increase the
This may lead to brain edema, mean arterial pressure. At
haemorrhage and dysfunction (usually the end of the procedure
transient). These hemodynamic diuretics are administered to
modifications are evident in the entire reduce edema in the cephalic
cephalic distribution. For this reason, a regions. Anticoagulation
cyanotic facies is almost always present therapy is mandatory during
during SVC clamping; however, it is and immediately after the
usually completely reversible after operation: intravenous
declamping. Petechiae may be evident in sodium heparin (0.5 mg/Kg) is
the immediate postoperative period and given before clamping and
disappear within a couple of weeks after continued during the
surgery. All these complications can be immediate postoperative
avoided completely using the period (adjust heparin dose to
Cardiopulmonary Bypass (CPB) in the achieve INR = 2 to 2.5). It is
different operations directly performed usually switched to warfarin
on the SVC. agents at the time of
discharge.
Cardiopulmonary Bypass (CPB) is 2. Surgical strategy and shunting
established and the patient’s body techniques: Every effort
temperature lowered to 16˚ to 20˚C. should be attempted to
When the target temperature is reached, reduce clamping time as
CPB is discontinued. Venous cannulae much as possible, in particular
may be removed to enhance exposure. when the SVC system is not
After performing the desired technique in completely occluded before
approximately 20 minutes of circulatory the operation. It has been
arrest, the access incision is closed. reported that up to 45 to 60
Incisions in the right atrium may be minutes of complete
excluded by vascular clamp to allow their clamping is usually tolerated
closure after CPB is resumed in order to with the appropriate
limit duration of circulatory arrest, and pharmacological support. For
rewarming is commenced. lung cancer resection, the
vascular step should be
The hemodynamic imbalance is reduced always performed before any
with an aggressive intraoperative other reconstructive
management by the anaesthetist, along procedure of the airway. For
with some technical tricks. mediastinal tumours involving
the upper lobes, the
1. Fluid implementation and dissection should be
pharmacological agents: this performed from the left to
strategy is devoted to the right side; the right part
increase venous return and of the excision is usually
maintain the normal arterial– performed after vascular
venous gradient in the brain. reconstruction, in particular
Macromolecules, blood and when a lobectomy is
 M. Alaa et al./ Journal of Egyptian Society of Cardiothoracic Surgery 34 (2009)

required. Intravascular or minute to let it stiffen and

extravascular shunts may be facilitate manipulation during
used to reduce the effects of suturing.
vascular clamping during 4. SVC replacement:
resection and reconstruction replacement of the whole
of the SVC. However, body of the SVC is the most
thrombosis of the shunt may frequent type of
occur; furthermore, these reconstruction (Figure A). In
devices occupy space in the patients with lung cancer, it is
operative field making the usually associated with right
anastomosis more difficult. upper lobectomy or

3. Tangential resection and pneumonectomy; however,

venous plasty: in cases in SVC reconstruction may be
which less than 30% of the required during carinal
SVC circumference is pneumonectomy, sleeve
involved, a partial resection lobectomy (Figure B), and
of the vessel can be reconstructive procedures of
performed. For minimal the pulmonary artery; the
invasion, a tangential latter two should always be
resection of the defect closed attempted if they help to
with a running suture or a avoid pneumonectomy. SVC
vascular stapler is usually replacement requires a
easy and leaves a patent tumours–free confluence of
vessel. Larger defects, both brachiocephalic veins.
especially if they are The reconstruction is usually
longitudinally extensive, performed using a straight
require reconstruction; this non-ringed PTFE graft (18 –
can be obtained by the 20 mm). An autologous or
interposition of a patch of bovine pericardial tube could
autologous or bovine also be used. After proximal
pericardium. Autologous and distal clamping, the SVC
pericardium may be fixed in is excised. The proximal
diluted glutaraldehyde (two anastomosis is performed
drops of 20% glutaraldehyde first, using a 5-0
in 50 cc of saline) for one polypropylene suture, starting
 M. Alaa et al./ Journal of Egyptian Society of Cardiothoracic Surgery 34 (2009)

from the posterior aspect of (especially if radiotherapy is

the prosthesis or the tube of administered) could
pericardium. The distal contribute to graft
anastomosis is subsequently compression. Simultaneous
performed with the same revascularization of both
technique. Before tying the brachiocephalic veins (Figure
distal suture line, the B) is rarely required since
proximal clamp is gently there are enough
released and deaeration is anastomotic venous
performed; afterwards, the communications in the neck.
distal clamp is released and Revascularization of both
knots are tied. After systems is indicated in case of
complete filling of the graft by previous neck surgery
blood, there should be no (laryngeal or thyroid surgery
tension of the suture lines or for cancer); a separate distal
torsion or kinking. anastomosis of the two grafts
5. Sometimes it may be is preferred to avoid
indicated to replace only one thrombosis of the accessory
brachiocephalic vein (either left limb of a Y graft, starting
the right or left, according to at the level of the graft–to–
local invasion). A ringed PTFE graft anastomosis.
graft should be used (Figure 6. Palliative bypass: the
A), especially for the left indications for palliative
vessel and the distal procedures of bypass are
anastomosis should be extremely rare due to the low
performed on the inferior venous blood flow obtained
stump of the SVC or on the from the axillary or jugular
right atrium. Use of the veins. Surgically created A–V
auricle should be avoided fistulae devoted to increase
because of the presence of flow through the bypass
the pectinate muscles. In this conduit are generally
situation, the prosthesis may unsuccessful.
be too long after closure of
median sternotomy and could
kink easily. Also postoperative
mediastinal fibrosis
 M. Alaa et al./ Journal of Egyptian Society of Cardiothoracic Surgery 34 (2009)
INDICATION FOR OPERATION
Current recommendations for operative
intervention in SVC obstruction are as
follows:
 Persistent severe SVC syndrome
caused by chronic SVC obstruction
from benign process.
 Acute SVC obstruction caused by
benign or malignant processes
with signs of cerebral or laryngeal
edema.
 Relief of life-threatening SVC
syndrome during palliation of
malignant process.
 Failure of non-operative treatment
to resolve SVC syndrome.
 Tumor or blood clot partially
obstructing SVC or IVC that is
hazardous or impossible to
remove without operation.
Reconstruction is contraindicated in
patients with:
 Adequate collateral circulation to
provide upper compartment
venous decompression.
 Extensive thrombosis of the SVC
and its tributaries such that there
is no suitable vein large enough to
provide outflow from the head
sufficient to decompress venous
hypertension.
 Large, bulky tumors of the
anterior mediastinum.
 Limited life expectancy because of
advanced malignancy or
associated medical disorders.
SPECIAL SITUATIONS AND
CONTROVERSIES
Femoral Vein Graft
Since the original successful bypass
operations were performed in the 1950s,
the femoral vein has rarely been used as a
bypass graft.B4, K5 Gladstone and
colleagues revived the concept of using
autologous femoral vein to construct a
bypass graft in two patients, one with
mediastinal fibrosis and the other with
poorly differentiated carcinoma.G3 After
median sternotomy to confirm feasibility
of the bypass operation, the femoral vein
is exposed from its junction with grater
saphenous vein as far distally as the
adductor hiatus, if necessary. Minor
branches are ligated and the appropriate
length of vein removed distal to the
femoral – saphenous junction. Following
heparinization, the femoral vein graft is
interposed between the innominate vein
and right atrial appendage, as described
for spiral vein graft bypass.
Femoral vein grafts are patent up to 18
months after operation, as reported by
Marshall and Kouchoukos.M3 Addition of a
ringed PTFE tube around the graft
provided external support to prevent
recurrent fibrosis in a patient who had
previously undergone spiral vein bypass.
There has been some concern about leg
edema after femoral vein removal, but
published reports have not indicated this
has been a problem, the real problem
with femoral bypass grafts is their fixed
diameter, which may not match the
inflow vein or may by too small to relieve
obstruction.
Autologous Paneled Saphenous Vein
Graft
Large-caliber venous bypass conduits can
be constructed using saphenous vein is a
composite or paneled manner as first
reported by Benvenuto and colleagues in
1962.B2
The saphenous vein is divided into several
segments, each of which is incised
longitudinally. The segments are
flattened, placed on a stent in a paneled
or tiled manner, and sewn together to
create the conduit. The problem with
paneled composite saphenous vein grafts
is complexity of construction; it is easier
to construct a spiral graft. In addition,
 M. Alaa et al./ Journal of Egyptian Society of Cardiothoracic Surgery 34 (2009)

there are two or more parallel suture lines and suture line irregularity than spiral
at any level of the graft, thereby grafts, which have only one suture line at
subjecting the blood to more foreign body any level.

AUTHOR N Etiology ConduitOperative Early graft Five-year

mortality failures patency
Dartevelle (1991) D2 22 Malignancy PTFE 4.5% 5% 86%
Moore (1991)M8 10 Benign SSVG, PTFE 0% 10% NS
Magnan (1994) M2 10 Both PTFE 0% 0% 86%
Narayan (1998) N2 1 Benign SSVG 0% % NS
Doty (1999)D4 16 Benign SSVG 0% 19% 88%
Calderon( 2001)C1 1 Malignancy PTFE 0% 0% 87%
Kalra (2003) K1 29 Benign SSVG, PTFE 0% 17% 80%
Billing (2003)B3 2 Benign AAHG 0% 0% 50%
Bays (2004) B1 2 Benign PTFE 0% 0% NS
Lau (2006) L2 2 Benign FV 0% 0% NS
Rizvi (2008)R2 42 Benign All 1% 14% 75%
AAHG, Aortic Arch Homograft; FV, Femoral Vein; PTFE, Polytetrafluoroethylene; SSVG, Spiral
Saphenous Vein Graft; NS, Not Stated

Allografts and Pericardial Conduits Non-operative Treatment

In some cases, autologous venous bypass
grafting cannot be accomplished.
Alternative tissue conduits in this setting
include aortic, SVC, or femoral vein
allografts and autologous pericardial tube
grafts. Aortic allografts have excellent
handling characteristics and perform well
when used arterial system replacements.
Aortic or venous allografts have high
patency in many applications in the
thorax. Long-term patency depends on
methods of graft preparation and complex
immune factors. In every case, allografts
should be viewed as palliative and the
graft should be expected to deteriorate
with time. Pericardial venous conduits are
probably no better than, and perhaps not
as good as, prosthetic conduits. On the
other hand, composite pericardial
conduits consisting of pericardium and
pedicled atrium should have a high
probability of remaining patent for a long
time because they include normal
endocardium.
Medical Therapy
Medical measures may be beneficial in
temporarily relieving symptoms of SVC
syndrome, especially in hospitalized
patients. Bed rest with head elevated
gradually brings improvement in most
cases. Diuretics and reduced sodium
intake usually reduce upper compartment
edema. Corticosteroids may be useful in
reducing cerebral edema.
Anticoagulants have been frequently
employed, but effectiveness has not been
demonstrated by controlled trial.P1
They probably are effective in preventing
propagation of clot into caval tributaries,
thereby retarding progression of the
syndrome. Anticoagulants most
frequently used include heparin during
hospitalization and warfarin for long-term
therapy. Long-acting heparin-like
medications (enoxaparin) may prove
beneficial for preventing clot propagation.
Patients best suited for anticoagulant
therapy are those with quiescent benign
disease, such as dormant granulomatous
 M. Alaa et al./ Journal of Egyptian Society of Cardiothoracic Surgery 34 (2009)

mediastinitis, or catheter placement in Chemotherapy

the SVC. Cancer chemotherapy can be effective as
Thrombolytic therapy may be valuable in primary therapy or as an adjunct to
patients with acute thrombosis of the SVC radiotherapy or surgery in selected cases.
if the cause of thrombosis can be Random use of chemotherapy has not
eliminated, such as by removing an been shown to be effective. L4, P1
offending catheter. Gray and colleagues Chemoradiotherapy is beneficial for
reported the Cleveland Clinic experience relieving SVC syndrome caused by
using urokinase or streptokinase for mediastinal lymphoma. Chemotherapy
treating SVC syndrome in 16 patients, 11 alone, using a combination of agents, may
of whom had indwelling venous be the treatment of choice for small-cell
catheters.G4 anaplastic bronchogenic carcinoma, with
Fifty-six percent (CL 40% - 71%) had symptom relief within 7 days. K3, S3 Best
complete clot lysis and relief of results occur with incomplete SVC
symptoms. Success was most likely to be obstruction and with extrinsic
achieved when thrombolytic medication compression from large tumors at the
was infused through the central venous thoracic inlet.
catheters and when thrombus had been
present less than 5 days. Transluminal Balloon Angioplasty and
Stents
Radiation Therapy
Radiation therapy is the primary
treatment modality for thoracic
malignancies causing SVC syndrome.
Because most cases are due to
malignancy, nearly all patients receive
radiation at some point in their clinical
course. This treatment should be
administered only after establishing a
tissue diagnosis of the cause of SVC
obstruction, because only a few patients
have life-threatening cerebral or laryngeal
edema that requires urgent
intervention.S7 Radiation is directed to the
tumor mass, to a 2-cm margin
surrounding it, and to mediastinal, hilar,
and supraclavicular lymph nodes.L4
Radiation is fractionated with the initial
midplane dose 4 Gy for 3 days and then
1.5 Gy per day, until an accumulated 30 to
50 Gy is achieved. Total dose depends on
the patient’s condition, extent of disease,
response of disease to treatment, and
tumor histology.
 M. Alaa et al./ Journal of Egyptian Society of Cardiothoracic Surgery 34 (2009)

Successful transluminal balloon use of intravascular stents.G1 They used

angioplasty and stentingS5 requires that the Gianturco Z self-expanding metallic
the SVC not be completely obstructed device (consisting of a stainless steel wire
because a vascular passageway is needed bent in Z configuration) as a single or
to guide the device. Endovascular therapy double stent in patients with malignancy –
initially relied on balloon angioplasty, induced SVC obstruction. Stents have also
which was successful for benign causes of been successfully used for treating of
SVC obstruction, but rarely so for benign causes of SVC obstruction,
malignant causes. However, the SVC is including stenosis caused by pacemaker
unable to resist external compression by electrodes.F1, L5
tumor or inflammation; therefore, the
report of Gaines and colleagues stipulated
AUTHOR N Restoration of patency Recurrence
Nicholson (1997)N4 76 100% 9%
Gross (1997) G6 13 100% NS
Tanigawa (1998) T1 23 78% 21%
Kee (1998)K4 43 95% NS
Miller (2000) M6 23 82% 17%
Smayra (2001) S8 30 100% 43%
Lanciego (2001)L1 52 100% 6%
Sasano (2001) S1 11 91% 9%
Teo (2002) T2 3 100% NS
Wilson (2002)W2 18 100% 6%
Chatziioannou (2003)C2 18 100% NS
Courtheoux (2003) C4 20 95% 15%
Garcia (2003)G2 44 100% 14%
Urruticoechea (2003) U1 52 100% 17%
Ariza (2003) A3 82 95% NS
Stamatelopoulos (2003)S10 17 98% NS
Yongsong (2003) Y1 9 98% 2%
Kalra (2003) K1 32 96% NS
Tzifa (2007)T4 63 94% 22%
Nagata (2007)N1 71 95% 12%
Rizvi (2008) R2 70 93% 14%

Table 2: Results of endovascular techniques for benign and malignant SVC obstruction
 M. Alaa et al./ Journal of Egyptian Society of Cardiothoracic Surgery 34 (2009)
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