437

Review

Superior vena cava syndrome

Peter Franz Klein-Weigel1, Saban Elitok2, Andreas Ruttloff1, Sabine Reinhold1,
Jessika Nielitz1, Julia Steindl1, Birgit Hillner3, Lars Rehmenklau-Bremer3,
Christian Wrase4, Heiko Fuchs4, Thomas Herold3, and Lukas Beyer4
1
Clinic for Angiology, Interdisciplinary Center of Vascular Medecine, Ernst von Bergmann Klinikum Potsdam, Potsdam, Germany
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2
Clinic for Nephrology, Endokrinology/Diabetology, Ernst von Bergmann Klinikum Potsdam, Potsdam, Germany
3
Radiology, Helios Klinikum Berlin-Buch, Berlin, Germany
4
Diagnostic and Interventional Radiology, Ernst von Bergmann Klinikum Potsdam, Potsdam, Germany

Summary: The superior vena cava syndrome (SVCS) is caused by compression, invasion, and/or thrombosis of the superior
vena cava and/or the brachiocephalic veins. Benign SVCS is separated from malignant SVCS. SVCS comprises a broad clinical
spectrum reaching from asymptomatic cases to rare life-threatening emergencies with upper airway obstruction and increased
intracranial pressure. Symptoms are correlated to the acuity and extent of the venous obstruction and inversely correlated to
the development of the venous collateral circuits. Imaging is necessary to determine the exact underlying cause and to guide
further interventions. Interventional therapy has widely changed the therapeutic approach in symptomatic patients. This article
provides an overview over this complex syndrome and focuses on interventional therapeutic methods and results.

Keywords: superior vena cava syndrome, tumor compression, superior vena cava thrombosis, venous stenting, thrombolysis,
thrombaspiration

Introduction
The superior vena cava-syndrome (SVCS) is caused by
mass compression, tumor invasion and/or thrombosis of
the superior vena cava (SVC). It comprises a broad clinical
spectrum reaching from asymptomatic cases to life-
threatening emergencies [1–4].
In the past SVCS was preferentially caused by compres-
sion of the SVC by syphilitic aortic aneurysms and medi-
astinal lymphadenopathy due to tuberculosis. Nowadays,
compression or invasion of the SVC by malignant tumors
(about 60%) and thrombosis or stenosis caused by central
lines or medical devices (about 30–40%) predominate.
Other underlaying conditions like fibrosing mediastinitis
are rare [1, 5]. Table I lists the common and rare causes
of malignant and non-malignant SVCS.
The following review provides an overview over this
complex syndrome to enable the reader to suspect SVCS
and to support clinical decision making in case of
emergency as well as in elective settings. It will also focus
on interventional techniques as these modalities have
basically changed the therapeutic approach in highly
symptomatic patients [1, 4].
Etiology, anatomy, and
pathophysiology
The venous backflow from the head and upper extremities
usually drains through the right and left brachiocephalic
veins into the SVC and the right atrium. The SVC feeds
about one third of the venous return to the heart. Blood
flow in the SVC is supported by the respiration cycle
(increased flow during inspiration) and by changes of the
tricuspid valve level and atrial geometry associated with
the cardiac cycle.
The average length of the SVC is 7.1 cm ± 1.4, and its
maximum diameter in adults is 2.1 cm ± 0.7 measured by
CT [5]. Obviously, the diameter of the SVC varies with
the volume status [6]. With CE-CT, Lin et al. demonstrated
that the SVC is irregular in shape on cross-sectional images
ranging from 1.5–2.8 cm for the major axis to 1–2.4 cm in the
minor axis [7]. The same authors demonstrated that an
SVC area of less than 1.07 cm2 is indicative for SVC
obstruction or compression [7].
Physiologically, there is no pressure gradient between the
SVC and the right atrium. Gradients up to 3 mmHg are
considered insignificant, while in patients selected for inter-
ventional therapy pressure gradients usually reach double-
digit values in adults, adolescents, and children [8, 9].
Increases venous pressure in the brachial, cervical, and
cerebral veins and leads to venous congestion of the head,
neck, upper thorax, and arms. Furthermore, plethora, respi-
ratory distress due to laryngeal and tracheal edema and/or
headache, visual disturbances, impaired consciousness,
and neurological abnormalities due to increased cerebral
pressure may develop [3, 4]. On the other hand, enlarge-
ment of preformed venous collaterals facilitates venous
backflow and normalizes venous pressure. Thus, the sever-
ity of symptoms in SVCS seems to be directly correlated
to the acuity and extent of the venous obstruction and

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Table I. Contemporary common and rare causes of SVCS
Malignant SVCS
Common causes Non-small cell lung cancer (NSCLC)
Small cell lung cancer (SCLC)
Non-Hodgkin lymphoma (NHL)
Mediastinal metastatic disease
Rare causes Thymoma and other thymic neoplasms
Germ cell neoplasms
Mesothelioma
Esophagus carcinoma
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Thyroid malignoma
inversely correlated to the development of the venous col-
lateral circuits [3, 10, 11].
Collateral pathways in SVCS have been extensively
studied and classified by Stanford and colleagues. [10,
11]. The most important of these is the acygos-hemiazygos
pathway also including intercostal and lumbar veins. SVC
obstructions below the insertion of the azygos vein typically
result in more severe symptoms of SVCS. Other collateral
routes consist of the internal thoracic veins including the
epigastric veins and superficial thoracic veins, the lateral
thoracic route via the superficial circumflex and long
saphenous and femoral vein, and the vertebral and
paravertebral venous system [10, 11]. Rarely, the “hot
quadrate sign”-pathway is activated, which connects
branches of the superior epigastric and internal thoracic
veins to peripheral portal veins of the left hepatic lobe [4].
Based on their venographic findings, Stanfort and
Doty classified the pattern of SVC-obstruction in 4 types
(Table II) according to the degree of SVC-obstruction
and the presence and direction of flow in the azygos-
hemiazygos system [11].
Cardiac output might be reduced in SVCS, especially in
more severe and rapidly developing cases like in acute
SVC thrombosis or rapidly increasing tumor compression,
in cases with pre-existing chronic heart failure, and/or in
cases of mass compression not only of the SVC but also
of the heart and/or pulmonary artery [3, 12].
Nowadays, VCS thrombosis in adults is often induced by
central lines, dialysis access catheters, ports, pacemakers,
or other cardiac devices [1, 3]. In contrast, spontaneous
VCS thrombosis in younger patients is often associated
with major thrombophilia or Behcet’s disease, while in
the elderly malignancy should primarily be suspected
[1, 3, 13–17]. VCS thrombosis might be associated with
pulmonary embolism, which aggravates hemodynamic
consequences and compromises gas exchange, or might
even end-up in a “catastrophic-SVCS” [18, 19].
Malignant SVCS develops in about 2–4% of all lung
cancer patients [1, 4]. Among these, non-small cell lung
cancer is the most common cause (approximately 40–
50%), followed by small cell lung cancer (approximately
20%) [1, 4]. Other tumors often associated with SVCS are
non-Hodgkin-lymphomas (approximately 10–15%), germ
cell tumors, adenocarcinomas, sarcomas, metastatic
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P. Klein-Weigel et al., SVCS
Non-malignant SVCS
Catheter-, port-, or cardiac device-associated thrombosis
SVC-obstruction associated with upper extremity hemodialysis access
Thrombophilia
Morbus Behçet
Infectious related mediastinal granuloma and fibrosing mediastinitis
Aortic aneurysm
Table II. Stanford and Doty types of SVC obstruction
Type of Degree of Flow in
obstruction SVC-obstruction acygos vein
I Partial Antegrade
II Near-complete Antegrade
III Complete Reversed
IV Complete No flow due to complete
obstruction
disease of known or unknown origin, or local tumor
formations like thymomas, thyroid masses, or esophageal
carcinoma [1, 4] (see Table I). Right-sided masses are
generally more likely to cause SVCS for anatomical reasons
[4]. Although there is curative treatment and long-term sur-
vival especially in patients with NHL, the prognosis of SVCS
caused by malignancies is generally poor (life-expectancy is
calculated in months) and primarily determined by the
tumor type, tumor stage, and the therapeutic possibilities,
but does not differ significantly between cancer patients
who develop SVCS and those who don’t [4, 20, 21].
Clinical symptoms and scoring
instruments
The diagnosis of SVCS is based on typical clinical signs.
According to Freidman et al. clinical symptoms of SVCS
can be categorized into neurological, laryngopharyngeal,
facial, and chest wall/upper extremity related. Table III
shows typical symptoms in each of these categories [4].
Typically, symptoms increase in a supine position and
many patients will not tolerate a supine position without
elevating the torso and/or head. Additionally, symptoms
resulting from reduced cardiac filling might be present like
hypotension and syncope, which most often occurs during
coughing or bending [3]. On the other hand, due to good
collateralization only mild symptoms may be present
despite extensive VCS compression [4, 20].
The pattern of collateral veins on the patient’s body sur-
face indicates whether the obstruction is located above or
below the azygos-hemiazygos-outlet and thus whether
there is an increased risk of cerebral and laryngeal edema.
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Table III. Symptoms of SVCS (modified according to Friedman et al.)

Neurological Laryngo-pharyngeal Facial Chest wall/upper extremities

Headache Coughing Nasal stuffiness Neck- and chest wall swelling

Blurred vision Mucosa and tongue swelling and proptosis Conjunctival and periorbital edema Upper extremity swelling
Confusion Stridor Facial edema Distended jugular veins
Decreased level Dyspnoe-orthopnoe Plethora, cyanosis Neck and chest wall collaterals
of conscious

Table IV. Grading System of SVCS proposed by Yu JB et al. [4]

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Grade Category Estimated Definition

incidence (%)

0 Asymptomatic 10 Absence of symptoms

1 Mild 25 Edema and vein distension in the head and neck, plethora, cyanosis
2 Moderate 50 Edema and vein distension in the head and neck, coughing, mild to moderate impairment of head, jaw
or eye lid movement, eye edema with visual disturbances
3 Severe 10 Mild to moderate cerebral edema causing headache and dizziness or/and mild to moderate laryngeal
edema and diminished cardiac reserve with syncope after coughing or bending
4 Life-threatening 5 Significant cerebral edema with confusion or apathy and/or significant laryngeal edema and/or
significant hemodynamic compromise (syncope without provocation, hypotension, renal impairment)
5 Fatal <1 Death

When the obstruction occurs below the azygos channel the
thoraco-epigastric veins and the epigastric veins are dis-
tended and the patient is more likely to develop severe to
life threatening complications [22].
The kind, severity, and temporal development of symp-
toms is important in determining the need and urgency of
an intervention. For this purpose, Yu et al. proposed a grad-
ing system that allows to differentiate between severe, life-
threatening, and non-life-threatening clinical conditions
(Table IV) [3].
As can be derived from Table IV patients with SVCS usu-
ally present in a stable condition and acute fatalities are
extremely rare [3]. Nevertheless, one should keep in mind,
that the grading system developed by Yu et al. implies
stable clinical conditions (as can be seen in slow growing
tumors), while in superimposing acute thrombosis and/or
aggressive tumor growth clinical deterioration of the
patient might develop rapidly.
Another scoring system has been developed to assess the
need for interventional therapy. The Kishi-score system
incorporates neurological, pharyngo-laryngeal, facial,
and vessel signs and symptoms of SVCS [23] (Table V).
A Kishi-score  4 argues for an intervention over con-
servative treatment. However, the kind of obstruction
(thrombosis, tumor entity), alternative treatment options
(anticoagulation, chemotherapy, radiation), and the overall
prognosis of the patient should be appreciated for proper
clinical decision making.
Differential diagnosis
SVCS is sometimes confused with allergic reactions or
Quincke edema. Furthermore, right heart failure, tricuspid
stenosis or -incompetence, constrictive pericarditis,
pericardial effusion/tamponade, and mediastinal emphy-
sema might mimic SVCS [4].
Imaging
Plain X-rays
A substantial number of pathologies especially in tumor
patients can be found on plain X-rays in SVCS [24]. X-rays
might show masses and/or pleural effusions indicative for
malignant SVCS in the case of typical clinical symptoms or
venous catheters or cardiac devices as well as indirect signs
of pulmonary embolism but can neither rule out nor deter-
mine SVCS. Plain X-rays are therefore not recommended in
emergency situations.
Duplex ultrasound
Ultrasound cannot directly image the SVC but might
demonstrate enlarged collaterals [25]. Doppler ultrasound
as well as echocardiography might reveal an obstructive
flow pattern in the proximal subclavian or jugular veins,
in the brachiocephalic veins, or in collaterals [25, 26]. In
patients who already developed intrathoracal collaterals
this flow pattern might be missing. Flow reversal in the
internal thoracic vein was also found to be indicative of
SVC and brachiocephalic vein obstruction [27]. Duplex
ultrasound is not recommended for emergency cases, as
it consumes precious time without defining the pathology
and might be misleading.
Contrast enhanced CT and MRI
The method of choice for imaging SVCS in emergency and
elective conditions is contrast enhanced CT with multiple

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Table V. Kishi-Scoring system for SVCS [27]
Signs and symptoms Weighting
Neurologic
Impaired awareness or coma
Visual disturbances, headache, vertigo
Mental disorders, impaired memory
Malaise
Thoracic, pharyngeal-laryngeal
Orthopnea, laryngeal edema
Stridor, dysphagia or dyspnoe
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Coughing or pleurisy
Facial
Lip edema, nasal obstruction, epistaxis
Facial edema
Vessel dilation
Venous distension neck, face, arms
Notes. Scoring value  4: Interventional therapy should be considered.
phase imaging, as it has a high sensitivity and specificity
and reliably allows to define the underlying pathology
[1, 2, 4, 28, 29, 30]. Contrast enhanced multislice CT is also
suitable for the detection of effusions, metastatic intra- and
extrapulmonary manifestations, assessment of collateral
vasculature [28, 29, 30] and planning of interventional
procedures [28]. CE-MRI might be used as an alternative
diagnostic tool in case of intolerance to iodine contrast
media [4, 30, 31].
Cavography
Formerly, cavography and upper extremity phlebography
was considered as the golden diagnostic standard [1, 4,
31, 32]. It’s strength was the detection of intraluminal pro-
cesses like thrombus formation and the determination of
the degree of obstruction as well as the evaluation of the
collateral pathways, but compared with CE-CT it is less
useful for detecting causes of obstruction other than
thrombi [1]. With modern contrast enhanced CT or MRI
techniques cavography/phlebography is restricted to inter-
ventional therapy. If cavography is performed at least two
projections (posterior-anterior and lateral) are necessary.
Things might appear normal in one projection but turn
out to be pathologic in another perspective [32]. Pressure
measurements might also be helpful in determining the
significance of SVC-lesion (see section Etiology, Anatomy,
and Pathophysiology of Superior Vena Cava-Syndrome).
Establishing tumor diagnosis
of patients who present without
prior diagnosis of malignancy
Approximately 90% of all malignancies in SVCS consist of
lung cancer or non-Hodgkin lymphoma [1, 2, 4]. Sputum
cytology, pleural puncture with fluid cytology, and
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P. Klein-Weigel et al., SVCS
sonographic or CT-guided needle biopsy of lymph nodes
or intrathoracic masses are diagnostic in most cases
[2, 4]. Needle biopsy and bone marrow aspiration may be
required for patients with suspected lymphoma [2, 4]. More
4 invasive procedures like bronchoscopy, mediastinoscopy,
3 video-assisted thoracoscopy, or even thoracotomy may be
2 indicated when a definitive diagnosis cannot be established
1 with minimal invasive procedures [2, 4]. Established stag-
ing strategies depending on the tumor histology should
3 be appreciated.
2
1
Therapeutic strategies
2
1 Figure 1 illustrates the clinical management algorithm for
primary thrombosis and tumor-induced SVCS.
1 Therapeutic decision making in SVCS is determined by
the etiology (thrombus, tumor, miscellaneous), kind of
onset, and severity of symptoms, and the availability of
therapeutic procedures in the institution [4].
In rare cases, patients require emergency diagnosis and
treatment. Nevertheless, most patients present in a rela-
tively stable condition requiring urgent or deferred care
[3, 33].
Head and chest should be kept in an elevated position
and patients should receive supportive care as needed.
Oxygen, diuretics, and steroids are recommended but evi-
dence for their use in symptomatic SVCS is low [4, 34, 35].
Emergency care for grade 4 patients
According to Yu et al. classification system a grade 4
indicates a life-threatening condition defined by confusion
and obtundation indicative for significant cerebral edema
and/or stridor indicating respiratory distress due to laryn-
geal edema and/or hemodynamic compromise indicated
by syncope, and/or hypotension [3, 34].
These patients require intensive care, an emergency
contrast enhanced CT and – depending on the cause of
the compression – emergency stent placement in case of
a tumor compression or emergency thrombaspiration
and/or thrombolytic therapy in case of a thrombotic occlu-
sion of the SVC [34].
Urgent care for grade 3 patients
Grade 3 patients with headache and dizziness or/and mild
to moderate laryngeal edema and diminished cardiac
reserve with syncope after coughing or bending with other-
wise stable hemodynamics need urgent care [3, 34]. They
should be monitored closely in an intermediate care unit
and urgently receive contrast enhanced CT for further
interdisciplinary assessment.
In case of VCS thrombosis anticoagulation should be
initiated and an interdisciplinary vascular medical team
should decide about additional procedures like thrombaspi-
ration and/or thrombolytic therapy as well as their timing.
In tumor patients obtaining a histologic diagnosis
is essential for optimal treatment and further oncologic
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Figure 1. Clinical management of VCS.
decision making but implicates some time delay. Stent
therapy in tumor patients has been shown to provide faster
symptomatic relieve than radiotherapy or chemotherapy
and does not delay or interfere with biopsy [1, 2, 4,
35, 36]. Thus, in a patient with unknown histologic diagno-
sis stenting is now the preferred option for grade 3
patients in many centers, while patients with known radio-
or chemotherapy-sensitive tumors like lymphomas might
preferably be treated with these options [4, 35, 36, 37].
Typical time-intervals for symptom relieve after radia-
tion therapy and chemotherapy in sensitive tumors are
3–14 days, while after stenting symptoms resolve usually
within 0–4 days [4, 35–37].
Figures 2a and 2b show high-grade compression of
the SVC by a large tumor mass (B cell non-Hodgkin
lymphoma) in the ventral and upper mediastinum in a grad
3 patient treated by stent placement with a dedicated
venous stent.
Elective care for grade 1 and 2 patients
In Grade 1 and 2 patients with stable clinical condition
there is always enough time for elective diagnosis and
interdisciplinary treatment decisions in the vascular and
oncologic centers.
Interventional therapy
The first description of stent therapy in SVCS was launched
by Charnsangavej et al. in 1986 [38]. Due to high technical
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441
success rates, acceptable complication and mortality rates,
and almost immediate symptom relief stenting soon
became leading in the management of highly symptomatic
malignant SVC obstruction [39–41].
According to Friedman et al. stenting of the SVC in SVCS
is indicated: (1) In patients with severe acute symptoms
such as respiratory distress from laryngeal edema or airway
obstruction and altered mental status from elevated
intracranial pressure, (2) in patients with persisting moder-
ate symptoms despite radio- and/or chemotherapy, and
(3) in patients with contraindications for chemotherapy
and radiation [4].
The individual anatomy, the exact extent of the tumor-
ous mass, the collateral circulation, and the diameter of
the central veins should be assessed before starting an
intervention using CE-CT or CE-MRI data.
The intervention is usually performed under local anes-
thesia and conscious sedation if necessary [39]. Patients
are kept in a supine position but often need some elevation
of the head and/or upper body.
VSC is usually accessed via a single femoral vein
approach but might be supplemented by vein punctures
of the upper extremities or a jugular access. Venograms
of the bilateral brachiocephalic veins, the confluence
region, and the SVC in at least two planes should be taken
[32, 39].
When simple recanalization techniques with hydrophilic
wires fail, sharp recanalization techniques or the use of
radiofrequency wires have been published, but these tech-
niques cover a substantial risk of hemopericardium or
hematothorax [41, 42].
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(a)
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(b)
Figure 2. (a) Tumor-induced compression of the SVC and the left brachiocephalic vein by a non-Hodgkin lymphoma. Arrows indicate VCS
compression by large mediastinal mass. (b) Cavography showing VCS stenosis and dedicated venous stenting (16 mm) of the VCS.
According to Fagedet et al. thrombosis of the superior
vena cava was the only independent factor for treatment
failure, while the use of stents over 16 mm in diameter
was a predictive factor for complications [43]. Thus, in case
of additional thrombosis thrombolysis or thrombaspiration
prior to stenting should be performed before stent place-
ment (see chapter thrombus aspiration and thrombolysis)
and care must be taken if large stent diameters are used
[39, 41].
Venous stenting and angioplasty are required to achieve
SVC patency [39, 41]. In case of an occluded or highly
compressed SVC predilation with smaller balloon sizes is
necessary. According to the CIRSE Quality Assurance
Guidelines stents should be sized appropriate to the dimen-
sions of the individual patient with many operators over-
sizing stents by up to 2 mm reference vessel diameter, in
a non-involved segment on MDCT or calibrated venogra-
phy, to help reduce delayed stent migration. Optimum
stent length should cover the lesion at least with approxi-
mately 10 mm of free extension at the proximal and distal
margins [39].
Mostly, self-expanding metal stents are used. Stainless
steel stents were identified as inferior to nitinol stents [41,
43]. In their 2014 overview Rachapalli V and Boucher LM
listing all case studies with patient population of more than
50 published in the English literature the stent most often
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P. Klein-Weigel et al., SVCS
placed as the Wallstent (Boston Scientific, Natick, MA,
U.S.A.) [41]. Reports on dedicated venous stents are rare
[44–46]. In these reports and small series dedicated venous
stents performed well with good deployment properties and
achieved comparable results to other self-expanding stents
[44–46]. Dedicated venous stents are characterized by a
higher radial force and flexibility due to unique stent
designs, which implies a theoretical advantage. Moreover,
they are available in larger diameters and greater length
preventing multiple stent placements as a safety margin
of at least 1 cm at both sides of the compressing structure
should be maintained [39]. However, there is no scientific
evidence for superiority of dedicated venous stents so far.
In the overview provided by Rachapalli and Boucher an
overall primary patency rate, secondary patency rate, and
technical success rate of 71%, 95%, and 98% was reported
[41]. In a more recently published series by Büstgens et al.
comprising 141 patients with malignant SVCS the technical
success rate was 97.9% and the primary patency after 30 d
and 180 d was 95.2 and 83.7%, respectively [47]. Moreover,
there were no procedural fatalities [47].
Up to now only one phase II and one phase III controlled
clinical trial has been published to clarify the role of stent
placement in patients with malignant SVCS [48]. In the
phase II trial, 28 patients were treated with stent place-
ment. In the phase III trial, 32 patients were enrolled and
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(a)
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(b)

Figure 3. (a) CE-CT showing port-related complete chronic thrombotic obstruction of the SVC. (b) Phlebography showing collaterals and complete
occlusion of the SVC and left brachiocephalic vein. (c) Recanalization and stenting of the SVC and both brachiocepheal veins (dedicated venous
stents). (d) Final result after recanalization, stenting with dedicated venous stents, and postdilation.

randomly assigned to the stent (n = 16) and control groups
(n = 16). In the phase II trial, the patients’ median symptom
score decreased significantly after the procedure. Techni-
cal success and technical feasibility rates were 96.4% and
100%, respectively. The incidence of major adverse events
was 14.3%. In the phase III trial, significant superiority of
stent placement was observed [48]. The authors concluded
that stent placement should be regarded as first-line proce-
dure, but one should keep in mind the low number of cases
included in these studies.
In case of involvement of both brachiocephalic veins,
only one side needs to be recanalized to gain symptom
relief [41, 49]. In the study published by Dinkel et al. total
occlusion rate and overall complication rate were signifi-
cantly lower in the unilateral group. Patency tended to last
longer in the unilateral group, but the difference was not
significant [49]. Thus, although technically feasible with
kissing stent technique it is inadvisable to primarily aim
for bilateral recanalization in most cases. However, in the
overview published by Rachapalli V and Boucher L-M most
authors obviously preferred bilateral over unilateral stent
placement [41].
Figures 3a–3d show recanalization and kissing-stent-
implantation with dedicated venous stents in a port-related
complete chronic occlusion of the SVC and the left brachio-
cephalic vein.
Some authors reported the use of covered stents as a bail-
out maneuver in iatrogenic injury of the SVC [50]. Based on
the theoretical advantage of prohibiting tumor transmigra-
tion as one possible cause of stent failure [51], some authors
advocated the use of covered stents to prevent this compli-
cation. Gwon et al. first reported improved patency of
unilateral covered stenting using a triple-layered ePTFE-
covered stent in 37 consecutive patients compared with
retrospective data of 36 consecutive patients who under-
went uncovered stent placement for SVC syndrome [52].

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(c)
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(d)
Figure 3. Continued.
Kaplan-Meier analysis revealed that covered stents had
higher cumulative patency (97%, 94%, 94%, and 94% at
1, 3, 6, and 12 months, respectively) than uncovered stents
(97%, 79%, 67%, and 48% at 1, 3, 6, and 12 months, respec-
tively), but clinical success rates did not differ nor did
patients’ survival [52]. In a follow-up publication of the
same group reporting outcomes of 40 consecutive patients
covered stent occlusion occurred in 10% of 40 patents and
cumulative stent patency rates at 1, 3, 6, and 12 months
were somewhat lower than previously reported (95%,
92%, 86%, and 86%, respectively) [53].
The Mayo Clinic study group from Rochester retrospec-
tively compared uncovered with covered stents in benign
SVCS including 59 patients with a mean follow-up of 2.7
years (70% with central line or pacemaker-induced throm-
bosis, 30% with fibrosing mediastinitis) [54]. They found a
significant difference in recurrence of symptoms (29.4% in
the covered stent group, 60% in the uncovered stent group)
and in the mean percent stenosis after stent placement
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P. Klein-Weigel et al., SVCS
between the covered (17.9% ± 26.2) and uncovered
(48.3% ± 33.5) stent group [54]. They found a significant
difference in recurrence of symptoms (29.4% in the cov-
ered stent group, 60% in the uncovered stent group) and
in the mean percent stenosis after stent placement between
the covered (17.9% ± 26.2) and uncovered (48.3% ± 33.5)
stent group [54]. The authors concluded, that covered
stenting seems to be promising, but needs further clarifica-
tion by controlled prospective trials [54].
Stent placement in case of pacemaker
or defibrillator leads
There is no generally accepted consensus how to handle
patients with cardiac devices but to refrain from stent
placement if possible [55].
Leads from pacemakers and other cardiac devices
might cause thrombosis of the SVC or induce a chronic
inflammation of the SVC wall, which might lead to fibrosis
Ó 2020 Hogrefe
 P. Klein-Weigel et al., SVCS 445

(a)
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(b)

Figure 4. (a) Portinduced complete thrombotic occlusion of the SVC. (b) CE-CT after port-directed thrombolysis with 20 mg rtPA.

and stenosis [55, 56]. Risk factors have been identified Special care should be taken with all maneuvers in the
including thrombophilia, the use of hormone therapy, lower half of the SVC as this the pericardium-covered
infection, the presence of temporary stimulation before portion [61].
implantation, and the presence of multiple or retained
leads [56]. Additionally, leads of cardiac devices might
complicate and delay clinical and interventional decision
Interventional management of superior
making in case of malignant SVCS [55]. vena cava syndrome caused by
While some authors prefer retraction of leads and thrombosis
placement of new leads shortly after SVC stenting, some
Presence of thrombosis leads to a change in treatment
advocate implantation of a stent without lead retraction
strategy as thrombosis of the superior vena cava was
[57]. At best, an interdisciplinary preinterventional consen-
identified as an independent predictive factor for stent
sus should be reached between cardiologists and interven-
failure in the study published by Fagedet D et al. [43].
tionalist to manage the problem.
The presence of a thrombus should be anticipated, if SVCS
is associated with central lines, dialysis access catheters,
Complications of SVC stenting
cardiac device wires, more acute onset of symptoms, and
Minor and major complication rates were reported to be
when intraluminal masses can easily be passed by the wire
0–19% [41] and 3.2–7.8% [58] with acute stent thrombosis
[modified according to 62]. Removal by thrombaspiration,
being the most acute major complication [41, 58]. Never-
thrombectomy, local thrombolysis via the central line, and/
theless, potentially lethal complications include SVC perfo-
or catheter-directed thrombolysis should be attempted in
ration, hemopericardium, hemothorax, sinus arrest, stent
highly symptomatic patients while incomplete thrombosis
dislocation into the atrium or pulmonary artery, and
or less symptomatic patients might be treated with antico-
pulmonary edema [4, 41, 43–50, 59]. In an overview pub-
agulation alone [62–66]. Best results for catheter-directed
lished by Nguyen et al. including 884 stent placements in
thrombolysis were obtained when thrombolysis was started
malignant SVCS, 17 deaths occurred (2%) during or shortly
within 5 days [63].
after the intervention [60]. 41% of these lethal events
Figures 4a and 4b illustrate complete port-induced
were attributable to hemorrhages (2 cerebral, 3 pulmonary
thrombosis of the SVC and result after port-directed throm-
and 2 unspecified sites), 23% were lethal cardiac events
bolysis with rt-PA.
(2 arrhythmias, 1 myocardial infarction, and 1 percardial
tamponade), 17% were attributed to respiratory failure, Anticoagulation
while 12% were unattributable and 6% were due to pul- In cases of device-induced thrombosis as well as in pri-
monary embolism [60]. mary thrombosis anticoagulation is indicated at least for

Ó 2020 Hogrefe Vasa (2020), 49 (6), 437–448

 446
3 months according to the actual guidelines [67]. Before
initiating anticoagulation therapy bleeding risks should be
assessed and contraindications should be ruled out [67].
Until now, there is no consensus whether anticoagulation
is beneficial or antiplatelet therapy is necessary to prevent
recurrence after a successful intervention. Retrospective
studies comparing the effect of anticoagulation after stent-
ing in malignant IVCS and in benign causes other than
acute thrombosis where unable to show a substantial
benefit [68, 69]. Unfortunately, prospective studies
addressing this important issue are not available.
https://econtent.hogrefe.com/doi/pdf/10.1024/0301-1526/a000908 - Saturday, April 16, 2022 11:53:38 AM - IP Address:179.14.245.252
In a recent paper published by Razon and colleagues
addressing malignant SVCS, 30 out of 127 patients with
SCVS (24%) showed thrombosis of the SVC or tributaries
[70]. 70% of the patients with thrombosis and 52% of the
patients without thrombosis received anticoagulation,
mostly in therapeutic dosages. During follow-up, there
was no statistical difference in the occurrence of new
thrombosis and there was only a tendency towards less
interventional therapeutic procedures in those receiving
anticoagulation. Major bleeding occurred in 4% of all
patients, six of whom received anticoagulation. Neither
thrombosis nor anticoagulation affected survival [70].
Prophylaxis of non-malignant SVCS
As nowadays the predominating cause of non-malignant
SVCS is catheter- or device associated thrombosis central
lines and catheters should be indicated restaintly. Even
more important, ports should be removed after successful
tumor treatment and not left for years. In device-related
thrombosis, all devices which are not actively used should
be removed after a first thrombotic event as otherwise
the trigger-factor persist.
Conclusions
SVCS is a challenging and complex condition best managed
by strict standard operating procedures and an interdisci-
plinary team approach. In the last decades percutaneous
interventional techniques have emerged and are now con-
sidered first line therapy for highly symptomatic patients in
benign and malignant SVCS. Nevertheless, many questions
remain unsolved and many recommendations remain pre-
liminary because of a lack of scientific evidence, which
should be tackled.
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