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34
Superior Vena Caval Obstruction
Enrico Ascher and Anil Hingorani
Division of Vascular Surgery, Department of Surgery, Maimonides Medical Center,
Brooklyn, New York, U.S.A.
ETIOLOGY
The initial paper on superior vena caval (SVC) obstruction was reported in 1757 by
William Hunter in a case caused by a syphilitic aortic aneurysm (1). Presently, the most
common cause of this syndrome is malignancy (80–90% of presentations) (2). The most
frequent reported malignancy causing this syndrome is bronchogenic cancer; however
many other types of mediastinal neoplasms have also been cited to cause this syndrome
including lymphomas, thymomas, teratomas, germ cell tumors, metastatic tumors etc.
Benign causes of this syndrome consist of mediastinal fibrosis (greater than 40%
of the benign cases), graulomatous disease such as histoplasmosis and sarcoidosis,
constrictive pericarditis, aneurysms of the aortic arch, prior radiation, retrostenal goiter,
thrombophilia, dialysis access, Bechet’s disease (3) and idiopathic thrombosis. The
increased use of short- and long-term venous catheters and pacemakers make their usage a
factor as well (4,5).
PRESENTATION
The most common presenting symptoms of SVC obstruction are fullness of the head
or neck. These symptoms may become more severe when the patients bends over or lies
flat in bed. Other patients may also present with dyspnea, othopnea, tongue swelling,
nasal stuffiness, stridor or cough. Additionally, nausea, dizziness, and mental confusion,
headache, visual disturbance or syncope may result from cerebral venous hypertension.
In the worst case scenario, this can result in cerebral edema and cerebellar herniation.
Physical signs consist of head swelling, prominent chest wall and neck collateral
vessels, facial cyanosis, proptosis, arm swelling, stridor, hoarseness, respiratory distress,
conjunctival edema and ecchymosis. SVC syndrome can also result in laryngeal and
airway edema.
The determinant factors in the severity of symptoms include duration, progression,
extent of venous occlusive disease and the amount of collaterals that develop. The major
collaterals that develop involve the azygos and hemiazygos veins, and these can be
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established only if obstruction occurs below the entrance of the azygos vein into the SVC.
Lumbar veins subsequently drain into the inferior vena cava. The second pathway involves
the internal mammary venous system, with its tributaries and communication with the
inferior epigastric vein. The third and fourth collateral routes include the thoracoepigastric
vein, with its connection to the saphenous vein, and the vertebral veins (6).
DIAGNOSIS
The initial work-up begins with a detailed history and physical examination. Chest X-ray
and computed tomography with intravenous contrast are the mainstays of the diagnostic
testing that is needed. Currently, magnetic resonance venography plays a limited role.
Duplex scans can assess the patency of the internal jugular vein for an inflow vein.
However, invasive procedures such as brochoscopy, mediasinoscopy, thorascopy,
throrocotomy or median sternotomy may be needed to provide tissue diagnosis.
If surgical reconstruction is planned, diagnostic venography via simultaneous injection
of bilateral superficial arm veins is mandatory.
TREATMENT
The first SVC bypass was reported in 1951 (7). In 1974, Chiu et al. (8) helped to further
progress this field when they first suggested autologous spiral vein grafts for replacement
of larger veins. However, it was Doty et al. (9–11) who established this technique for
reconstruction of the occluded SVC using autologous saphenous vein.
Initial conservative therapy consisting of head elevation, anticoagulation, oxygen,
steroids and diuretics can at times relieve acute SVC syndrome. If this therapy is
unsuccessful, the additional types of treatment are determined by evaluation of the
underlying cause(s) of the SVC syndrome. In benign and malignant causes, thrombolytic
therapy can also be used to help resolve acute thrombosis (12,13).
Additionally, in malignant SVC syndrome, if conservative therapy and radiation or
chemotherapy fail to resolve the symptoms, some authors have suggested that good short-
term results can be obtained with endovascular therapy (14–17). However, for malignant
SVC syndrome following balloon angioplasty, stents are needed to avoid early restenosis
and recurrence. A pressure gradient should be measured before and after the intervention
to document the benefit of the intervention in addition to the documentation of resolution
of the clinical symptoms.
Since many of these patients have a limited life span and the endovascular therapy is
minimally invasive, the role of open surgery in this patient population has been limited to
patients with a life expectancy of greater than one year (such as cases of lymphoma,
thymoma, metastatic medullary or follicular carcinoma of the thyroid). In patients with
residual carcinoma, some authors have suggested that using PTFE for the bypasses as this
would be less likely to be compressed by recurrence (18).
It has been suggested that the type of therapy to be employed is affected by the
anatomy of the lesion. Venographic classification of SVC syndrome has been divided into
four types (19). Type I has a !90% stenosis of the SVC with patency and antegrade flow of
the azygous-right atrium pathway. Type II has a O90% stenosis or occlusion of the SVC
with patency and antegrade flow in the azygous-right atrial pathway. Type III has O90%
stenosis or occlusion of the SVC with reversal of azygous blood flow. TypeIV hasocclusion
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of the SVC and one or more other caval tributary including the azygous systems. Some
authors have suggested using endovascular therapy for type I and II lesions (20).
Open surgical bypass has been largely employed for benign disease. The types of
conduits that have been used include: spiral vein graft, superficial femoral vein bypass,
human allograft, PTFE and pericardial tube graft (21). When using a spiral vein graft,
some authors, when dealing with fibrosing mediastinitis, have suggested external support
with a PTFE graft to prevent extrinsic compression due to the recurrence (18).
To construct a spiral saphenous vein bypass graft (SSVG), the saphenous vein is
harvested and opened longitudinally, and valve leaflets are excised under loop
magnification. The opened vein is wrapped around a 32F or 36F polyethylene chest
tube, and the edges are stapled or sutured with 7.0 continuous monofilament nonabsorbable
suture, interrupting the suture line every three-quarter turn. To obtain adequate length as in
those patients where the SSVG originates from the internal jugular vein, the saphenous
vein from both legs often has to be harvested. The additional operating time required to
prepare a 10 cm long spiral vein graft ranges been between 60 and 90 minutes. This is
performed while a separate team performs the median sternotomy (22). If clamping of the
vessels result in hemodynamic changes with an increase in the venous pressure greater than
30 mmHg, one may consider using a temporary venovenous shunt (21).
If the peripheral anastomosis is performed to the subclavian vein or more distally, an
addition of a brachial artery arteriovenous fistula is suggested to maintain patency. If the
peripheralanastamosisis performedto the internal jugular vein, a veinconduitfor thebypassis
needed as the relatively low flow in this system will not maintain patency. If the greater
saphenous vein is not available, some authors have used the superficial femoral vein with
good results (7,23–25). In general the patency of these bypasses has been better with vein as
compared to PTFE. However, PTFE with a minimum diameter of 10 mm has been used with
good results for the lesions 5–10 cm long (26). These bypasses and endovascular procedures
only need to decompress one side even with bilateral innominate vein thrombosis, as
collaterilization across the midline is adequate to decompress both sides with a single
graft (27).
Post-operative heparin is started in 24–48 hours and then long-term coumadin is
initiated. If a vein graft was used, then only three months of coumadin is needed. Life-long
anticoagulation is used if PTFE was used for the bypass or if the underlying disorder is a
hypercoaguable state (6).
With both endovascular and open procedures, long term patency can be maintained
with surveillance (28). Gloviczki et al. (6) have suggested venography as a surveillance
tool. Attempts at checking patency with contrast tomography and magnetic resonance
venography does not seem to offer the needed resolution, and lesions can be missed. With
these surveillance techniques, often patency can be extended with secondary endovascular
procedures. Therefore, surveillance with venography every three months for one year is
essential. After one year, venography is needed if symptoms recur (6).
Often the immediate results in terms of the resolution of the symptoms can be quite
prompt and dramatic, and the patients can be some of the most grateful, which can make
treating these patients a most rewarding experience.
KEY POINTS
† The superior vena cava obstruction is due to malignancy in 80–90% of cases.
† Patients usually present with head swelling, prominent chest wall and neck
collateral vessels, facial cyanosis, proptosis, arm swelling, stridor, hoarseness,
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respiratory distress, conjunctival edema and ecchymosis and sometimes with
laryngeal and airway edema.
† Chest X-ray and computed tomography with intravenous contrast are the
mainstays of the diagnostic testing that is needed.
† Conservative therapy consists of head elevation, anticoagulation, oxygen,
steroids and diuretics.
† Good short-term results can be obtained with balloon angioplasty and stenting.
This is usually done for patients with limited life span.
† Surgery with various types of grafts is performed in patients with benign disease.
ACKNOWLEDGMENT
Special thanks to Anne Ober for editorial assistance.
REFERENCES
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gerneral. Med Obsinq 1757; 1:323–357.
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11. Doty DB. Composite spiral saphenous vein graft for occlusion of the superior vena cava. In:
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occlusive disease. Ann Vasc Surg 2005.
13. Bornak A, Wicky S, Ris HB, Probst H, Milesi I, Corpataux JM. Endovascular treatment of
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14. Kee ST, Kinoshita L, Razavi MK, Nyman UR, Semba CP, Dake MD. Superior vena cava
syndrome: treatment with catheter-directed thrombolysis and endovascular stent placement.
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16. Thony F, Moro D, Witmeyer P, et al. Endovascular treatment of superior vena cava obstruction
in patients with malignancies. Eur Radiol 1999; 9:965–971.
17. Young N, Yeghiaian-Alvandi R, Chin YS. Use of endovascular metal stents to alleviate
malignant superior vena cava syndrome. Intern Med J 2003; 33:542–544.
18. Marshall WG, Kouchoukos NT. Management of recurrent superior vena caval syndrome with
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superior vena cava obstruction. Ann Thorac Surg 1986; 41:158–163.
20. Dondelinger RF, Trotteur, G. Expandable stents in the venous system. Abstracts of the
International Symposium, Leuven, Belgium. 1996.
21. Seelig MH, Oldenburg WA, Klingler PJ, Odell JA. Superior vena cava syndrome caused by
chronic hemodialysis catheters: autologous reconstruction with a pericardial tube graft. J Vasc
Surg 1998; 28:556–560.
22. Kalra M, Gloviczki P, Andrews JC, et al. Open surgical and endovascular treatment of superior
vena cava syndrome caused by nonmalignant disease. J Vasc Surg 2003; 38:215–223.
23. Hagino RT, Bengtson TD, Fosdick DA, Valentine RJ, Clagett GP. Venous reconstructions
using the superficial femoral-popliteal vein. J Vasc Surg 1997; 26:829–837.
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an externally supported femoral vein bypass graft. Ann Thorac Surg 1988; 46:239–241.
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35
Congenital Venous Malformations:
Venous Tumors
Sachiendra V. Amaragiri
Freeman Hospital, University of Newcastle upon Tyne, Newcastle upon Tyne, U.K.
Nicos Labropoulos
Vascular Laboratory, Division of Vascular Surgery, New Jersey Medical School, Newark,
New Jersey, U.S.A.
CONGENITAL VENOUS MALFORMATIONS
When one considers that venous anatomical variations are common, it is surprising that
congenital venous malformations are seen quite uncommonly in specialist venous clinics.
There is a wide spectrum of congenital variation—absence of major veins, incomplete
development, multiple vessels, dextra-position of vessels and hereditary diseases.
Attempts are being made to map the genetic signatures for these venous malformations
but no single chromosome or gene has yet been implicated. There is however evidence that
some of the hereditary forms are associated with some chromosomal defects, but the
findings have not been consistent. Awareness of these anomalies, such as double inferior
vena cava, left side inferior vena cava, etc., have implications in surgical practice,
especially for vascular surgeons and radiologists. Some of these such as venous aneurysm,
agenesis, congenital and hereditary anomalies, etc., are associated with complications
such as varicose veins, thrombosis, embolism, and the secondary effects of venous
thrombosis—venous hypertension leading to chronic venous disease.
Venous Aneurysm
There are numerous published case reports of venous aneurysms but it a relatively rare
disorder. The term venous aneurysm is synonymous with the terms phlebectasia, venous
congenital cyst, venous ectasia and essential venous dilatation. It is an isolated abnormal
fusiform or saccular dilatation of a vein. They are either primary, which is idiopathic
(congenital), or secondary due to trauma.
Venous aneurysm differs from varicose vein in that it is a solitary lesion that can
affect any vein and there is no associated venous elongation as in a varicosity. It has no
relation to sex and it can occur at any age and has been reported even in a child as young as
2 years (1).
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