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Superior vena cava (SVC) syndrome comprises a constellation of clinical signs and symptoms caused by obstruction of blood flow through the SVC. The management of patients with life-threatening SVC syndrome is evolving from radiation therapy to endovascular therapy as the first-line treatment. There is a paucity of data and societal guidelines with regard to the management of SVC syndrome. This paper aims to update the practicing interventionalists with the contemporary and the evolving therapeutic approach to SVC syndrome. In addition, the review will focus on endovascular techniques, including catheter-directed thrombolysis, angioplasty, and stenting, and their associated complications.

Chronic upper extremity (UE) occlusive disease and superior vena cava syndrome (SVCS) can be debilitating to the patient. Chronic UE venous occlusion is more often because of a benign lesion, whereas SVCS is more likely the result of malignant obstruction. Endovascular treatment with percutaneously placed intravascular stents is increasingly being used to provide relief of symptoms.

Large cell neuroendocrine carcinoma of the ovary (LCNC) is a rare malignancy. We present the first description of superior vena cava syndrome (SVCS) and cardiac tamponade resulting from LCNC. A 58 year-old female with history of recurrent LCNC resulting in SVCS and SVC stent placement, presented

Patient initials or identifier number Tang QS, 45 year old gentleman ### Relevant clinical history and physical exam This 45 year-old man was a case of NSCLC, squamous cell carcinoma, stage IIIB, WGFR wild type, complicated with SVC syndrome, and recurrent laryngeal nerve involvement. He

Thrombosis is a rare cause of superior vena cava (SVC) syndrome. We report a 37-year-old man hospitalized because of swelling of the face and neck. A computed tomography angiography showed a thrombotic obstruction of SVC. The patient was treated by percutaneous transluminal balloon angioplasty of the SVC and placement of a stent. The symptoms disappeared, but the patient was hospitalized again after 3 months for the same complaints. Computed tomography angiography showed thrombosis in the stent in the SVC. The SVC was replaced with a prosthetic blood vessel. The patient's postoperative recovery was uneventful, and SVC syndrome did not occur during 2 years of postoperative follow-up.

Cardiac tamponade is usually a differential diagnosis of SVC syndrome. We discuss management of a case of SVC syndrome presenting with pericardial effusion and tamponade. A 34 year old lady presented with shortness of breath and facial puffiness for 7 days. Examination revealed pulsus paradoxus and

ous tenons a feliciter Da Ines, et al. pour leur evaluation retrospective du « traitement endovasculaire du syndrome cave superieur (SCS) d’origine neoplasique a propos de 34 patients » (1). Celui-ci fait etat d’un taux de permeabilite primaire et secondaire de 80 et 100 % respectivement, sans echec technique, et de 5,8 % de complications majeures. Nous aimerions faire part de notre experience complementaire qui utilise des endoprotheses Gianturco en acier (COOK, Charenton le Pont, France) et Smart en nitinol (Cordis, Issy-Les Moulineaux, France) a propos de 78 patients oncologiques. Si le cliche thoracique identifie la cause tumorale dans plus de 80 % des cas, sa « normalite » fait discuter les causes benignes, notamment la thrombose cruorique et la stenose post-radique (2, 3). Nous utilisons toujours l’echographie Doppler en pre-operatoire afin de selectionner et guider l’abord veineux percutane, et predefinir le siege de l’obstruction. En effet, l’analyse de la courbe Doppler des veines sousclavieres et jugulaires internes (4) ainsi que l’inversion du flux veineux thoracique interne (5) sont d’excellents signes indirects d’obstruction cave superieure. En outre, le SCS etant souvent revelateur (53 % dans l’etude (1)), l’echographie permet la realisation rapide de la ponction percutanee d’une lesioncible dont le resultat histologique permet de predire la sensibilite au traitement. En effet, en cas de lymphome ou de carcinome a petites cellules, l’urgence est-elle plus a la pose d’une voie veineuse centrale qui permet a la chimiotherapie de reduire rapidement la compression mediastinale. Enfin, la reapparition des anomalies Doppler decrites confirme la recidive du syndrome cave superieur lors du suivi. En scanner multi-coupes, nous utilisons les reformations de type MIP (parfois obliques) dans l’axe veineux cave qui precise, mieux que l’angiographie, l’etendue exacte de l’obstruction (atteinte de la convergence innominee et de la veine sous-claviere soulevant le risque de fracture prothetique et de permeabilite jugulaire), la nature et le degre d’obstruction cave, le stade phlebographique pronostique (flux azygos, occlusion cave ou des affluents) (6), et la presence d’elements aggravants associes ; tamponnade pleurale, pericardique, atelectasie, fibrose post-radique, thrombose extensive et embolie pulmonaire. Comme Da Ines et al, nous preferons egalement la thrombectomie mecanique a la fibrinolyse in situ, potentiellement plus iatrogene et recommandons, dans le deuxieme cas, l’IRM cerebrale a la recherche de metastases cerebrales infra-cliniques (7). La gravite du SCS est fonction de la rapidite d’installation du syndrome, de l’absence de developpement de collaterales veineuses, et de la presence de lesions et tares associees du patient. Les stades 3 et 4 de la classification de Stanford (6) et une pression d’amont > 22 mm Hg sont les elements radiologiques de gravite qui nous incitent a poser l’indication de stenting, d’autant plus que le syndrome cave superieur est cliniquement mal tolere. Dans notre experience exclusivement effectuee sous anesthesie locale, le succes immediat radiologique (reouverture de la stenose, regression de la circulation collaterale) est corrobore par l’amelioration sensible de la saturation d’oxygene et une sensation de « mieux-etre » du patient. Comme l’a recommande la SFICV, nous prescrivons un traitement anticoagulant. Notre choix va actuellement au Fondaparinux sodique, qui n’induit pas de risque thrombopenique et n’interfere pas avec les produits de chimiotherapie. Son inconvenient actuel est de ne pas avoir l’autorisation d’utilisation au long cours. Contrairement aux endoprotheses de Wallstent utilisees par Da Ines et al, les endoprotheses Gianturco (50x30mm, double corps, introducteur 11French, Cook) ont une expansion lente (48 heures), adaptees aux stenoses rectilignes de l’axe droit qui representent plus de 80 % des cas (fig. 1) (1). La prothese Gianturco « monocorps » presente un fort risque d’« expulsion » brutale en cas de stenose courte et ne doit pas, a notre sens, etre utilisee. Les « triples corps » de Gianturco sont egalement de maniement difficile et exposent au risque de fracture sous-claviculaire et/ou de protrusion intra-atriale. En cas de stenose veineuse tortueuse serree etendue a la veine sous-claviere ou a l’axe gauche, nous utilisons preferentiellement les protheses en nitinol, de diametre maximal limite a 16 mm Smart (Cordis) (fig. 2). Leur positionnement percutane est accessible a l’operateur junior, offrant un calibrage immediat sans raccourcissement y compris en region sous-claviculaire. Le succes technique eleve du traitement cave percutane ne doit pas occulter la survenue de complications majeures. Celles-ci sont cliniquement de deux ordres : la recidive du SCS (thrombose du stent, fracture, migration) et le choc cardio-vasculaire avec jugulaires distendues. Ce dernier comprend trois diagnostics etiologiques : l’embolie pulmonaire, l’OAP et la tamponnade pericardique. Certains ont decrit l’interet de la thromboaspiration in situ ou de la fragmentation par rotation du catheter pig-tail, en cas d’embole pulmonaire tronculaire. La disparition du troisieme secteur œdemateux genere par l’hyperpression

There has been an increase in superior vena cava (SVC) syndrome secondary to the growing use of indwelling catheters and pacemaker wire insertions. These 2 factors can account up to 74% cases of benign SVC syndrome. Endovascular therapy is considered the first line of treatment. Surgery is an excellent option and is generally reserved for SVC syndrome not amenable to traditional endovascular procedures. We report a case of central venous reconstruction including an SVC reconstruction using the femoropopliteal vein as a panel graft in a patient with SVC syndrome due to pacemaker wires who failed multiple endovascular interventions.

The symptoms of superior vena cava (SVC) obstruction can be extremely debilitating, and current medical and surgical treatments have been only partially successful in providing relief to afflicted patients. Endovascular techniques of venous recanalization have recently shown excellent short-term and mid-term success in patients with both benign and malignant causes of SVC obstruction. Endovascular therapy may be reasonably used as a first-line approach to the palliation of malignant SVC obstruction, and its mid-term patency rates compare favorably with those of modern surgical methods of venous bypass in patients with benign SVC obstruction. In this article, the percutaneous management: of SVC syndrome is discussed, with particular attention to the anatomical considerations and clinical priorities that impact endovascular decision making.

Abbreviation: SVC 5 superior vena cava PERCUTANEOUS stent placement in the superior vena cava (SVC) has evolved as an attractive alternative to traditional therapies for benign and malignant SVC syndrome (1– 6). Symptomatic stenosis or occlusion of the SVC is a rare but wellrecognized complication of transvenous permanent pacemaker implantation (7,8). Several factors may increase the occurrence of venous thrombosis related to a pacemaker. The presence of more than one lead has been associated with a higher likelihood of SVC obstruction (9,10). Retention of a severed lead or previous lead infection have also been implicated as potential etiologic factors (11). Little information is available about the effect of stent placement over pacemaker wires in the SVC (12,13). We report our experience with placement of SVC stents over pacemaker wires to treat SVC syndrome.

A case of aberrant right subclavian artery (RSA) aneurysm presenting solely with symptoms and signs of superior vena cava obstruction (the SVC syndrome) is described. The SVC syndrome is usually a consequence of mediastinal malignancy and only rarely due to compression by an arterial aneurysm.

Relief of superior vena cava (SVC) syndrome due to non-neoplastic mediastinal disease presents a formidable challenge. Long-term patency of surgically created bypass grafts has been poor, and the morbidity associated with these procedures is substantial. We report a case of SVC syndrome, caused by fibrosing mediastinitis, treated with Palmaz balloon expandable intravascular stents. Intravascular stents are a promising alternative for relief of non-neoplastic SVC obstruction.

Superior vena cava (SVC) syndrome is most commonly due to direct compression of the SVC by a tumor. Recently, there has been an increase in the number of cases of SVC syndrome associated with chronic indwelling central venous catheters. We present a case history of a patient with prolonged symptoms of SVC syndrome that was successfully treated with catheter-directed (intraclot) infusion thrombolytic therapy with urokinase. The treatment, prevention, and incidence of SVC syndrome caused by thrombosis associated with catheters is discussed. (J V ASC S URG 1994;20:108-13.)

Superior vena caval (SVC) syndrome may be caused by extravascular compression or intravascular obstruction. Knowing the mechanism of SVC syndrome enables the physician to choose appropriate treatment. Transesophageal echocardiography (TEE) is a safe bedside procedure that is excellent for evaluating the SVC and its surrounding structures. We report the valuable role of TEE in demonstrating the mechanism of SVC syndrome.