Cause Of Superior Vena Cava Syndrome Research Articles

In-hospital outcomes of patients with lung cancer with and without superior vena cava thrombosis: A nationwide analysis.

e23322 Background: Malignant superior vena cava syndrome (SVCS) is a clinical problem that results from the obstruction of blood flow in the superior vena cava by an underlying malignancy. It may be caused by external compression or internal obstruction due to a thrombus or direct invasion by tumor cells. Though lung malignancy is the most common cause of SVCS, there is a lack of data on in-hospital outcomes in these patients. Methods: We queried the National Inpatient Sample 2018-2020 to identify hospitalizations with lung cancer including both small cell and non small cell lung cancer. Hospitalizations with diagnosis of acute SVC thrombosis were determined by using ICD-10 codes.Demographics and mortality rates were compared between two groups using chi square for categorical variables and t test for continuous variables. Multivariate regression analysis was further performed to study the impact of SVC thrombosis on mortality, LOS and total hospitalization cost. Results: A total of 2011620 hospitalizations with lung cancer were identified. Of these, 2855 (0.0014%) had acute SVC thrombosis. These patients were younger with a mean age of 63 years. African-Americans and Hispanics were in a higher proportion in the cohort of hospitalizations with SVC thrombus as compared to those without. (Table 1). Multivariate regression analysis revealed higher odds of mortality (OR-1.94; C.I: 1.53-2.47; P < 0.001), LOS (OR 1.66; C.I:1.20- 2.31; P < 0.005) and total hospitalization cost (26211.15; C.I:22183.56- 30238.74; P < 0.001) in lung cancer hospitalizations. Conclusions: Our study shows that SVCT, has higher odds of mortality, length of stay and total hospital cost. Though the general recommendation is to continue anticoagulation, sometimes patients may require endovascular stent placement with/without thrombectomy. Though rare, SCVT can be life threatening and requires prompt attention.[Table: see text]

Focal hepatic hot spot sign: Clinical image

A 51‐year‐old women was hospitalized to start chemotherapy for small cell lung cancer diagnosed one months earlier. She underwent Computed Tomography (CT) of the chest and abdomen to re‐evaluate the progression of the lung tumour. Contrast-enhanced CT of the chest indicated an invasive anterior left lung tumour that caused an obstruction of the Superior Vena Cava (SVC) (Figure 1). Contrast-enhanced CT of the abdomen revealed an intense focal wedge-shaped homogeneous enhancement area in the quadrate lobe of the liver, which is known as the hot spot sign (Figure 2). Focal hepatic hot spot sign was first described by Ishikawa in 1983. The sign can be observed on technetium 99m (99mTc) Sulphur colloid scans or on contrast, material enhanced CT scans [1]. Hot spot sign is caused by portosystemic venous shunting between the superior vena cava and the left portal vein via the internal mammary and paraumbilical veins along the ligamentum teres, secondary to superior vena cava obstruction. The hot spot is created by areas of focally increased blood flow that result from this shunting [2]. Stanford and colleagues classified SVC syndrome into four types - type I and type II referred as supra-azygous partial and near complete obstruction of SVC with antegrade flow in azygous vein. Type III is defined as complete obstruction of SVC with reversal of azygous blood flow and type IV as complete obstruction of SVC and azygous system with development of chest wall collaterals [3]. This sign has been reported in Budd-Chiari syndrome, the causes of SVC syndrome (neoplasms of the thorax as lung carcinoma and lymphoma, Vasculo‐Behcet’s disease, fibrosing mediastinitis, and luetic aneurysm), and masses of the liver (abscess, haemangioma, focal nodular hyperplasia, and hepatocellular carcinoma) [4].

SAT486 A Case of Superior Vena Cava Syndrome Caused by Untreated Multinodular Goiter

Abstract Disclosure: K. Blanchard: None. C. Musurakis: None. A. Ojha: None. C.P. Barsano: None. A. Havrylyan: None. A 92-year-old female with heart failure, COPD, obstructive sleep apnea, longstanding exertional dyspnea, and a 15-year history of a toxic multinodular thyroid on methimazole presented to our emergency department with one week of right arm swelling. Physical exam showed a 4 cm midline goiter with right-sided jugular venous distention and right upper extremity pitting edema. On admission, TSH, free T4 and free T3 levels were within normal limits on methimazole 5 mg daily. PTT, PT and INR were normal. Thyroglobulin antibodies and TSI measured two years prior were normal. Right arm venous duplex was negative for acute deep venous thrombosis (DVT) but showed heterogenous structures in the right neck with collateral vessels, likely related to a large multinodular thyroid gland with substernal extension. Left arm venous duplex showed chronic sequela of DVT in the left central subclavian vein. Chest x-ray revealed right-sided tracheal deviation due to goiter. A CT chest performed 6 months prior revealed a massive multinodular goiter with mass effect on the trachea, narrowing the tracheal opening to only 7 mm (ref 10-21 mm in females) and significant mass effect upon adjacent venous structures with resultant collateralized flow. Of note, the patient has a 15-year documented history of this goiter and repeatedly declined aggressive surgical intervention. We recommended ENT consultation for minimally invasive treatment options. ENT recommended thoracic surgery evaluation at a tertiary center and suggested tracheal stenting as a possible solution. Regarding the chronic left subclavian vein thrombosis, the patient opted to forego anticoagulation therapy after discussion of risk versus benefit. She again declined surgical evaluation and was discharged home with primary care and Endocrinology outpatient follow-up. Superior vena cava (SVC) syndrome is the result of either a partial or complete obstruction of the SVC, resulting in symptoms such as upper extremity swelling, dyspnea, cough, face or neck swelling, and dilated venous collaterals in the chest. Compression of the SVC by a mediastinal malignancy is the most common cause of SVC syndrome. However, retrosternal goiter as a cause is extremely rare, with only a few cases previously reported in the literature. Interestingly, the incidence of malignancy in retrosternal goiters is reported to be as high as 35 percent. Large intrathoracic goiters are primarily seen in long periods of neglected disease, as in our patient. The presence of a substernal goiter, regardless of symptoms, is an indication for thyroidectomy, as this is the only way to prevent mediastinal enlargement of the goiter. Non-surgical treatment options documented in the literature include temporary tracheal stent placement followed by radiofrequency thyroid ablation and ultrasound-guided needle aspiration of a dominant thyroid cyst. Presentation Date: Saturday, June 17, 2023

Superior Vena Cava Syndrome: An Umbrella Review.

Superior vena cava syndrome (SVCS) is a medical emergency that encompasses an array of signs and symptoms due to obstruction of blood flow through the superior vena cava (SVC). It poses a significant healthcare burden due to its associated morbidity and mortality. Its impact on the healthcare system continues to grow due to the increasing incidence of the condition. This incidence trend has been attributed to the growing use of catheters, pacemakers, and defibrillators, although it is a rare complication of these devices. The most common cause of SVCS remains malignancies accounting for up to 60% of the cases. Understanding the pathophysiology of SVCS requires understanding the anatomy, the SVC drains blood from the right and left brachiocephalic veins, which drain the head and the upper extremities accounting for about one-third of the venous blood to the heart. The most common presenting symptoms of SVCS are swelling of the face and hand, chest pain, respiratory symptoms (dyspnea, stridor, cough, hoarseness, and dysphagia), and neurologic manifestations (headaches, confusion, or visual/auditory disturbances). Symptoms generally worsen in a supine position. Diagnosis typically requires imaging, and SVCS can be graded based on classification schemas depending on the severity of symptoms and the location, understanding, and degree of obstruction. Over the past decades, the management modalities of SVCS have evolved to meet the increasing burden of the condition. Here, we present an umbrella review providing an overall assessment of the available information on SVCS, including the various management options, their indications, and a comparison of the advantages and disadvantages of these modalities.

Interventions for superior vena cava syndrome.

Superior vena cava (SVC) syndrome refers to the clinical manifestations of cerebral venous hypertension secondary to obstruction of the SVC and/or the innominate veins. The most common cause of SVC syndrome is malignancy like small cell lung cancer and non-Hodgkin lymphoma, but there is an increasing trend of benign etiologies secondary to thrombosis due to central lines/ pacemakers or mediastinal fibrosis. Supportive measures include head elevation, diuresis, supplemental oxygen, and steroids. Thrombolysis with or without endovenous stenting is required emergently in those with airway compromise or symptoms secondary to cerebral edema. Definitive treatment in those with malignancy is multidisciplinary; this requires radiotherapy, chemotherapy, SVC stenting, oncologic surgery and SVC bypass or reconstruction. Endovascular treatment is the primary modality for palliation in malignancy and in those with benign etiology. Surgery is reserved for those who have failed or are unsuitable for endovascular treatment. In patients with benign disease endovenous stenting and open surgery provide excellent symptom relief and are safe and effective.

Superior vena cava syndrome management in limited source setting: a case report

Superior vena cava syndrome (SVCS) is syndrome caused by mass compression, tumor invasion, and/or thrombosis of SVC. In the past, SVCS was mostly linked to infection. Nowadays, SVCS is mostly linked to malignant tumor and medical procedures. Most common malignant cause of SVCS is non small cell lung cancer. A 69-year-old man was presented with breathing difficulty. Symptom began 4 months before admission, with worsening of symptom since 2 weeks before admission. Symptom improved with sitting position, and worsened with supine position. Patient had been sleeping with 2 pillows. Patient had productive cough and hoarseness. Swelling of face and neck were present. Collateral vein distention was visible in the area of head, neck, and chest. Physical examination of lung revealed decreased vesicular breath sound at right side. Non pitting edema was found at both sides of upper extremity. SVCS in this case can be categorized into grade 2, chronic SVCS case. CT showed center right lung mass, although malignant cells were not obtained from pleural puncture and CT guided needle biopsy. Staging of mass was T4N3M1a. Mass finding at the center of right lung is in accordance with the previous findings that SVCS generally arise from lung (not mediastinum), and that right sided masses are generally more likely to cause SVCS. Management in this case was done by giving corticosteroid and diuretic. Surgery, radiotherapy, and immunotherapy were not done since malignancy diagnosis hadn’t been able to be concluded.

The Role of Extracorporeal Membrane Oxygenation in the Anesthetic Management of Superior Vena Cava Syndrome: Is it Time to Use a Scoring System?

SUPERIOR VENA cava (SVC) syndrome is characterized by a mechanical obstruction to the SVC, decreasing preload to the heart and causing the constellation of neck vein distention, facial, and upper extremity edema, and sometimes cerebral edema. 1 Kishi K Sonomura T Mitsuzane K et al. Self-expandable metallic stent therapy for superior vena cava syndrome: Clinical observations. Radiology. 1993; 189: 531-535 Crossref PubMed Scopus (109) Google Scholar ,2 Qanadli S El Hajjam M Bruckert F et al. Helical CT phlebography of the superior vena cava: Diagnosis and evaluation of venous obstruction. Am J Roentgenol. 1999; 172: 1327-1333 Crossref PubMed Scopus (53) Google Scholar Malignancy has been the historic cause of SVC syndrome, although there has been a shift toward nonmalignant etiologies accounting for up to half of cases. 3 Nossair F Schoettler P Starr J et al. Pediatric superior vena cava syndrome: An evidence-based systematic review of the literature. Pediatri Blood Cancer. 2018; 65: e27225 Crossref PubMed Scopus (12) Google Scholar ,4 Siegel Y Kuker R. Superior vena cava obstruction in hemodialysis patients: Symptoms, clinical presentation and outcomes compared to other etiologies. Ther Apher Dial. 2016; 20: 390-393 Crossref PubMed Scopus (5) Google Scholar Malignancies arising in the anterior mediastinum are well-known to cause SVC syndrome by direct tumor invasion or SVC compression. These typically advanced tumors also may cause external compression of the respiratory tract, complicating mechanical ventilation and the provider's options for securing an airway sufficient for ventilation and oxygenation. 5 Straka C Ying J Kong F et al. Review of evolving etiologies, implications and treatment strategies for the superior vena cava syndrome. Springerplus. 2016; 5: 229 Crossref PubMed Scopus (43) Google Scholar Although general anesthesia generally is considered high risk, it routinely is required for surgical biopsy, before resection, or for palliative treatments. The imminent risks of cardiovascular and respiratory collapse during induction of general anesthesia pose a real challenge for the anesthesiologist, and may require extracorporeal membrane oxygenation (ECMO) perioperativelt to safely manage patients with SVC syndrome.

HEMOPTYSIS SECONDARY TO SUPERIOR VENA CAVA SYNDROME

SESSION TITLE: Tuesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/22/2019 01:00 PM - 02:00 PM INTRODUCTION: Superior Vena Cava (SVC) syndrome is caused by obstruction of the SVC, impeding venous drainage into the right atrium. SVC syndrome is responsible for a rare subset of acute upper gastrointestinal bleeding from downhill esophageal varices.(1) We present a case of hemoptysis thought to be due to bronchial vein bleeding by a similar mechanism. CASE PRESENTATION: A 23 year old male with end stage renal disease on chronic hemodialysis presented with hematemesis. He had severe facial swelling, cervical plethora and peak airway pressures greater than 50. Emergent esophagogastroduodenoscopy demonstrated diffuse esophageal varices with no focal source of bleeding. Bronchoscopy was performed after frank blood was suctioned from the endotracheal tube, which revealed blood clots, diffuse airway hyperemia, and no focal source of bleeding. Computed tomography of chest and abdomen demonstrated total occlusion of the SVC with enlarged azygous and hemiazygous veins as well as extensive chest wall and abdominal venous collaterals. He did not have underlying liver pathology or portal hypertension. The patient underwent venoplasty and stenting of the SVC with restoration of SVC patency. His facial and cervical plethora resolved, and there was no further hemoptysis or hematemesis. DISCUSSION: Although SVC syndrome is classically described by malignancies that cause direct mass effect on the SVC, our patient is an example of a growing subset of SVC syndrome caused by catheter associated SVC stenosis. SVC obstruction forces blood to return to the heart via the azygous vein, hemiazygous vein, and mediastinal collaterals, resulting in the formation of downhill varices in the esophagus. (1,2) Although the mechanism for hemoptysis in SVC syndrome is not well described, ulceration or rupture of bronchial vein varices in patients with mitral stenosis (MS) has been used to explain hemoptysis in the absence of acute pulmonary edema or pulmonary infarction.(3) Injection studies in the autopsy specimens of patients with MS showed engorged bronchial vein varices from increased left atrial pressure and reversal of blood flow from the pulmonary circulation into the bronchial veins and into the right side of the heart via the azygos system.(3) In our patient, increased hydrostatic pressure from SVC occlusion and intrathoracic pressures from positive pressure ventilation likely led to microruptures in the bronchial veins causing hemoptysis. CONCLUSIONS: Catheter-associated SVC stenoses are becoming a more frequent cause of SVC syndrome. Chronic fluid build-up in the venous system can result in complications such as downhill esophageal and bronchial vein distension. Diagnosis should be considered when patients present with upper gastrointestinal bleeding or hemoptysis and the classic symptoms of SVC syndrome. Reference #1: Calderwood AH, Mishkin DS. Downhill esophageal varices caused by catheter-related thrombosis. Clin Gastroenterol Hepatol. 2008;6(1):e1. Reference #2: Felson, B. and Lessure, A.P. “Downhill” varices of the esophagus. Dis Chest. 1964; 46: 740–746 Reference #3: Schwartz R, Myerson RM, Lawrence T, Nichols HT. Mitral stenosis, massive pulmonary hemorrhage, and emergency valve replacement. N Engl J Med. 1966;275(14):755-8. DISCLOSURES: No relevant relationships by Meredith Greer, source=Web Response No relevant relationships by William Hunt, source=Web Response No relevant relationships by Jeeyon Rim, source=Admin input No relevant relationships by Manasi Tannu, source=Web Response

Síndrome de Veia Cava Superior: Relato de Caso

A Síndrome de Veia Cava Superior (SVCS) ocorre quando há obstrução da veia cava superior. As causas mais comuns da SVCS são as malignidades, sendo o câncer de pulmão do subtipo histológico de pequenas células a segunda principal causa. Os autores descrevem um caso de síndrome de veia cava superior por carcinoma neuroendócrino de pequenas células (tipo oat cell) em uma paciente tabagista com queixa de tosse, dispneia, edema e pletora facial. O alívio dos sintomas obstrutivos representa o tratamento inicial. A radioterapia não deve ser indicada empiricamente, já que requer o diagnóstico histológico de malignidade.

Management of superior vena cava syndrome in critically ill cancer patients.

The purpose of this study is to describe the management and outcome of critically ill cancer patients with Superior Vena Cava Syndrome (SVCS). All cancer patients admitted to the medical intensive care unit (ICU) of the Saint-Louis University Hospital for a SVCS between January 2004 and December 2016 were included. Of the 50 patients included in the study, obstruction of the superior vena cava was partial in two-thirds of the cases and complete in one-third. Pleural effusion was reported in two-thirds of the patients, pulmonary atelectasis in 16 (32%), and pulmonary embolism in five (10%). Computed tomography of the chest showed upper airway compression in 18 (36%) cases, while echocardiography revealed 22 (44%) pericardial effusions. The causes of SVCS were diagnosed one (0-3) day after ICU admission, using interventional radiology procedures in 70% of the cases. Thirty (60%) patients had hematological malignancies, and 20 (40%) had solid tumors. Fifteen (30%) patients required invasive mechanical ventilation, seven (14%) received vasopressors, and renal replacement therapy was implemented in three (6%). ICU, in-hospital, and 6-month mortality rates were 20, 26, and 48%, respectively. The cause of SVCS was the only factor independently associated with day 180 mortality by multivariate analysis. Patients with hematological malignancies had a lower mortality than those with solid tumors (27 versus 80%) (odds ratio 0.12, 95% confidence interval (0.02-0.60), p<0.01). Airway obstruction and pleural and pericardial effusions contributed to the unstable condition of cancer patients with SVCS. The vital prognosis of SVCS was mainly related to the underlying diagnosis.

Superior vena cava syndrome: Clinical considerations

BackgroundThe superior vena cava syndrome (SVCS) is a rare pathological process caused by the superior vena cava obstruction (SVCO). AimTo know the main causes of SVCS in a third level hospital. Material and methodsObservational, prospective and descriptive study in 31 patients with SVCS treated between June 2013 and December 2014. Yale, Stanford scores and tumour biopsy were obtained at diagnosis. ResultsThe main causes of SVCS were malignant tumours: lung cancer (22.5%) and lymphoma (16.1%). For lung cancer, the most common was non small cells (57.1%) and lymphoma was non-Hodgkin (80%). ConclusionsThe main causes of SVCS are advanced malignant tumours like lung cancer and lymphomas, benign obstruction causes are relatively rare.

PUB095 Computed Tomography Imaging of Superior Vena Cava Involvement in T4-Classed Lung Cancer

Superior vena cava (SVC) can be involved in many ways in patients with lung cancer. This latter is considered to be the most frequent cause of SVC syndrome which is a medical emergency requiring prompt evaluation and treatment. The SVC syndrome can reveal the disease or can be discovered on computed tomography (CT) of the chest. The objectives of our study are to specify CT characteristics of SVC involvement in T4-classed lung cancer and to estimate the frequency of its total obstruction in this patients category. Retrospective review of CT scans of 177 consecutive patients with T4-classed lung cancer, newly and fully diagnosed in our institution during the year 2015. All CT examinations were performed after contrast agent administration. Only patients with mediastinal involvement were retained. Every aspect of SVC involvement was noticed separately. Among the 177 patients, mediastinal invasion was observed in 132 cases (74.5%). SVC was involved in 32 cases (24%). Lung cancer was located on the right side in 91% of cases. The involvement included: - A contact with the tumor with loss of the fat layer (n= 7) - An inclusion of the vessel in the tumoral mass with narrowing of the lumen (n=17) - An intraluminal tumoral bud (n=8) - A complete obliteration (n= 6) Collateral venous circulation was observed in 8 cases. Adenocarcinoma and small cell lung cancer were the most frequent histological types responsible for SVC involvement Clinical signs of SVC syndrome were obvious in only 6 patients. Superior vena cava involvement is quite frequent in advanced stage of lung cancer. However, the total tumoral obstruction of this vessel is rare. CT helps defining the mechanism and the severity of the SVC involvement.

A Case of Malignant Superior Vena Cava Syndrome Presenting as Syncope

SESSION TITLE: Student/Resident Case Report Poster - Disorders of the Mediastinum SESSION TYPE: Student/Resident Case Report Poster PRESENTED ON: Tuesday, October 25, 2016 at 01:30 PM - 02:30 PM INTRODUCTION: Superior Vena Cava Syndrome (SVCS) is a constellation of clinical symptoms and signs caused by either extrinsic compression or SVC thrombosis. Lung Cancer is the most common cause of SVCS. We present an uncommon case of malignant SVCS presenting with syncope. CASE PRESENTATION: A 55-year-old male presented to the emergency department after passing out in his niece’s parked car. He had lightheadedness and blurred vision before the witnessed, one minute, syncopal episode. He denied any previous history of syncope, heart disease or seizure. He endorsed having progressive neck pain and swelling over the past six months, a twenty-two pounds weight loss over the past year and a forty year pack history of tobacco smoking. Physical examination revealed normal vital signs except for heart rate of 105 bpm. Multiple solid, non-mobile masses were noted on the neck and the chest wall (Figure 1). Distended superficial veins were observed on the diffusely swollen right upper extremity. Significant clubbing was noted in all extremities. Routine syncope workup was unremarkable. CT scan of the neck and chest with intravenous contrast showed the presence of a speculated nodule in the right upper lobe, a large right neck mass, evidence of venous collaterals and soft tissue edema, and extensive upper mediastinal lymphadenopathy significantly narrowing the SVC (Figure 2). Surgical incisional biopsy of a chest wall mass was performed. Histology and immunohistochemistry studies (Figure 2) along with the clinical and radiographic findings confirmed the diagnosis of malignant SVCS secondary to stage IV (T4 N3 M1) poorly differentiated adenocarcinoma of lung origin. Imaging of the brain revealed no evidence of metastases. The patient was hemodynamically stable and with no significant cardiorespiratory compromise. Combined palliative treatment with radiation and chemotherapy was elected. Two years later, the patient continues to maintain good functional capacity. DISCUSSION: This is a case of malignant SVCS presenting uncommonly as syncope. Proper diagnosis, grading, and staging of malignant SVCS are key to its management. Worrisome signs like laryngeal or cerebral edema might warrant an emergent placement of an endovascular stent. Our patient’s SVCS was secondary to stage IV lung adenocarcinoma and was severe based on proposed grading system by Yu et al. Patient has responded well to palliative radiation and chemotherapy. CONCLUSIONS: Accurate diagnosis and staging of SVCS are necessary and help determine the modality and goal of therapy. Reference #1: Wilson, L. D. (2007, 05). Superior Vena Cava Syndrome with Malignant Causes. NEJM, 356(18), 1862-1869. Reference #2: Yu, J. B. (2008, 08). Superior Vena Cava Syndrome—A Proposed Classification System and Algorithm for Management. Journal of Thoracic Oncology, 3(8), 811-814. DISCLOSURE: The following authors have nothing to disclose: Mahrous Abo Hassan, Yahya Kurdi, Xiaoyi Yu, Eric Speakman, Rupesh Raina, Harish Kakarala, Osei-Tutu Owusu No Product/Research Disclosure Information

Superior vena cava syndrome idiopathic: case report

The Superior Vena Cava Syndrome(SVCS) is a set of signs and symptoms resulting from venous stasis caused by the obstruction of the superior vena cava(VCS) due to thrombosis, extrinsic compression or direct invasion of the vein. The most common causes of SVCS are malignant, lung cancer being the leading cause. There are few reports in the literature on SVCS of benign etiology. We describe a case of SVCS of idiopathic origin, where the author studied and excluded all benign etiologies of SVCS, until arriving at etiological diagnosis.

Unexpected cause of superior vena cava syndrome.

Superior vena cava syndrome (SVCS) may be caused by an extrinsecal vessel compressing or by thrombosis. Symptoms are edema of the face and arms and development of swollen collateral veins on the front of the chest wall, shortness of breath, coughing, headache and stridor. Bronchogenic carcinoma, Burkitt’s lymphoma, lymphoblastic lymphomas, pre-T-cell lineage acute lymphoblastic leukemi, and other acute leukemia are the main cause of SVCS (1).

Percutaneous management of chronic central venous occlusive disease.

Stenosis or occlusion of the central veins and/or vena cava can cause painful and debilitating symptoms for affected patients. Superior vena cava syndrome (SVCS) can develop acutely or progressively from external compression or intrinsic obstruction. The clinical signs and symptoms result from venous hypertension and reduced blood flow in the superior vena cava (SVC) or central veins emptying into the SVC. Depending on the anatomic location of the narrowing, clinical symptoms, and presentation will vary. Clinical signs include cyanosis, plethora, distention of subcutaneous veins, and edema of the upper extremities, head and neck. Edema may compromise laryngeal or pharyngeal function, causing dyspnea, stridor, cough, hoarseness, and dysphagia.1 Although there may be symptom overlap with congestive heart failure, a physical examination will usually delineate between the two diagnoses. The etiology of SVCS varies and can be broadly grouped into benign and malignant causes, with most strictures of the caval system and venous tributaries being malignant.2 3 Non–small-cell lung cancer (NSCLC) is the most common malignant cause of SVCS, followed by small-cell lung cancer (SCLC) and non-Hodgkin lymphoma.4 The most common causes of benign venous stenosis involve the presence of an indwelling intravascular device (i.e., catheters, pacemaker/defibrillators, ports). Arteriovenous fistula related obstruction, mediastinal fibrosis, and prior thoracic external bean radiation therapy are additional benign causes. Treatment of central venous occlusions depends on the etiology and clinical presentation. The ultimate goal of therapy is to correct the obstruction and alleviate the symptoms. Conservative measures depend on the etiology and include limb elevation, steroids, anticoagulation, chemotherapy and/or radiation therapy, and diuretics.5 Interventional therapies include surgical bypass and/or endovascular stent placement. Guide wire recanalization and endovascular stenting is a minimally invasive procedure that can be performed on an outpatient basis with standard equipment available in an angiography suite. The procedure below describes the authors approach to treating chronic central venous occlusive disease.

Urothelial Superior Vena Cava Syndrome with Limited Response to Radiation Therapy.

Radiation therapy (RT) is the standard of care for cases of superior vena cava (SVC) syndrome secondary to metastatic adenopathy. Histologies vary in radiosensitivity and response time, making alternative therapies such as chemotherapy and/or intravenous stenting preferable alternative options for certain diagnoses. Metastatic urothelial carcinoma is a particularly rare cause of SVC syndrome with only 3 cases reported in the literature. Consequently, optimal management remains challenging, particularly in cases of high tumor burden. Here we present a case of highly advanced metastatic urothelial cancer with SVC syndrome and tracheal compression. The patient started urgent RT but expired midway through her treatment course due to systemic progression of disease, requiring SVC and tracheal stenting. The authors review the literature including discussion of the few other known cases of SVC syndrome due to urothelial carcinoma and a review of this histology's response to RT. This experience suggests, that in cases of SVC syndrome with widespread advanced disease, stenting and chemotherapy with or without RT may be the most important initial treatment plan, depending on goals of care.

Superior vena cava syndrome caused by a malignant tumor: a retrospective single-center analysis of 124 cases

Superior vena cava syndrome (SVCS) results from compression of the superior vena cava. SVCS is an emergency requiring immediate diagnosis and treatment. We hypothesized that the outcome of patients (pts.) admitted during regular work hours may differ from that of pts. admitted on weekends. From 1992 to 2011, we analyzed all pts. admitted with SVCS due to a malignancy. Clinical outcome was analyzed, focusing on the work-up of pts. hospitalized on a weekend compared with those hospitalized during the week. One hundred and twenty-four pts. with malignant causes of SVCS were analyzed. Causes were as follows: small cell lung cancer (SCLC) 28.2%, non-small cell lung cancer 25%, non-Hodgkin's lymphoma 25%, metastasis of other malignant tumors 19.4% and Hodgkin's disease 2.4%. Sixty-five percent of pts. were admitted during the week and 35% on a weekend. Sixty-one percent received chemotherapy, 24% radiation, 4% radiochemotherapy, 9% palliative treatment and 2% no treatment at all. No difference in choice of treatment between pts. admitted on a weekday versus weekend was seen. Response was as follows: 7 pts. complete remission, 20 pts. partial response, 38 pts. progressive disease, 3 pts. NC and 15 pts. died. Overall response rate was as follows: Hodgkin's disease 100%, non-Hodgkin's lymphoma 29%, SCLC 22.8%, non-small cell lung cancer 9.6% and metastatic cancer 16.6%. Only 2 of the 34 pts. with relapsing carcinoma responded. None of the pts. died due to SVCS. The outcome of pts. with SVCS is not dependent on the day of admission (weekend or weekday) but is related to underlying disease in the setting of a tertiary care center.

Superior vena cava syndrome caused by a swollen absorbable haemostat after repair of ischaemic mitral regurgitation

Surgicel, an absorbable haemostat, is widely used in cardiovascular surgery. An 81-year-old woman, who was diagnosed with ischaemic mitral regurgitation, underwent mitral valve plasty and coronary artery bypass grafting. On postoperative day two, her superior vena cava (SVC) pressure gradually rose to 38 mmHg and she developed low output syndrome. Emergent surgery revealed that the cause of SVC syndrome was external compression from a haematoma at the posterior surface of the SVC, which formed around the Surgicel.

An Unusual Case of Superior Vena Cava Syndrome Caused by the Intravascular Invasion of an Invasive Thymoma

Superior vena cava syndrome (SVCS) is usually caused by extrinsic compression or invasion of the superior vena cava (SVC) by malignant tumors involving mediastinal structures. Although thymomas are well-known causes of SVCS, cases of SVCS caused by malignant thymomas protruding into adjacent vessels draining the SVC with thrombosis have been very rarely reported worldwide. We experienced a 39-year-old female patient with SVCS that developed after the direct invasion of the left brachiocephalic vein (LBCV) and SVC by an anterior mediastinal mass with a high maximum standardized uptake value on the chest computed tomography (CT) and positron emission tomography-CT. Based on these results, she underwent en bloc resection of the tumor, including removal of the involved vessels, and was eventually diagnosed as having a type B2 thymoma permeating into the LBCV and SVC. We present this case as a very rare form of SVCS caused by an invasive thymoma.