Superior vena cava syndrome after pacemaker implantation treated with direct oral anticoagulation

Background Superior Vena Cava (SVC) syndrome, is a quite rare but serious complication after pacemaker lead implantation; most patients are asymptomatic due to the development of adequate venous collateral circulation. Case presentation We report a case of a 75-year-old woman who developed SVC syndrome after transvenous pacemaker implantation with complete resolution of the thrombosis after 3 months of oral anticoagulation. Conclusions Generally other causes as malignancy are considered to be the most common etiology of SVC syndrome, but benign iatrogenic causes, mainly intravascular devices (central vein catheters, cardiac defibrillators and pacemaker wires), are becoming increasingly common. Procedures performed on venous vasculature, causing a possible intimal injury or vein stenosis, provoked by transvenous leads, seem to be the most reasonable explanation for the observed complication.

296 Case Report: Pacemaker Lead-Induced Fibrosis Resulting in Right Atrial and Tricuspid Stenosis Managed with An Open Surgical Approach

Pacemaker leads can result in localised inflammation and, over time, fibrosis. Rarely, this can significantly alter the anatomy of the heart and impair cardiac function. In this case, a fifty-year-old female had undergone pacemaker placement in her teens having experienced symptomatic bradycardia. Due to pacemaker pocket erosion, she had undergone a lead extraction where lead fragments had been left in-situ. Years after a new generator and leads were placed, she presented with symptoms of proximal venous congestion and superior vena cava (SVC) syndrome. A venogram demonstrated completely occluded brachiocephalic and innominate veins with significant adjacent venous collateralization. Computed tomography showed partial obstruction of the SVC and tricuspid stenosis. Initially, a decision was made not to intervene. After developing abdominal distension, she was diagnosed with hepatic congestion and cirrhosis secondary to elevated right sided pressures and right atrial congestion due to tricuspid stenosis. It was concluded that the patient’s symptoms were the result of occluded proximal veins, SVC syndrome, and functional tricuspid stenosis, all of which were likely the result of fibrotic tissue secondary to pacemaker lead-induced inflammation. Due to the severity of her symptoms, the patient accepted the risks associated with surgical management. Intra-operatively, electrocautery was used to debride the fibrotic tissue inhibiting the leaflets of the tricuspid valve. This worked to great effect and additional valve repair/replacement was not necessary. Whilst the patient has been left with SVC syndrome, her tricuspid stenosis symptoms are greatly improved. To our knowledge, such a case has not been previously described.

SUPERIOR VENA CAVA SYNDROME SECONDARY TO ADULT T-CELL LYMPHOBLASTIC LYMPHOMA

Superior vena cave (SVC) obstruction can be a substantial contributor to morbidity and mortality in cancer and non-cancer patients. It is currently known to be almost exclusively secondary to malignancy, most frequently lung cancer. A case of SVC syndrome presenting with worsening right-sided chest pain, shortness of breath, facial swelling, neck distension, and cough developing over a period of 12 days is reported. The approach to diagnosis included imaging studies and tissue diagnosis. CT scan of the chest revealed a large right pericardial mass, hilar infrahilar adenopathy, moderate increased right base posterior effusion, and compressive atelectasis. A mediastinal lymph node CT guided core biopsy subsequently revealed adult T-cell lymphoblastic lymphoma. Due to rapid symptom progression, the patient was started on hyper-CVAD regimen and tumor lysis prophylaxis. The etiology, diagnosis, and treatment modalities of the SVC syndrome are discussed further in detail. Given the wide range of symptom severity, identifying and treating severe SVC syndrome promptly can be critical to patient outcomes.

A144 ISOLATED UPPER ESOPHAGEAL VARICES DUE TO SUPERIOR VENA CAVA SYNDROME: A CASE OF UPPER GI BLEEDING

Background Esophageal varices represent a cause of upper gastrointestinal bleeding (UGI) with significant associated morbidity and mortality. The majority of variceal bleeds are due to portal hypertension and cirrhosis. In some very rare cases isolated upper esophageal varices may occur. These present management challenges, as typical management options for varices in cirrhosis are not applicable due to differences in pathophysiology. Infusions to decrease portal pressure and TIPS procedures may be used in cirrhosis, but are not effective in patients with SVC syndrome. Aims We present a literature review on isolated upper esophageal varices due to SVC syndrome, and present a case that provides further confirmation that surgical vascular reconstruction is a viable option in these cases. Methods The case of a 49 year old female with variceal hemorrhage secondary to SVC syndrome was reviewed. A search of the literature was undertaken using the terms “varices + superior vena cava syndrome” and “upper esophageal varices + management.” Results Overall, the majority of cases of isolated upper esophageal varices are secondary to SVC syndrome. They typically occur in cases of benign, rather than malignant SVC syndrome. Only one previous case was reported to be managed with surgical vascular reconstruction. We present the case of a 49-year old woman with SVC syndrome secondary to a thrombosed dialysis line who went on to develop isolated upper esophageal varices and large volume UGI bleeding. The pathophysiology of these “downhill” varices differs enough from portal hypertension that typical variceal management options may not be appropriate. Given a previous history of unsuccessful balloon angiography and the risk associated with variceal bleeding, she was taken back to the operating room for surgical vascular reconstruction. A surgical bypass was performed. She did well post-surgery and was discharged. She had no recurrence of bleeding and had a resolution of her edema at 6 month follow up. Conclusions Isolated upper esophageal varices are a potentially serious complication of SVC syndrome, and should be considered in cases of upper GI bleeding in patients with dialysis lines as they can have limited management options. This case was successfully managed by surgical vascular reconstruction, which represents an important treatment option in these difficult cases. Funding Agencies None

Combined cut down and endovascular retrieval of orphaned ventriculoatrial shunt with stenting of chronic superior vena cava occlusion

Revascularization of the superior vena cava (SVC) in the context of symptomatic luminal obstruction is a therapeutic intervention performed for SVC syndrome of benign or malignant etiology. Venous occlusion can preclude future access and cause symptoms ranging from mild chest discomfort to the more serious effects of SVC syndrome. This case report demonstrates the treatment of a novel case of SVC syndrome arising from a previously placed SVC stent. An intravascular, extraluminal orphaned ventriculoatrial shunt was used to go through the SVC but around the existing lumen-limiting stent to place a new larger stent for revascularization. This case highlights the need for an innovative approach for complex foreign body retrieval and treatment of chronic SVC occlusion.

Superior vena cava syndrome during veno-venous extracorporeal membrane oxygenation for COVID-19

Superior vena cava (SVC) syndrome is typically associated with malignant tumors obstructing the SVC, but as many as 40% of cases have other etiologies. SVC obstruction was previously described during veno-venous extracorporeal membrane oxygenation therapy (VV ECMO) in children. In this report, we describe a woman with adult respiratory distress syndrome resulting from infection with coronavirus-19 who developed SVC syndrome during VV ECMO. A dual-lumen ECMO cannula was inserted in the right internal jugular vein, but insufficient ECMO circuit flow, upper body edema, and signs of hypovolemic shock were observed. This clinical picture resolved when the right internal jugular vein was decannulated in favor of bilateral femoral venous cannulae. Our report demonstrates that timely recognition of clinical signs and symptoms led to the appropriate diagnosis of an uncommon ECMO complication.